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We are very delighted that you have shown interest in the Foundation. Data protection is of a particularly high priority for the management of the International CML Foundation. The use of the Internet pages of the International CML Foundation is possible without any indication of personal data; however, if a data subject wants to use special services via our website, processing of personal data could become necessary. If the processing of personal data is necessary and there is no statutory basis for such processing, we generally obtain consent from the data subject.

The processing of personal data, such as the name, address, e-mail address, or telephone number of a data subject shall always be in line with the General Data Protection Regulation (GDPR), and in accordance with the country-specific data protection regulations applicable to the International CML Foundation. By means of this data protection declaration, our organisation would like to inform the general public of the nature, scope, and purpose of the personal data we collect, use and process. Furthermore, data subjects are informed, by means of this data protection declaration, of the rights to which they are entitled.

As the controller, the International CML Foundation has implemented numerous technical and organizational measures to ensure the most complete protection of personal data processed through this website. However, Internet-based data transmissions may in principle have security gaps, so absolute protection may not be guaranteed. For this reason, every data subject is free to transfer personal data to us via alternative means, e.g. by telephone.

1. Definitions

The data protection declaration of the International CML Foundation is based on the terms used by the European legislator for the adoption of the General Data Protection Regulation (GDPR). Our data protection declaration should be legible and understandable for the general public, as well as our customers and business partners. To ensure this, we would like to first explain the terminology used.

In this data protection declaration, we use, inter alia, the following terms:

a)    Personal data Personal data means any information relating to an identified or identifiable natural person (“data subject”). An identifiable natural person is one who can be identified, directly or indirectly, in particular by reference to an identifier such as a name, an identification number, location data, an online identifier or to one or more factors specific to the physical, physiological, genetic, mental, economic, cultural or social identity of that natural person.

b)    Data subject Data subject is any identified or identifiable natural person, whose personal data is processed by the controller responsible for the processing.

c)    Processing Processing is any operation or set of operations which is performed on personal data or on sets of personal data, whether or not by automated means, such as collection, recording, organisation, structuring, storage, adaptation or alteration, retrieval, consultation, use, disclosure by transmission, dissemination or otherwise making available, alignment or combination, restriction, erasure or destruction.

d)    Restriction of processing Restriction of processing is the marking of stored personal data with the aim of limiting their processing in the future.

e)    Profiling Profiling means any form of automated processing of personal data consisting of the use of personal data to evaluate certain personal aspects relating to a natural person, in particular to analyse or predict aspects concerning that natural person's performance at work, economic situation, health, personal preferences, interests, reliability, behaviour, location or movements.

f)   Pseudonymisation Pseudonymisation is the processing of personal data in such a manner that the personal data can no longer be attributed to a specific data subject without the use of additional information, provided that such additional information is kept separately and is subject to technical and organisational measures to ensure that the personal data are not attributed to an identified or identifiable natural person.

g)    Controller or controller responsible for the processing Controller or controller responsible for the processing is the natural or legal person, public authority, agency or other body which, alone or jointly with others, determines the purposes and means of the processing of personal data; where the purposes and means of such processing are determined by Union or Member State law, the controller or the specific criteria for its nomination may be provided for by Union or Member State law.

h)    Processor Processor is a natural or legal person, public authority, agency or other body which processes personal data on behalf of the controller.

i)   Recipient Recipient is a natural or legal person, public authority, agency or another body, to which the personal data are disclosed, whether a third party or not. However, public authorities which may receive personal data in the framework of a particular inquiry in accordance with Union or Member State law shall not be regarded as recipients; the processing of those data by those public authorities shall be in compliance with the applicable data protection rules according to the purposes of the processing.

j)   Third party Third party is a natural or legal person, public authority, agency or body other than the data subject, controller, processor and persons who, under the direct authority of the controller or processor, are authorised to process personal data.

k)    Consent Consent of the data subject is any freely given, specific, informed and unambiguous indication of the data subject's wishes by which he or she, by a statement or by a clear affirmative action, signifies agreement to the processing of personal data relating to him or her.

2. Name and Address of the controller

Controller for the purposes of the General Data Protection Regulation (GDPR), other data protection laws applicable in Member states of the European Union and other provisions related to data protection is:

International CML Foundation

20 Eversley Road, Bexhill-on-Sea

TN40 1HE East Sussex

UK

Email: info@cml-foundation.org

Website: www.cml-foundation.org

3. Cookies

The Internet pages of the International CML Foundation use cookies. Cookies are text files that are stored in a computer system via an Internet browser.

Many Internet sites and servers use cookies. Many cookies contain a so-called cookie ID. A cookie ID is a unique identifier of the cookie. It consists of a character string through which Internet pages and servers can be assigned to the specific Internet browser in which the cookie was stored. This allows visited Internet sites and servers to differentiate the individual browser of the dats subject from other Internet browsers that contain other cookies. A specific Internet browser can be recognized and identified using the unique cookie ID.

Through the use of cookies, the International CML Foundation can provide the users of this website with more user-friendly services that would not be possible without the cookie setting.

By means of a cookie, the information and offers on our website can be optimized with the user in mind. Cookies allow us, as previously mentioned, to recognize our website users. The purpose of this recognition is to make it easier for users to utilize our website. The website user that uses cookies, e.g. does not have to enter access data each time the website is accessed, because this is taken over by the website, and the cookie is thus stored on the user's computer system. Another example is the cookie of a shopping cart in an online shop. The online store remembers the articles that a customer has placed in the virtual shopping cart via a cookie.

The data subject may, at any time, prevent the setting of cookies through our website by means of a corresponding setting of the Internet browser used, and may thus permanently deny the setting of cookies. Furthermore, already set cookies may be deleted at any time via an Internet browser or other software programs. This is possible in all popular Internet browsers. If the data subject deactivates the setting of cookies in the Internet browser used, not all functions of our website may be entirely usable.

4. Collection of general data and information

The website of the International CML Foundation collects a series of general data and information when a data subject or automated system calls up the website. This general data and information are stored in the server log files. Collected may be (1) the browser types and versions used, (2) the operating system used by the accessing system, (3) the website from which an accessing system reaches our website (so-called referrers), (4) the sub-websites, (5) the date and time of access to the Internet site, (6) an Internet protocol address (IP address), (7) the Internet service provider of the accessing system, and (8) any other similar data and information that may be used in the event of attacks on our information technology systems.

When using these general data and information, the International CML Foundation does not draw any conclusions about the data subject. Rather, this information is needed to (1) deliver the content of our website correctly, (2) optimize the content of our website as well as its advertisement, (3) ensure the long-term viability of our information technology systems and website technology, and (4) provide law enforcement authorities with the information necessary for criminal prosecution in case of a cyber-attack. Therefore, the International CML Foundation analyzes anonymously collected data and information statistically, with the aim of increasing the data protection and data security of our organisation, and to ensure an optimal level of protection for the personal data we process. The anonymous data of the server log files are stored separately from all personal data provided by a data subject.

5. Registration on our website

The data subject has the possibility to register on the website of the controller with the indication of personal data. Which personal data are transmitted to the controller is determined by the respective input mask used for the registration. The personal data entered by the data subject are collected and stored exclusively for internal use by the controller, and for his own purposes. The controller may request transfer to one or more processors (e.g. a parcel service) that also uses personal data for an internal purpose which is attributable to the controller.

By registering on the website of the controller, the IP address—assigned by the Internet service provider (ISP) and used by the data subject—date, and time of the registration are also stored. The storage of this data takes place against the background that this is the only way to prevent the misuse of our services, and, if necessary, to make it possible to investigate committed offenses. Insofar, the storage of this data is necessary to secure the controller. This data is not passed on to third parties unless there is a statutory obligation to pass on the data, or if the transfer serves the aim of criminal prosecution.

The registration of the data subject, with the voluntary indication of personal data, is intended to enable the controller to offer the data subject contents or services that may only be offered to registered users due to the nature of the matter in question. Registered persons are free to change the personal data specified during the registration at any time, or to have them completely deleted from the data stock of the controller.

The data controller shall, at any time, provide information upon request to each data subject as to what personal data are stored about the data subject. In addition, the data controller shall correct or erase personal data at the request or indication of the data subject, insofar as there are no statutory storage obligations. The entirety of the controller’s employees are available to the data subject in this respect as contact persons.

6. Subscription to our newsletters

On the website of the International CML Foundation, users are given the opportunity to subscribe to our organisation's newsletter. The input mask used for this purpose determines what personal data are transmitted, as well as when the newsletter is ordered from the controller.

The International CML Foundation informs its customers and business partners regularly by means of a newsletter about organisation offers. The organisation's newsletter may only be received by the data subject if (1) the data subject has a valid e-mail address and (2) the data subject registers for the newsletter shipping. A confirmation e-mail will be sent to the e-mail address registered by a data subject for the first time for newsletter shipping, for legal reasons, in the double opt-in procedure. This confirmation e-mail is used to prove whether the owner of the e-mail address as the data subject is authorized to receive the newsletter.

During the registration for the newsletter, we also store the IP address of the computer system assigned by the Internet service provider (ISP) and used by the data subject at the time of the registration, as well as the date and time of the registration. The collection of this data is necessary in order to understand the (possible) misuse of the e-mail address of a data subject at a later date, and it therefore serves the aim of the legal protection of the controller.

The personal data collected as part of a registration for the newsletter will only be used to send our newsletter. In addition, subscribers to the newsletter may be informed by e-mail, as long as this is necessary for the operation of the newsletter service or a registration in question, as this could be the case in the event of modifications to the newsletter offer, or in the event of a change in technical circumstances. There will be no transfer of personal data collected by the newsletter service to third parties. The subscription to our newsletter may be terminated by the data subject at any time. The consent to the storage of personal data, which the data subject has given for shipping the newsletter, may be revoked at any time. For the purpose of revocation of consent, a corresponding link is found in each newsletter. It is also possible to unsubscribe from the newsletter at any time directly on the website of the controller, or to communicate this to the controller in a different way.

7. Newsletter-Tracking

The newsletter of the International CML Foundation contains so-called tracking pixels. A tracking pixel is a miniature graphic embedded in such e-mails, which are sent in HTML format to enable log file recording and analysis. This allows a statistical analysis of the success or failure of online marketing campaigns. Based on the embedded tracking pixel, the International CML Foundation may see if and when an e-mail was opened by a data subject, and which links in the e-mail were called up by data subjects.

Such personal data collected in the tracking pixels contained in the newsletters are stored and analyzed by the controller in order to optimize the shipping of the newsletter, as well as to adapt the content of future newsletters even better to the interests of the data subject. These personal data will not be passed on to third parties. Data subjects are at any time entitled to revoke the respective separate declaration of consent issued by means of the double-opt-in procedure. After a revocation, these personal data will be deleted by the controller. The International CML Foundation automatically regards a withdrawal from the receipt of the newsletter as a revocation.

8. Contact possibility via the website

The website of the International CML Foundation contains information that enables a quick electronic contact to the Foundation, as well as direct communication with us, which also includes a general address of the so-called electronic mail (e-mail address). If a data subject contacts the controller by e-mail or via a contact form, the personal data transmitted by the data subject are automatically stored. Such personal data transmitted on a voluntary basis by a data subject to the data controller are stored for the purpose of processing or contacting the data subject. There is no transfer of this personal data to third parties.

9. Routine erasure and blocking of personal data

The data controller shall process and store the personal data of the data subject only for the period necessary to achieve the purpose of storage, or as far as this is granted by the European legislator or other legislators in laws or regulations to which the controller is subject to.

If the storage purpose is not applicable, or if a storage period prescribed by the European legislator or another competent legislator expires, the personal data are routinely blocked or erased in accordance with legal requirements.

10. Rights of the data subject

a) Right of confirmation Each data subject shall have the right granted by the European legislator to obtain from the controller the confirmation as to whether or not personal data concerning him or her are being processed. If a data subject wishes to avail himself of this right of confirmation, he or she may, at any time, contact any employee of the controller.

b) Right of access Each data subject shall have the right granted by the European legislator to obtain from the controller free information about his or her personal data stored at any time and a copy of this information. Furthermore, the European directives and regulations grant the data subject access to the following information:

  • the purposes of the processing;
  • the categories of personal data concerned;
  • the recipients or categories of recipients to whom the personal data have been or will be disclosed, in particular recipients in third countries or international organisations;
  • where possible, the envisaged period for which the personal data will be stored, or, if not possible, the criteria used to determine that period;
  • the existence of the right to request from the controller rectification or erasure of personal data, or restriction of processing of personal data concerning the data subject, or to object to such processing;
  • the existence of the right to lodge a complaint with a supervisory authority;
  • where the personal data are not collected from the data subject, any available information as to their source;
  • the existence of automated decision-making, including profiling, referred to in Article 22(1) and (4) of the GDPR and, at least in those cases, meaningful information about the logic involved, as well as the significance and envisaged consequences of such processing for the data subject.

Furthermore, the data subject shall have a right to obtain information as to whether personal data are transferred to a third country or to an international organisation. Where this is the case, the data subject shall have the right to be informed of the appropriate safeguards relating to the transfer. If a data subject wishes to avail himself of this right of access, he or she may, at any time, contact any employee of the controller.

c) Right to rectification Each data subject shall have the right granted by the European legislator to obtain from the controller without undue delay the rectification of inaccurate personal data concerning him or her. Taking into account the purposes of the processing, the data subject shall have the right to have incomplete personal data completed, including by means of providing a supplementary statement. If a data subject wishes to exercise this right to rectification, he or she may, at any time, contact any employee of the controller.

d) Right to erasure (Right to be forgotten) Each data subject shall have the right granted by the European legislator to obtain from the controller the erasure of personal data concerning him or her without undue delay, and the controller shall have the obligation to erase personal data without undue delay where one of the following grounds applies, as long as the processing is not necessary:

  • The personal data are no longer necessary in relation to the purposes for which they were collected or otherwise processed.
  • The data subject withdraws consent to which the processing is based according to point (a) of Article 6(1) of the GDPR, or point (a) of Article 9(2) of the GDPR, and where there is no other legal ground for the processing.
  • The data subject objects to the processing pursuant to Article 21(1) of the GDPR and there are no overriding legitimate grounds for the processing, or the data subject objects to the processing pursuant to Article 21(2) of the GDPR.
  • The personal data have been unlawfully processed.
  • The personal data must be erased for compliance with a legal obligation in Union or Member State law to which the controller is subject.
  • The personal data have been collected in relation to the offer of information society services referred to in Article 8(1) of the GDPR.

If one of the aforementioned reasons applies, and a data subject wishes to request the erasure of personal data stored by the International CML Foundation, he or she may, at any time, contact any employee of the controller. An employee of International CML Foundation shall promptly ensure that the erasure request is complied with immediately. Where the controller has made personal data public and is obliged pursuant to Article 17(1) to erase the personal data, the controller, taking account of available technology and the cost of implementation, shall take reasonable steps, including technical measures, to inform other controllers processing the personal data that the data subject has requested erasure by such controllers of any links to, or copy or replication of, those personal data, as far as processing is not required. An employees of the International CML Foundation will arrange the necessary measures in individual cases.

e) Right of restriction of processing Each data subject shall have the right granted by the European legislator to obtain from the controller restriction of processing where one of the following applies:

  • The accuracy of the personal data is contested by the data subject, for a period enabling the controller to verify the accuracy of the personal data.
  • The processing is unlawful and the data subject opposes the erasure of the personal data and requests instead the restriction of their use instead.
  • The controller no longer needs the personal data for the purposes of the processing, but they are required by the data subject for the establishment, exercise or defence of legal claims.
  • The data subject has objected to processing pursuant to Article 21(1) of the GDPR pending the verification whether the legitimate grounds of the controller override those of the data subject.

If one of the aforementioned conditions is met, and a data subject wishes to request the restriction of the processing of personal data stored by the International CML Foundation, he or she may at any time contact any employee of the controller. The employee of the International CML Foundation will arrange the restriction of the processing.

f) Right to data portability Each data subject shall have the right granted by the European legislator, to receive the personal data concerning him or her, which was provided to a controller, in a structured, commonly used and machine-readable format. He or she shall have the right to transmit those data to another controller without hindrance from the controller to which the personal data have been provided, as long as the processing is based on consent pursuant to point (a) of Article 6(1) of the GDPR or point (a) of Article 9(2) of the GDPR, or on a contract pursuant to point (b) of Article 6(1) of the GDPR, and the processing is carried out by automated means, as long as the processing is not necessary for the performance of a task carried out in the public interest or in the exercise of official authority vested in the controller. Furthermore, in exercising his or her right to data portability pursuant to Article 20(1) of the GDPR, the data subject shall have the right to have personal data transmitted directly from one controller to another, where technically feasible and when doing so does not adversely affect the rights and freedoms of others. In order to assert the right to data portability, the data subject may at any time contact any employee of the International CML Foundation.

g) Right to object Each data subject shall have the right granted by the European legislator to object, on grounds relating to his or her particular situation, at any time, to processing of personal data concerning him or her, which is based on point (e) or (f) of Article 6(1) of the GDPR. This also applies to profiling based on these provisions. The International CML Foundation shall no longer process the personal data in the event of the objection, unless we can demonstrate compelling legitimate grounds for the processing which override the interests, rights and freedoms of the data subject, or for the establishment, exercise or defence of legal claims. If the International CML Foundation processes personal data for direct marketing purposes, the data subject shall have the right to object at any time to processing of personal data concerning him or her for such marketing. This applies to profiling to the extent that it is related to such direct marketing. If the data subject objects to the International CML Foundation to the processing for direct marketing purposes, the International CML Foundation will no longer process the personal data for these purposes. In addition, the data subject has the right, on grounds relating to his or her particular situation, to object to processing of personal data concerning him or her by the International CML Foundation for scientific or historical research purposes, or for statistical purposes pursuant to Article 89(1) of the GDPR, unless the processing is necessary for the performance of a task carried out for reasons of public interest. In order to exercise the right to object, the data subject may contact any employee of the International CML Foundation. In addition, the data subject is free in the context of the use of information society services, and notwithstanding Directive 2002/58/EC, to use his or her right to object by automated means using technical specifications.

h) Automated individual decision-making, including profiling Each data subject shall have the right granted by the European legislator not to be subject to a decision based solely on automated processing, including profiling, which produces legal effects concerning him or her, or similarly significantly affects him or her, as long as the decision (1) is not is necessary for entering into, or the performance of, a contract between the data subject and a data controller, or (2) is not authorised by Union or Member State law to which the controller is subject and which also lays down suitable measures to safeguard the data subject's rights and freedoms and legitimate interests, or (3) is not based on the data subject's explicit consent. If the decision (1) is necessary for entering into, or the performance of, a contract between the data subject and a data controller, or (2) it is based on the data subject's explicit consent, the International CML Foundation shall implement suitable measures to safeguard the data subject's rights and freedoms and legitimate interests, at least the right to obtain human intervention on the part of the controller, to express his or her point of view and contest the decision. If the data subject wishes to exercise the rights concerning automated individual decision-making, he or she may, at any time, contact any employee of the International CML Foundation.

i) Right to withdraw data protection consent Each data subject shall have the right granted by the European legislator to withdraw his or her consent to processing of his or her personal data at any time. If the data subject wishes to exercise the right to withdraw the consent, he or she may, at any time, contact any employee of the International CML Foundation.

11. Data protection provisions about the application and use of Facebook

On this website, the controller has integrated components of the enterprise Facebook. Facebook is a social network.

A social network is a place for social meetings on the Internet, an online community, which usually allows users to communicate with each other and interact in a virtual space. A social network may serve as a platform for the exchange of opinions and experiences, or enable the Internet community to provide personal or business-related information. Facebook allows social network users to include the creation of private profiles, upload photos, and network through friend requests.

The operating company of Facebook is Facebook, Inc., 1 Hacker Way, Menlo Park, CA 94025, United States. If a person lives outside of the United States or Canada, the controller is the Facebook Ireland Ltd., 4 Grand Canal Square, Grand Canal Harbour, Dublin 2, Ireland.

With each call-up to one of the individual pages of this Internet website, which is operated by the controller and into which a Facebook component (Facebook plug-ins) was integrated, the web browser on the information technology system of the data subject is automatically prompted to download display of the corresponding Facebook component from Facebook through the Facebook component. An overview of all the Facebook Plug-ins may be accessed under https://developers.facebook.com/docs/plugins/. During the course of this technical procedure, Facebook is made aware of what specific sub-site of our website was visited by the data subject.

If the data subject is logged in at the same time on Facebook, Facebook detects with every call-up to our website by the data subject—and for the entire duration of their stay on our Internet site—which specific sub-site of our Internet page was visited by the data subject. This information is collected through the Facebook component and associated with the respective Facebook account of the data subject. If the data subject clicks on one of the Facebook buttons integrated into our website, e.g. the "Like" button, or if the data subject submits a comment, then Facebook matches this information with the personal Facebook user account of the data subject and stores the personal data.

Facebook always receives, through the Facebook component, information about a visit to our website by the data subject, whenever the data subject is logged in at the same time on Facebook during the time of the call-up to our website. This occurs regardless of whether the data subject clicks on the Facebook component or not. If such a transmission of information to Facebook is not desirable for the data subject, then he or she may prevent this by logging off from their Facebook account before a call-up to our website is made.

The data protection guideline published by Facebook, which is available at https://facebook.com/about/privacy/, provides information about the collection, processing and use of personal data by Facebook. In addition, it is explained there what setting options Facebook offers to protect the privacy of the data subject. In addition, different configuration options are made available to allow the elimination of data transmission to Facebook. These applications may be used by the data subject to eliminate a data transmission to Facebook.

12. Data protection provisions about the application and use of Google Analytics (with anonymization function)

On this website, the controller has integrated the component of Google Analytics (with the anonymizer function). Google Analytics is a web analytics service. Web analytics is the collection, gathering, and analysis of data about the behavior of visitors to websites. A web analysis service collects, inter alia, data about the website from which a person has come (the so-called referrer), which sub-pages were visited, or how often and for what duration a sub-page was viewed. Web analytics are mainly used for the optimization of a website and in order to carry out a cost-benefit analysis of Internet advertising.

The operator of the Google Analytics component is Google Inc., 1600 Amphitheatre Pkwy, Mountain View, CA 94043-1351, United States.

For the web analytics through Google Analytics the controller uses the application "_gat. _anonymizeIp". By means of this application the IP address of the Internet connection of the data subject is abridged by Google and anonymised when accessing our websites from a Member State of the European Union or another Contracting State to the Agreement on the European Economic Area.

The purpose of the Google Analytics component is to analyze the traffic on our website. Google uses the collected data and information, inter alia, to evaluate the use of our website and to provide online reports, which show the activities on our websites, and to provide other services concerning the use of our Internet site for us.

Google Analytics places a cookie on the information technology system of the data subject. The definition of cookies is explained above. With the setting of the cookie, Google is enabled to analyze the use of our website. With each call-up to one of the individual pages of this Internet site, which is operated by the controller and into which a Google Analytics component was integrated, the Internet browser on the information technology system of the data subject will automatically submit data through the Google Analytics component for the purpose of online advertising and the settlement of commissions to Google. During the course of this technical procedure, the enterprise Google gains knowledge of personal information, such as the IP address of the data subject, which serves Google, inter alia, to understand the origin of visitors and clicks, and subsequently create commission settlements.

The cookie is used to store personal information, such as the access time, the location from which the access was made, and the frequency of visits of our website by the data subject. With each visit to our Internet site, such personal data, including the IP address of the Internet access used by the data subject, will be transmitted to Google in the United States of America. These personal data are stored by Google in the United States of America. Google may pass these personal data collected through the technical procedure to third parties.

The data subject may, as stated above, prevent the setting of cookies through our website at any time by means of a corresponding adjustment of the web browser used and thus permanently deny the setting of cookies. Such an adjustment to the Internet browser used would also prevent Google Analytics from setting a cookie on the information technology system of the data subject. In addition, cookies already in use by Google Analytics may be deleted at any time via a web browser or other software programs.

In addition, the data subject has the possibility of objecting to a collection of data that are generated by Google Analytics, which is related to the use of this website, as well as the processing of this data by Google and the chance to preclude any such. For this purpose, the data subject must download a browser add-on under the link https://tools.google.com/dlpage/gaoptout and install it. This browser add-on tells Google Analytics through a JavaScript, that any data and information about the visits of Internet pages may not be transmitted to Google Analytics. The installation of the browser add-ons is considered an objection by Google. If the information technology system of the data subject is later deleted, formatted, or newly installed, then the data subject must reinstall the browser add-ons to disable Google Analytics. If the browser add-on was uninstalled by the data subject or any other person who is attributable to their sphere of competence, or is disabled, it is possible to execute the reinstallation or reactivation of the browser add-ons.

Further information and the applicable data protection provisions of Google may be retrieved under https://www.google.com/intl/en/policies/privacy/ and under http://www.google.com/analytics/terms/us.html. Google Analytics is further explained under the following Link https://www.google.com/analytics/.

13. Data protection provisions about the application and use of LinkedIn

The controller has integrated components of the LinkedIn Corporation on this website. LinkedIn is a web-based social network that enables users with existing business contacts to connect and to make new business contacts. Over 400 million registered people in more than 200 countries use LinkedIn. Thus, LinkedIn is currently the largest platform for business contacts and one of the most visited websites in the world.

The operating company of LinkedIn is LinkedIn Corporation, 2029 Stierlin Court Mountain View, CA 94043, UNITED STATES. For privacy matters outside of the UNITED STATES LinkedIn Ireland, Privacy Policy Issues, Wilton Plaza, Wilton Place, Dublin 2, Ireland, is responsible.

With each call-up to one of the individual pages of this Internet site, which is operated by the controller and on which a LinkedIn component (LinkedIn plug-in) was integrated, the Internet browser on the information technology system of the data subject is automatically prompted to the download of a display of the corresponding LinkedIn component of LinkedIn. Further information about the LinkedIn plug-in may be accessed under https://developer.linkedin.com/plugins. During the course of this technical procedure, LinkedIn gains knowledge of what specific sub-page of our website was visited by the data subject.

If the data subject is logged in at the same time on LinkedIn, LinkedIn detects with every call-up to our website by the data subject—and for the entire duration of their stay on our Internet site—which specific sub-page of our Internet page was visited by the data subject. This information is collected through the LinkedIn component and associated with the respective LinkedIn account of the data subject. If the data subject clicks on one of the LinkedIn buttons integrated on our website, then LinkedIn assigns this information to the personal LinkedIn user account of the data subject and stores the personal data.

LinkedIn receives information via the LinkedIn component that the data subject has visited our website, provided that the data subject is logged in at LinkedIn at the time of the call-up to our website. This occurs regardless of whether the person clicks on the LinkedIn button or not. If such a transmission of information to LinkedIn is not desirable for the data subject, then he or she may prevent this by logging off from their LinkedIn account before a call-up to our website is made.

LinkedIn provides under https://www.linkedin.com/psettings/guest-controls the possibility to unsubscribe from e-mail messages, SMS messages and targeted ads, as well as the ability to manage ad settings. LinkedIn also uses affiliates such as Eire, Google Analytics, BlueKai, DoubleClick, Nielsen, Comscore, Eloqua, and Lotame. The setting of such cookies may be denied under https://www.linkedin.com/legal/cookie-policy. The applicable privacy policy for LinkedIn is available under https://www.linkedin.com/legal/privacy-policy. The LinkedIn Cookie Policy is available under https://www.linkedin.com/legal/cookie-policy.

14. Legal basis for the processing

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CML Publications 2017 

 

Clinical Publications Scientific Publications
December 2017
Treatment-free remission in CML: who, how, and why?
(Mahon FX. Hematology Am Soc Hematol Educ Program, December 2017)
Exosomes derived from imatinib-resistant chronic myeloid leukemia cells mediate a horizontal transfer of drug-resistant trait by delivering miR-365
(Min QH et al. Exp Cell Res, December 2017)
(epub ahead of print)
Cardiovascular care of patients with chronic myeloid leukemia (CML) on tyrosine kinase inhibitor (TKI) therapy
(Barber MC et al. Hematology Am Soc Hematol Educ Program,
December 2017)
Ecotopic viral integration site 1 (EVL1) transcriptionally targets talin 1 (TLN1) and upregulates its expression in chronic myeloid leukemia
(Halder A et al. Leuk Lymphoma, December 2017)
(epub ahead of print)
Novel approaches to therapy in CML
(Bhatia R et al. Hematology Am Soc Hematol Educ Program, December 2017)
C1206, a novel curcumin derivate, potently inhibits Hsp90 and human chronic myeloid leukemia cells in vitro
(Fan YL et al. Acta Pharmacol, December 2017)
(epub ahead of print)
Front-line treatment options for chronic-phase chronic myeloid leukemia
(Shah NP et al. J Clin Oncol, December 2017)
(epub ahead of print)
Monocytic myeloid-derived suppressor cells as prognostic factor in chronic myeloid leukaemia patients treated with dasatinib
(Giallongo C et al. J Cell Mol Med, December 2017)
(epub ahead of print)
Mechanisms of resistance to targeted therapies in chronic myeloid leukemia
(Lussana F et al. Handb Exp Pharmacol, December 2017)
(epub ahead of print)
Controversies regarding use of myeloid growth factors in leukemia
(Poston JN et al. J Natl Compr Canc Netw, December 2017)
Management of chronic myeloid leukemia in the setting of pregnancy: when is leukocytapharesis appropriate? A case report and review of the literature
(Staley EM et al. Transfusion, December 2017)
(epub ahead of print)

Atypcial chronic myeloid leukemia: a rare entity with management challenges

(Dhakal P et al. Future Oncol, December 2017)
(epub ahead of print)

Successful ovarian stimulation for fertility preservation in a patient with chronic myeloid leukemia: switch from nilotinib to interferon-alpha
(Gazdaru S et al. Oncologist, December 2017)
(epub ahead of print)

November 2017
Bosutinib versus imatinib for newly diagnosed chronic myeloid leukemia: Results from the randomized BEFORE trial
(Cortes JE et al. J Clin Oncol, November 2017)
(epub ahead of print)
Targeting BCR-ABL-independent TKI resistance in chronic myeloid leukemia by mTOR and authophagy inhibition
(Mitchell R et al. J Natl. Cancer Inst, November 2017)
(epub ahead of print)
 Bosutinib more effective than imatinib in CML
(Gourd E. Lancet Oncol, November 2017)
(epub ahead of print)

Off-target effect of imatinib and nilotinib on human vitamin D3 metabolism
(Kroschwald L et al. Mol Med Rep, November 2017)
(epub ahead of print)

  Clinical efficacy and safety of first-line dasatinib therapy and the relevance of velocity of BCR-ABL1 transcript decline for achievement of molecular chronic-phase chronic myeloid leukemia: Report from the Juntendo Yamanashi Cooperative Study Group
(Takaku T et al. Oncology, November 2017)
(epub ahead of print)
  Immature CML cells implement a BMP autocrine loop to escape TKI treatment
(Grockowiak E et al. Blood, November 2017)
  Prognostic relevance of CCAs/Ph- CML settled
(Hehlmann R et al. Blood, November 2017)
 

Off-target effect of imatinib and nilotinib on human vitamin D3 metabolism
(Kroschwald L et al. Mol Med Rep, November 2017
(epub ahead of print)

  Chk1 inhibitors overcome imatinib resistance in chronic myeloid leukemia cells
(Lei H et al. Leuk Res, November 2017)
(epub ahead of print)
  Altered intracellular signaling by imatinib increases the anti-cancer effects of tyrosine kinase inhibitors in CML cells
(Hirao T et al. Cancer Sci, November 2017)
(epub ahead of print)
October 2017
Long-term patient-reported outcomes from an open-label safety and efficacy study on bosutinib in Philadelphia chromosome-positive chronic myeloid leukemia patients resistant or intolerant to prior therapy
(Kantarjian HM et al. Cancer, October 2017)
(epub ahead of print)
Transgenic expression of human cytokines in immunodeficient mice does not facilitate myeloid expansion of BCR-ABL1 transduces human cord blood cells
(Askmyr M et al. PLoS One, October 2017
How I manage relapse of chronic myeloid leukemia after stopping tyrosine kinase inhibitor therapy
(Rea D et al. Br J Haematol, October 2017)
(epub ahead of print)
Micro RNA-7 inhibits cell proliferation of chronic myeloid leukemia and sensitizes it to imatinib in vitro
(Jiang MJ et al. Biochem Biophys Res Comm, October 2017)
(epub ahead of print
Life after ponatinib failure: outcomes of chronic and accelerated phase CML patients who discontinued ponatinib in the salvage setting
(Boddu P et al. Leuk Lymphoma, October 2017)
(epub ahead of print)
Balaglitazone reverses P-glycoprotein-mediated multidrug resistance via upregulation of PTEN in a PPARy-dependent manner in leukemia cells
(Yousefi B et al. Tumour Biol, October 2017
Effects of bosutinib treatment on renal function in patients with Philadelphia chromosome-positive leukemias
(Cortes JE et al. Clin Lymphoma Myeloma Leuk, October 2017)
Prognostic significance of additional chromosomal abnormalities at the time of diagnosis in patients with chronic myeloid leukemia treated with frontline tyrosine kinase inhibitors
(Alhuraiji A et al. Am J Hematol, October 2017)
(epub ahead of print)
Dasatinib cessation after deep molecular response exceeding 2 years, and NK cell transition during dasatinib consolidation
(Kumagai T et al. Cancer Sci, October 2017)
(epub ahead of print)
Membrane perturbation through novel cell-penetrating peptides influences intracellular accumulation of imatinib mesylate in CML cells
(Mukherjee D et al. Cell Biol Toxicol, October 2017)
(epub ahead of print)

Physicians’ attitude towards selection of second line therapy with nilotinib and dasatinib in chronic myeloid leukemia patients
(Breccia M et al. Health Qual Life Outcomes, October 2017)

Absolute bioavailability of bosutinib in healthy subjects from an open-label randomized, 2-period crossover study
(Hsyu PH et al. Clin Pharmacol Drug Dev, October 2017)
(epub ahead of print)

 
Pleural effusion and molecular response in dasatinib treated chronic myeloid leukemia patients in a real-life Italian multicenter series
(Iurlo A et al. Ann Hematol, October 2017)
(epub ahead of print)
Synergistic antiproliferative activity of the RAD51 inhibitor IBR2 with inhibitors of receptor tyrosine kinases and microtubule protein
(Ferguson PJ et al. J Pharmacol Exp Ther, October 2017)
(epub ahead of print)

First-line therapy for chronic phase CML: selecting the optimal BCR-ABL-1-targeted TKI
(Saglio G et al. Leuk Lymphoma, October 2017)
(epub ahead of print)

 

Sudden blast phase in chronic myeloid leukemia developed during nilotinib therapy after major molecular response was achieved
(Okada Y et al. Int J Hematol, October 2017)
(epub ahead of print)

 

The efficacy of reduced-dose dasatinib as a subsequent therapy in patients with chronic myeloid leukemia in the chronic phase: The LD-CML study of the Kanto CML Study Group
(Iriyama N et al. Intern Med, October 2017)
(epub ahead of print)

 
September 2017
 Deeper molecular response is a predictive factor for treatment-free remission after imatinib discontinuation in patients with chronic phase myeloid leukemia: the JALSG-STIM213 study
(Takahashi N et al. Int J Hematol, September 2017)
(epub ahead of print)
High BCR-ABL/Gusis levels at diagnosis of chronic phase CML are associated with unfavorable responses to standard-dose imatinib
(Vigneri P et al. Clin Cancer Res, September 2017)
Rapid reduction of BCR-ABL1 transcript predicts deep molecular response in dasatinib-treated chronic-phase chronic myeloid leukemia patients
(Murai K et al. Eur J Haematol, September 2017)
(epub ahead of print
Targeting mitochondrial oxidative phosphorylation eradicates therapy-resistant chronic myeloid leukemia stem cells
(Kuntz EM et al. Nat Med, September 2017)
(epub ahead of print)
  Expression differences of genes in the PI3K/AKT, WNT/b-catenin, SHH, NOTCH and MAPK signaling pathways in CD34+ hematopoietic cells obtained from chronic-phase patients with chronic myeloid leukemia and from healthy controls
(de Cássia Viu Carrara R et al. Clin Tranl Oncol, Sept. 2017)
(epub ahead of print)
 

A method for next-generation sequencing of paired diagnostic and remission samples to detect mitochondrial DNA mutations associated with leukemia
(Pagani IS et al. J Mol Diagn, September 2017)

 

Diagnostic and prognostic cytogenetics of chronic myeloid leukemia: an update
(Molica M et al. Expert Rev Mol Diagn, September 2017
(epub ahead of print)

August 2017
 The safety of bosutinib for the treatment of chronic myeloid leukemia
(Kong JH et al. Expert Opin Drug Saf, August 2017)
(epub ahead of print)
CT-721, a potent BCR-ABL inhibitor, exhibits excellent in vitro and in vivo efficacy in the treatment of chronic myeloid leukemia
(Sun Y et al. J Cancer, August 2017)
Safety and efficacy of blinatumomab in combination with a tyrosine kinase inhibitor for the treatment of relapsed Philadelphia chromosome-positive leukemia
(Assi R et al. Clin Lymphoma Myeloma Leuk, August 2017)
(epub ahead of print)

A new mechanism of resistance to ABL1 tyrosine kinase inhibitors in a BCR-ABL1-positive cell line
(Airiau K et al. Leuk Res, August 2017
(epub ahead of print)

Assessment of imatinib as first-line treatment of chronic myeloid leukemia: 10-year survival results of the randomized CML Study IV and impact of non-CML determinants
(Hehlmann R et al. Leukemia, August 2017)
(epub ahead of print)
Dasatinib reversibly disrupts endothelial vascular integrity by increasing non-muscle myosin II contractility in a ROCK-dependent manner
(Kreutzmann A et al. Clin Cancer Res, August 2017)
(epub ahead of print)
Impact of imatinib on the fertility of male patients with chronic myelogenous leukaemia in the chronic phase
(Chang X et al. Target Oncol, August 2017)
(epub ahead of print)
SHP1 is required for BCR-ABL1-induced hematologic neoplasia
(Gu S et al. Leukemia, August 2017)
(epub ahead of print)

Vascular adverse events during long-term nilotinib therapy in patients with chronic myeloid leukemia
(Eskazan AE et al. Clin Lymphoma Myeloma Leuk, August 2017
(epub ahead of print)

Reactive follicular hyperplasia on dasatinib treatment for chronic myeloid leukemia
(Iurlo A et al. Ann Hematol, August 2017
(epub ahead of print)

 

Cardiovascular toxicities of BCR-ABL tyrosine kinase inhibitors in chronic myeloid leukemia: preventive strategies and cardiovascular surveillance
(Aghel N et al. Vasc Health Risk Manag, August 2017)

A virtual screening approach for the identification of high affinity small molecules targeting BCR-ABL1 inhibitors for the treatment of chronic myeloid leukemia

(Sharda S et al. Curr Top Med Chem, August 2017)
(epub ahead of print)

 

Persistent detection of alternatively spliced BCR-ABL variant results in a failure to achieve deep molecular response
(Yuda J et al. Cancer Sci, August 2017)
(epub ahead of print)

 

NCG2D gene polyphormisms are associated with disease control of chronic myeloid leukemia by dasatinib
(Hara R et al. Int J Hematol, August 2017)
(epub ahead of print)

 
 

Sustained molecular response in chronic myeloid leukemia deep responders treated with low dose tyrosine kinase inhibitors
(Cayssials E et al. Leuk Lymphoma, August 2017)
(epub ahead of print)

 

Role and mechanisms of decitabine combined in advanced chronic myeloid leukemia cells
(Jiang LC et al. Oncol Lett, August 2017)

July 2017
Prognostic factors and survival outcomes in patients with chronic myeloid leukemia in blast phase in the tyrosine kinase inhibitor era: Cohort study of 477 patients
(Jain P et al. Cancer, July 2017)
(epub ahead of print)
Targeting BCR-ABL+ stem/progenitor cells and BCR-ABL-T315l mutant cells by effective inhibition of the BCR-ABL-Tyr177-GRB2 complex
(Chen M et al. Oncotarget, July 2017)
Second tyrosine kinase inhibitor discontinuation attempt in patients with chronic myeloid leukemia
(Legros L et al. Cancer, July 2017)
(epub ahead of print)
Association between proteomic profile and molecular response in chronic myeloid leukemic patients
(Garrisi VM et al. Leuk Lymphoma, July 2017)
(epub ahead of print)
Cardiovascular events after exposure to nilotinib in chronic myeloid leukemia: Long-term follow-up
(Aghel N et al. Clin Lymphoma Myeloma Leuk, July 2017)
(epub ahead of print)
Placental transfer of tyrosine kinase inhibitors used for chronic myeloid leukemia treatment
(Chelysheva E et al. Leuk Lymphoma, July 2017
(epub ahead of print)

How to report adherence to treatment as clinically relevant data-making – a case of CML and TKI 
(Okumura LM et al. Support Care Cancer, July 2017
(epub ahead of print)

New tool for monitoring molecular response in patients with chronic myeloid leukemia
(Badar T et al. Appl Immunohistochem Mol Morphol, July 2017)
(epub ahead of print)

Treatment-free rmission in patients with chronic myeloid leukemia 
(Rea D et al. Int J Hematol, July 2017) 
(epub ahead of print)

Specific monoclonal antibody against BCR/ABL out-of-frame alternative proteins as diagnostic tool in chronic myelogenous leukemia patients
(Casnici C et al. Monoclon Antib Immunodiagn Immunother, July 2017
(epub ahead of print)

Nilotinib dose-optimization in newly diagnosed chronic myeloid leukemia in chronic-phase: final results from ENESTxtnd
(Hughes TP et al. Br J Haematol, July 2017)
(epub ahead of print)

Somatic mutations identified at diagnosis by exome sequencing can predict response to imatinib in chronic phase CML patients 

(Mologni L et al. Am J Hematol, July 2017)
(epub ahead of print)

De-escalation of tyrosine kinase inhibitor dose in patients with chronic myeloid leukaemia with stable molecular response (DESTINY): an interim analysis of a non-randomised, phase 2 trial
(Clark RE et al. Lancet Haematol, July 2017)

Expansion of BCR/ABL1+ cells requires PAK2 but not PAK1 

(Edlinger L et al. Br J Haematol, July 2017)
(epub ahead of print)

Post-transplant feasibility study of nilotinib prophylaxis for high-risk Philadelphia chromosome positive leukaemia
(Carpenter PA et al. Blood, July 2017)
(epub ahead of print)

PTCH1 is a reliable marker for predicting imatinib response in chronic myeloid leukemia patients in chronic phase
(Alonso-Dominguez JM et al. PLoS One, July 2017)

 

Influence of WHO versus ELN advanced phase chronic myeloid leukemia definitions on overall survival
(Geelen IGP et al. Eur J Haematol, July 2017)
(epub ahead of print)

Clinical and prognostic significance of e1a2 BCR-ABL transcript subtype in chronic myeloid leukemia
(Gong Z et al. Blood Cancer J, July 2017)

 

Chronic myeloid leukemia: Global impact from a local laboratory
(Radich JP. Cancer, July 2017)

Imatinib and nilotinib off-target effects on human NK cells, monocytes, and M2 macrophages
(Bellora F et al. J Immunol, July 2017)
(epub ahead of print)

 
Chronic myeloid leukemia: room for improvement?
(Baccarani M et al. Haematologica, July 2017
 
June 2017
Analyses of treatment outcome according to age in patients with chronic myeloid leukemia receiving front-line imatinib therapy 
(Cojbasic I et al. Clin Lymphoma Myeloma Leuk, June 2017)
ASXL1 and BIM germ line variants predict response and identify CML patients with the greatest risk of imatinib failure
(Marum JE et al. Blood Advances, June 2017)
Incidence of second primary malignancies and related myeloid leukemia patients
(Gugliotta G et al. Haematologica, June 2017)
(epub ahead of print)

Understanding cancer from the stem cells up
(Eide CA, Nat Med, June 2017)

 

Evaluation of a new flow cytometry based method for detection of BCR-ABL1 fusion protein in chronic myeloid leukemia
(Dasgupta S et al. Blood Res, June 2017)

 

SHC004-221A1, a novel tyrosine kinase, potently inhibits T315l mutant BCR-ABL in chronic myeloid leukemia
(Wang D et al. Eur J Pharmacol, June 2017)
(epub ahead of print)

 

A new monoclonal antibody detects downregulation of protein tyrosine phosphatase receptor type y in chronic myeloid leukemia patients
(Vezzalini M et al. J Hematol Oncol, June 2017)

 

Genomic profiling of chronic myelogenous leukemia: Basis and clinical approach
(Keramatinia A et al. J Cancer Prev, June 2017)

  Chronic myeloid leukemia progenitor cells require autophagy when leaving hypoxia-induced quiescence
(Ianniciello A et al. Oncotarget, June 2017)
May 2017

De-escalation of tyrosine kinase inhibitor dose in patients with chronic myeloid leukaemia with stable major molecular response (DESTINY): an interim analysis of a non-randomised, phase 2 trial 
(epub ahead of print)
(Clark R et al. Lancet Haematol, May 2017)

Cryptic BCR-ABL fusion gene as variant rearrangement in chronic myeloid leukemia: molecular cytogenetic characterization and influence on TKI’s therapy
(Luatti S et al. Oncotarget, May 2017)

 

Natural killer cell counts are associated with molecular relapse-free survival after imatinib discontinuation in chronic myeloid leukemia: the IMMUNOSTIM study
(Rea D et al. Haematologica, May 2017)
(epub ahead of print)

Chronic myeloid leukemia: Immunobiology and novel immunotherapeutic approaches
(Cayssials E et al. Bio Drugs, June 2017)

 

Risk factors and mechanisms contributing to TKI-induced vascular events in patients with CML
(Valent P et al. Leuk Res, May 2017)
(epub ahead of print)

E14a2 BCR-ABL1 transcript is associated with a higher rate of treatment-free remission in persons with chronic myeloid leukemia after stopping tyrosine kinase inhibitor therapy
(Claudiani S. et al. Haematologica, May 2017)
(epub ahead of print)

 

Treatment of chronic myeloid leukemia: assessing risk, monitoring response, and optimizing outcome
(Shanmuganathan N et al. Leuk Lymphoma, May 2017) 
(epub ahead of print)

Single-cell transcriptomics uncovers distinct molecular signatures of stem cells in chronic-myeloid leukemia
(Giustaccini A et al. Nat Med, May 2017)
(epub ahead of print)

 
Maternal, fetal and neonatal imatinib levels with treatment of chronic myeloid leukemia in pregnancy
(Burwick RM et al. Obstet Gynecol, May 2017 
Single cell immune profiling by mass cytometry of newly diagnosed chronic phase chronic myeloid leukemia treated with nilotinib
(Gullaksen SE et al. Haematologica, May 2017)
(epub ahead of print)

New drugs and allogeneic hematopoietic stem cell transplantation for haematological malignancies: do they have a role in bridging, consolidating or conditioning transplantation treatment?
(Patriarca F. et al. Expert Opin Biol Ther, May 2017)
(epub ahead of print)

Micro RNA’s that affect the Fanconi Anemia / BRCA pathway are downregulated in imatinib-resistant chronic myeloid leukemia patients without detectable BCR-ABL kinase domain mutations
(Yap E et al. Leuk Res, May 2017)
(epub ahead of print)

The BCR-ABL1 transcript type influences response and outcome in Philadelphia chromosome-positive chronic myeloid leukemia patients treated frontline with imatinib
(Castagnetti F et al. Am J Hematol, May 2017)
(epub ahead of print)

A novel BCR-ABL1 fusion gene with genetic heterogeneity indicates a good prognosis in a chronic myeloid leukemia case
(Zhou F et al. Mol Cytogenet, May 2017)

Evaluation of cardiovascular ischemic event rates in dasatinib-treated patients using standardized incidence ratios
(Saglio G et al. Ann Hematol, May 2017)
(epub ahead of print)

Deregulated expression of MiR-299-3p, miR-494-3p and miR 660-5p affects sensitivity to tyrosine kinase inhibitors in CML leukemic stem cells
(Salati S et al. Oncotarget, May 2017
(epub ahead of print)

Running the marathon of chronic myeloid leukemia with no shoes (or without the right shoes)
(Mauro M. Cancer, May 2017
(epub ahead of print)

A rare e13a3 (b2a3) BCR-ABL1 fusion transcript with normal karyotype in chronic myeloid leukemia: The challenges in diagnosis and monitoring minimal residual disease (MRD)
(Duan MH et al. Leuk Res, May 2017)
(epub ahead of print)

Dasatinib rapidly induces deep molecular response in chronic-phase chronic myeloid leukemia patients who achieved major molecular response with detectable levels of BCR-ABL1 transcript by imatinib therapy
(Shiseki M et al. Int J Clin Oncol, May 2017)
(epub ahead of print)

BiRC6 mediates imatinib resistance independently of Mcl-1
(Okumu DO et al. PloS One, May 2017)

Clinical impact of pre-transplant use of multiple tyrosine kinase inhibitors on the outcome of allo-HSCT for CML
(Kondo T et al. Am J Hematol, May 2017)
(epub ahead of print)

Cancer progression by reprogrammed BCAA metabolism in myeloid leukemia
(Hattori A et al. Nature, May 2017)

CML in blast crisis: more common than we think?
(Hunger SP et al. Blood, May 2017)

Research on the epigenetic regulation mechanism of the PTPN6 gene in advanced chronic myeloid leukemia
(Zhang X et al. Br J Haematol, May 2017)
(epub ahead of print

Treating the chronic-phase myeloid leukemia patient: which TKI, when to switch and when to stop?
(Patel AB et al. Expert Rev Hematol, May 2017)
(epub ahead of print)

Role of NOX2 for leukemic expansion in a murine model of BCR-ABL1+ leukemia
(Grauers Wiktorin H et al. Br J Hematol, May 2017)
(epub ahead of print)

Are chronic myeloid leukemia patients ready to stop long-term treatment?
(Breccia M et al. Leuk Lymphoma, May 2017)
(epub ahead of print)

Baseline BCR-ABL1 transcript type of 13a2 and large spleen size are predictors of poor long-term outcomes in chronic phase chronic myeloid leukemia patients who failed to achieve an early molecular response after 3 months of imatinib therapy
(Lee SE et al. Leuk Lymphoma, May 2017)
(epub ahead of print)

 

Cryptic BCR-ABL fusion gene as variant rearrangement in chronic myeloid leukemia: molecular cytogenetic characterization

(Luatti S et al. Oncotarget, May 2017)
(epub ahead of print
  Single cell immune profiling by mass cytometry of newly diagnosed chronic phase chronic myeloid leukaemia treated with nilotinib
(Gullaksen SE. Haematologica, May 2017)
(epub ahead of print)
April 2017
Understanding CML, 1 cell at a time
(Radich J et al. Blood, April 2017)
Decreased Calpain activity in chronic myeloid leukemia impairs apoptosis by increasing Xiap1 in differentiating granulocytes

(
Huang W et al. Oncotarget, April 2017)
(epub ahead of print)
  

Overall survival with ponatinib versus allogeneic stem cell transplantation in Philadelphia chromosome-positive leukemias with the T315l mutation
(Nicolini FE et al. Cancer, April 2017)
(epub ahead of print)

A novel AHI-1-BCR-ABL-DNM2 complex regulated leukemic properties of primitive CML cells through enhanced cellular endocytosis and ROS-mediated authophagy
(Liu X et al. Leukemia, April 2017)
(epub ahead of print)

TKI rotation-induced persistent deep molecular response in multi-resistant blast crisis of Ph+ CML

(Hadzijusufovic E. et al. Oncotarget, April 2017)



Genotypes of SLC22A4 and SLC22A5 regulatory loci are predictive of the response of chronic myeloid leukemia patients to imatinib treatment
(Jaruskova M et al. J Exp Clin Cancer Res, April 2017)

The role of early molecular response in the management of chronic phase CML
(Harrington P et al. Curr Hematol Malig Rep, April 2017)
(epub ahead of print

BCR-ABL 1 transcript types showed distinct laboratory characteristics in patients with chronic myeloid leukemia

(Vasconcelos AP et al. Genet Mol Res, April 2017)
 

Treatment and molecular monitoring update in chronic myeloid leukemia management
(Sorel N et al. Ann Biol Clin, April 2017)


Impact of age on efficacy and tolerability of nilotinib in patients with chronic myeloid leukemia in chronic phase: ENEST1st subanalysis
(Giles FJ et al. J Cancer Res Clin Oncol, March 2017)
(epub ahead of print)

 

Association between a cardiovascular disease risk assessment and the molecular response to tyrosine kinase inhibitors in chronic-phase myeloid leukemia patients
(Osada Y et al. Med Oncol, April 2017)

 
March 2017
Systematic review and meta-analysis of standard-dose imatinib vs. high-dose imatinib and second generation tyrosine kinase inhibitors for chronic myeloid leukemia
(Hoffmann VS et al. J Cancer Res Clin Oncol, March 2017) 

The SCLtTAxBCR-ABL transgenic mouse model closely reflects the differential effects of dasatinib on normal and malignant hematopoiesis in chronic phase CML patients

(Schubert C et al. Oncotarget, March 2017) 
(epub ahead of print)


Imatinib discontinuation in chronic myeloid leukemia patients with undetectable BCR-ABL transcript level:
A systematic review and a meta-analysis

(Campiotti L et al. Eur J Cancer, March 2017)
(epub ahead of print)

Contributions of MET activation to BCR-ABL1 tyrosine kinase inhibitor resistance in chronic myeloid leukemia cells
(Tsubaki M et al. Oncotarget, March 2017
(epub ahead of print)

A BCR-ABL1 cutoff of 1,5 % at 3 months, determined by the GeneExpert System, predicts an optimal response in patients with chronic myeloid leukemia
(García-Gutiérrez V. et al. PLoS One, March 2017
Interleukin 3- receptor targeted exosomes inhibit in vitro and in vivo chronic myelogenous leukemia cell growth
(Bellavia D et al. Theranostics, March 2017)
Elderly patients with chronic myeloid leukemia benefit from a dasatinib dose as low as 20 mg
(Itamura H et al. Clin Lymphoma Myeloma Leuk, March 2017)
(epub ahead of print)
Stelletin B induces apoptosis in human chronic myeloid leukemia cells via targeting Pi3K and Stat 5

(Chen Y et al. Oncotarget, March 2017)
(epub ahead of print)


Predictive parameters for imatinib failure in patients with chronic myeloid leukemia

(Lekovic D et al. Hematology, March 2017)
(epub ahead of print)

The allosteric inhibitor ABL001 enables dual targeting of BCR-ABL 1
(Wylie AA et al. Nature, March 2017)

Imatinib changed everything
(Longo D et al. N Engl J Med, March 2017)

Is there an immune suveillance against chronic myeloid leukemia? Possibly, but not much
(Gale RP et al. Leuk Res, March 2017)

Phase I/II study of low-dose azacytidine in patients with chronic myeloid leukemia who have minimal residual disease while receiving therapy with tyrosine kinase inhibitors
(Maiti A et al. Leuk Lymphoma, March 2017) 

With no interaction, knockdown of Apollon and MDR1 reverse the multidrug resistance of human chronic myelogenous leukemia K562/ADM cells
(Chen JR et al. Oncol Rep, March 2017)
(epub ahead of print)

Can any patients with chronic myeloid leukemia outside of clinical trial have their tyrosine kinase inhibitors discontinued?
(
Mauro MJ. Curr Opin Hematol, March 2017) 

MPT0B002, a novel microtube inhibitor downregulates T315l mutant BCR-ABL and induces apoptosis of imatinib-resistant chronic myeloid leukemia cells
(Yet YYY et al. Invest New Drugs, March 2017)
(epub ahead of print)

Dasatinib versus imatinib in Japanese patients with newly diagnosed chronic phase chronic myeloid leukemia: a subanalysis of the DASISION 5 year final report
(Nakamae H et al. Int J Hematol, March 2017)
(epub ahead of print

Carfilzomib induces leukemia cell apoptosis via inhibiting ELK1/Ki AA1524 (ELK-1/CIP2A) and activating PP2A not related to proteasome inhibition
(Liu CY et al. Br J Haematol, March 2017)
(epub ahead of print)

Comparative analysis of pulmonary hypertension in patients treated with imatinib, nilotinib and dasatinib
(Minami M et al. Br J Haematol, March 2017)
(epub ahead of print) 

Tyrosine kinase inhibitor therapy-induced changes in humoral immunity in patients with chronic myeloid leukemia
(Rajala HL et al. J Cancer Res Clin Oncol, March 2017)
(epub ahead of print)

Treatment and outcome of 2904 CML patients from the EUTOS population-based registry
(Hoffmann VS. Leukemia, March 2017

p53 modulates the effect of ribosomal S6 kinase 1 (S6K1) cisplatin toxicity in chronic myeloid leukemia cells
(Xiao LY et al. Pharmacol Res, March 2017)
(epub ahead of print)

Long-term outcomes of imatinib treatment for CML
(Hochhaus A. et al. N Engl J Med, March 2017)

Combined inhibition of ß-catenin and BCR-ABL synergistically targets tyrosine kinase inhibitor-resistant blast crisis chronic myeloid leukemia blasts and progenitors in vitro and in vivo
(Zhou H et al. Leukemia, March 2017)
(epub ahead of print)

Factors influencing adherence in CML and ways to improvement: Results of a patient-driven survey of 2546 patients in 63 countries
(Geissler J et al. J Cancer Res Clin Oncol, March 2017
(epub ahead of print)

Association of the hOCT1/ABCB1 genotype with efficacy and tolerability of imatinib in patients affected by chronic myeloid leukemia
(Galeotti L et al. Cancer Chemother Pharmacol, March 2017
(epub ahead of print)

Treatment and outcomes of 2904 CML patients from the EUTOS population-based registry
(Hoffmann VS et al. Leukemia, March 2017)

Measurement of BCR-ABL1 by RT-qPCR in chronic myeloid leukemia: findings from an international EQA Programme
(Scott S et al. Br J Hematol. March 2017
(epub ahead of print)

Unleasing the Guardian: The targetable BCR-ABL/HAUSP/PML/PTEN Network in chronic myeloid leukemia
(Morotti A et al. Curr Drug Targets, March 2017

The HDAC inhibitor SB939 overcomes resistance to BCR-ABL kinase inhibitors conferred by the deletion polymorphism in chronic myeloid leukemia
(Rauzan M et al. PLoS One, March 2017

 

Blockade of Y177 and and nuclear translocation of BCR-ABL inhibits proliferation and promotes apoptosis in chronic myeloid leukemia cells
(Li Q et al. Int J Mol Sci, March 2017
)
February 2017
Pleural effusion in Dasatinib-treated patients with chronic myeloid leukemia in chronic phase: Identification and management
(Cortes J et al. Clin Lymphoma Myeloma Leuk, February 2017) 
Molecular techniques for the personalised management of patients with chronic myeloid leukemia
(Alikian M et al. Biomol Detect Quantif, February 2017)
Chronic myeloid leukemia with extreme thrombocytosis at presentation: incidence, clinical findings and outcome
(Sora F et al. Br J Haematol, February 2017)
(epub ahead of print)
 

Presence of novel compound BCR-ABL mutations in late chronic and advanced phase imatinib sensitive CML patients indicates their possible role in CML progression
(Akram AM et al. Cancer Biol, Ther, February 2017)
(epub ahead of print)

Differential depth of treatment response required for optimal outcome in patients with blast phase versus chronic phase of chronic myeloid leukemia
(Chen Z et al. Blood Cancer J, February 2017
(epub ahead of print)
 
Phase II trial of homoharringtonine with imatinib in chronic, accelerated, and blast crisis chronic myeloid leukemia
(Maiti A et al. Leuk Lymphoma, February 2017) 
(epub ahead of print)

Nilotinib first-line therapy in patients with Philadelphia chromosome-negative/BCR-ABL-positive chronic myeloid leukemia in chronic phase: ENEST1st subanalysis
(Hochhaus A et al. J Cancer Res Clin Oncol, February 2017) 
(epub ahead of print)
CobII1 is linked to drug resistance and blastic transformation in chronic myeloid leukemia
(Han SH et al. Leukemia, February 2017)
(epub ahead of print
Treatment-free remission following frontline nilotinib in patients with chronic myeloid leukemia in chronic phase: Results from the ENESTfreedom Study
(Hochhaus A et al. Leukemia, February 2017)
(epub ahead of print)
Up-regulated exosomal miRNA-140-3p in CML patients with musculoskeletal pain associated with discontinuation of tyrosine kinase inhibitors
(Asano M et al. Int J Hematol, February 2017
(epub ahead of print
Stopping second-generation TKI's in CML
(Laneuville P et al. Blood, February 2017)
Differential signaling networks of BCR-ABL p210 and p190 kinases in leukemia cells defined by functional proteomics
(Reckel et al. Leukemia, February 2017)
(epub ahead of print

Does the frequency of molecular monitoring after tyrosine kinase inhibitor discontinuation affect outcomes of patients with chronic myeloid leukemia?
(Kong JH et al. Cancer, February 2017)
(epub ahead of print)

Differentiation status of primary chronic myeloid leukemia cells affect sensitivity to BCR-ABL1 inhibitors
(Pietarinen PO et al. Oncotarget, February 2017)
(epub ahead of print) 
Smokers with chronic myeloid leukemia are at higher risk of disease progression and premature death
(Lauseker M et al. Cancer, February 2017
(epub ahead of print)
A review of the challenge in measuring and standardizing BCR-ABL1
(Yu S et al. Clin Chem Lab Med, Februar 2017)
(epub ahead of print) 

Targeted therapies: Remembrance of things past - discontinuation of second-generation TKI therapy for CML
(Hughes TP et al. Nat Rev Clin Oncol, February 2017)
(epub ahead of print)

The JAK2 blocker TG101209 is a potent inhibitor of clonogenic progenitor cell growth in patients with chronic myeloid leukemia
(Demyanets S et al. Br J Hematol, February 2017)
(epub ahead of print) 

Pleural effusion in Dasatinib-treated patients with chronic myeloid leukemia in chronic phase: Identification and management
(Cortes J et al. Clin Lymphoma Myeloma Leuk, February 2017)

The chronic myeloid leukemia stem cell: Stemming the tide of persistence
(Holyoake T. et al. Blood, February 2017)
  Increased peroxisome proliferator-activated receptor-gamma activity reduces imatinib uptake and efficacy in chronic myeloid leukemia mononuclear cells
(Wang J et al. Haematologica, February 2017
(epub ahead of print
January 2017
Characterization of patients with chronic myeloid leukemia unresponsive to tyrosine kinase inhibitors who underwent hemoatopoietic stem cell transplantation
(Carvalho FR et al. Int J Hematol Stem Cell Res, January 2017)
Reduced CD62L expression on T cells and increased CD62L levels predict molecular response to tyrosine kinase inhibitor therapy in early chronic-phase chronic myelogenous leukemia
(Sopper S et al. J Clin Oncol, January 2017) 
Current approach to the treatment of chronic myeloid leukemia
(Pasic I et al. Leuk Res, January 2017 

CML patients with deep molecular responses to TKI have restored immune effects, decreased PD-1 and immune suppressor
(Hughes A et al. Blood, January 2017
(epub ahead of print)

Long-term follow-up of the French Stop Imatinib (STIM1) Study in patients with chronic myeloid leukemia
(Etienne G. et al. J Clin Oncol, January 2017 

No influence of BCR-ABL1 transcript types e13a2 and e14a2 on long-term survival: Results in 1494 patients with chronic myeloid leukemia treated with imatinib
(Pfirrmann M et al. J Cancer Res Clin Oncol, January 2017)
(epub ahead of print)

Current approach in the treatment of chronic myeloid leukemia
(Pasic I et al. Leuk Res, January 2017)
(epub ahead of print)
Modelling predictors of molecular response to frontline imatinib for patients with chronic myeloid leukemia
(Banjar H et al. PLoS One, January 2017)
Exploratory study on the impact of switching to nilotinib in 18 patients with chronic myeloid leukemia in chronic phase with suboptimal response to imatinib
(Ailawadhi S. et al. Ther Adv Hematol, January 2017)    
The hypothesis of the human iNKT/innate CD8(+) T-cells axis applied to Cancer: Evidence for a defiency in chronic myeloid leukemia
(Jacomet F. et al. Front Immunol, January 2017)
Early BCR-ABL1 transcript decline after 1 month of tyrosine kinase inhibitor therapy as an indicator for treatment response in chronic myeloid leukemia
(El Missiry M et al. PLoS One, January 2017)
Induction of p53 suppresses chronic myeloid leukemia
(Peterson LF et al. Leuk Lymphoma, January 2017)
(epub ahead of print) 
 

Epression of the CTLA-4 ligand CD86 on plasmacytoid dendritic cells (pDC) predicts risk of disease recurrence after treatment discontinuation in CML
(Schütz C et al. Leukemia, April 2017)

 

 

 

 

Dasatinib may be considered a new standard of care for pediatric patients with CML-CP

Madrid, June 2017 -Findings from a large prospective trial with pediatric patients1 suggest that dasatinib provides benefits to children and adolescents in CML-CP who are resistant /intolerant to imatinib.

CML represents less than 3% of all leukemias in children worldwide, but more aggressive disease characteristics have been observed in this patient population.

Currently imatinib is the only approved tyrosine kinase inhibitor in children with CML and no approved therapies are available for children resistant or intolerant to imatinib. "There is an unmet need for safe and effective treatment options for children and adolescents who are resistant or intolerant to imatinib and also for alternative treatment formulations", Dr C. Zwaan opened his presentation at the 22th meeting of the European Hematology Association (EHA) in Madrid.

According to Dr. Zwaan, dasatinib has already shown to be effective in adults with newly diagnosed CML-CP, as well as those resistant/intolerant to imatinib however, "there is almost no published data available in children who are resistant or intolerant to imatinib".

Zwaan presented data from a Phase II open-label, randomized, prospective study conducted in 18 countries. In this large, ongoing prospective trial of pediatric patients with CML-CP, dasatinib was found to be safe and effective as first, or second-line therapy.

Patients aged <18 years were recruited into three separate cohorts: (1) IM-resistant/intolerant CML-CP treated with dasatinib 60 mg/m2 QD, (2) IM-resistant/intolerant CML-AP/BP or Ph+ ALL, and (3) newly diagnosed CML-CP treated with dasatinib 60 mg/m2 or dasatinib 72 mg/m2 powder for oral suspension QD for ≥1 year. Within the imatinib resistant/intolerant group of 29 patients, 25 patients were resistant, 2 intolerant and 2 undetermined.

The primary objectives were MCyR for imatinib resistant/intolerant CML-CP at any time with more than 30% MCyR as the protocol-defined rate of clinical interest and CCyR for newly diagnosed CML-CP at any time with more than 55% CCyR as the protocol-defined rate of clinical interest.

The cumulative rate of MCyR >30% was reached as early as 3 months for IM-resistant/intolerant CML-CP, and a cumulative rate of CCyR >55% was reached as early as 6 months for newly diagnosed CML-CP. Cytogenetic and molecular response continued to increase over time in each cohort. "Early and durable responses to dasatinib were observed, which met the study objectives for both cohorts”, Zwaan summed up the efficacy study results.

The safety profile of dasatinib was comparable to previous reports in adults treated with dasatinib except that no cases of pleural/pericardial effusion or pulmonary arterial hypertension were observed. 

Additional advantages include; once-daily dosing and administration with, or without food.

In conclusion, according to Zwaan, this is the largest prospective trial with pediatric patients and dasatinib was found to be a safe and effective treatment for pediatric patients in chronic-phase CML. The safety profile was slightly favourable to adult data with respect to the absence of effusions. “Further investigation is needed to determine whether the reasons for this slightly better safety profile in pediatric patients are due to a better immune system or any other reason”, Zwaan concluded at the end of his presentation.

1. Dasatinib in children and adolescents with chronic myeloid leukemia in chronic phase (CML-CP) from a phase 2 trial, abstract presented by CM Zwaan during the 22nd Congress of the European Hematology Association (EHA), June 22-25, 2017 in Madrid, Spain.

 

Free abstract
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CML Publications 2016

 

Clinical Publications Scientific Publications
December 2016
Response to overexpresssion of ABCB1 as prediction marker for CML: How close we are to translation into clinics?
(Eadie LN et al. Leukemia, December 2016)
(epub ahead of print)
CYP2C8 genotype significantly alters imatinib metabolism in chronic myeloid leukemia patients
(Barrat DT et al. Clin Pharmacokinet, December 2016)
(epub ahead of print)
Cardiologist's perspective to the European LeukemiaNet recommendations for the management and avoidance of adverse events of treatment in chronic myeloid leukemia
(Constance C. et al. Leukemia, December 2016)
(epub ahead of print)
RT-q PCR and RT-Digital PCR: A comparison of different platforms for the evaluation of residual diseease in chronic myeloid leukemia
Alikian M et al. Clin Chem, December 2016
(epub ahead of print)

Chronic myeloid leukemia: sequencing of TKI therapies
(Cortes JE et al. Hematology Am Soc Hematol Educ Program, December 2016)

Pioglitazone together with imatinib in chronic myeloid leukemia: A proof of concept study
(Rousselot P et al. Cancer, December 2016)
(epub ahead of print)
 

Molecular monitoring in chronic myeloid leukemia - how low can you go?
(Branford S. Hematology Am Soc Hematol Educ Program, December 2016)

Frequency of rare BCR-ABL1 fusion transcripts in chronic myeloid leukemia patients
(Arun AK et al. Int J Lab Hematol, December 2016) 
(epub ahead of print)
Long-term bosutinib for chronic phase myeloid leukemia after failure of imatinib plus dasatinib and/or nilotinib
(
Cortes JE et al. Am J Hematol, December 2016)
Enhanced targeting of CML stem and progenitor cells by inhibition of porcupine acyltransferase in combination with TKI
(Agarwal P et al. Blood, December 2016)
(epub ahead of print)
 
The value of quality of life assessment in chronic myeloid leukemia patients receiving tyrosine kinase inhibitors
(
Efficace F et al. Hematology Am Soc Hematol Educ Program, December 2016)

Response to overexpresssion of ABCB1 as prediction marker for CML: How close we are to translation into clinics?
(Eadie LN et al. Leukemia, December 2016)
(epub ahead of print)

 

Increased proportion of mature NK cells is associated with successful imatinib discontinuation in chronic myeloid leukemia
(Ilander M et al. Leukemia, December 2016
(epub ahead of print)

 

Role of complexity of variant Philadelphia chromosome in chronic myeloid leukemia in the era of tyrosine kinase inhibitor therapy
(Gong Z. et al. Ann Hematol, December 2016)

 
November 2016

How can I treat atypical CML?
(Gotlib J. Blood, November 2016
(epub ahead of print)

Nickel pyrithione induces apoptosis in chronic myeloid leukemia cells resistant to imatinib via both BCR/Abl-dependent and BCR/Abl-independent mechanisms
(Lan X et al. J Hematol Oncol, November 2016) 
Second line small molecule therapy options for treating chronic myeloid leukemia
(Molica M et al. Expert Opin Pharmacotherapy, November 2016) 
Cyclic AMO (cAMP) confers drug resistance against DNA damaging agents via PKAIA in CML cells
(
Xiao LY et al. Eur J Pharmacol, November 2016)
(epub ahead of print)
Clinical efficacy of fecal occult blood test and colonoscopy for dasatinib-induced hemorrhagic colitis in CML patients
(Nishiwaki S. et al. Blood, November 2016)
(epub ahead of print)
 
Upreguating miR-146a by pyscion reverses multidrug resistance in human chronic myelogenous leukemia K562/ADM cells
(Liu W et al. Am J Cancer Res, November 2016)
Standardization of molecular monitoring for chronic myeloid leukemia in Latin America using locally produced secondary cellular calibrators
(Ruiz MS et al. Leukemia, November 2016) 
Axl blockade by BGB324 inhibits BCR-ABL tyrosine kinase inhibitor-sensitive and -resistant chronic myeloid leukemia
(
Ben Batalla et al. Clin Cancer Res, November 2016)
(epub ahead of print)
How can patient reported outcomes improve patient management in chronic myeloid leukemia?
(De Marchi F. et al. Expert Rev Hematol, November 2016)
(epub ahead of print)
 

Different BCR/ABL protein suppression patterns as a converging trait of chronic myeloid leukemia cell adaptation to energy restriction
(Bono S et al. Oncotarget, November 2016) 
(epub ahead of print)

Risk of arterial and venous occlusive events in chronic myeloid leukemia patients treated with new generation BCR-ABL tyrosine kinase inhibitors: A systematic review and meta-analysis
(
Haguet H et al. Expert Opin Drug Saf, November 2016
(epub ahead of print)

Casiopeina III-Ea, a copper-containing small molecule, inhibits the in viro growth of primitive hematopoietic cells from chronic myeloid leukemia
(Chavez-Gonzalez A et al. Leuk Res, November 2016) 
(epub ahead of print)

Charlson comorbidity index predicts poor outcome in CML patients treated with tyrosine kinase inhibitor
(Uemura M et al. Int J Hematol, November 2016) 
(epub ahead of print)
IncRNA UCA1 contributes to imatinib resistance by acting as a ceRNA against miR-16 in chronic myeloid leukemia cells
(Xiao Y et al. DNA Cell Biol, November 2016)
(epub ahead of print)

A propensity score matching analysis of dasatinib and nilotinib as a frontline therapy for patients with chronic myeloid leukemia in chronic phase
(Takahashi K et al. Cancer, November 2016
(epub ahead of print)

 

Gas6/AXL signaling regulates self-renewal of chronic myelogenous leukemia stem cells by stabilizing ß-catenin
(Jin Y et al. Clin Cancer Res, November 2016)
(epub ahead of print)

 

  Celecoxib inhibits proliferation and survival of chronic myelogenous leukemia cells via AMPK-dependent regulation of ß-catenin and mTORC 1/2
(Riva B et al. Oncotarget, November 2016)
(epub ahead of print)
  Plasma proteomics in CML patients before and after initiation of tyrosine kinase inhibitor therapy reveals induced Th1 immunity and loss of angiogenetic stimuli
(Söderlund S. et al. Leuk Res, Nov, 2016)
  The Rho-ROCK pathway is a new pathological mechanism of innate immune subversion in chronic myeloid leukaemia
(Basbous S et al. J Pathol, November 2016)
  Resistance to imatinib in patients with chronic myelogenous leukemia and the splice variant BCR-ABL1 (35INS)
(Berman E et al. Leuk Res, Oct 2016)
October 2016

A population-based study of chronic myeloid leukemia patients treated with imatinib in first-line
(Castagnetti F. et al. Am J Hematol, October 2016) 
(epub ahead of print

PBA2, a novel inhibitor of imatinib-resistant BCR-ABL T315I mutation in chronic myeloid leukemia
(Gupta P et al. Cancer Lett, October 2016
(epub ahead of print)
Tyrosine kinase inhibitors in chronic myeloid leukaemia: which, when, for whom? 
(Rosti G. et al. Nat Rev Clin Oncol, October 2016)
(epub ahead of print)
CML cells actively evade host immune surveillance through cytokine-mediated downregulation of MHC-II expression
(Tarafdar A. et al. Blood, October 2016
(epub ahead of print)
Chronic myeloid leukemia among patients with a history of prior malignancies: A tale of dual survivorship
(Koller PB et al. Cancer, October 2016)
(epub ahead of print)
miRNAs in chronic myeloid leukemia: small molecules, essential function
(Litwínska Z. et al. Leuk Lymphoma, October 2016)

Current developments in molecular monitoring in chronic myeloid leukemia
(Marum JE et al. Ther adv Hematol, Oct 2016

Programmed cell death 4 and BCR-ABL fusion gene expression are negatively correlated in chronic myeloid leukemia
(Zhang X et al. Oncol Lett, Oct 2016)
September 2016

Monitoring and defining early response: Where to draw the line?
(Branford S. Best Pract Clin Haematol, September 2016)

Epigenetic reprogramming sensitizes CML stem cells to combined EZH2 and tyrosine kinase inhibition
(Scott MT et al. Cancer Discov, Sept 2016)
(epub ahead of print) 

Discontinuation of TKI therapy and 'functional' cure for CML
(Mahon FX. Best Pract Res Clin Hematol, September 2016)

Inhibition of interleukin-1 signaling enhances elimination of tyrosine kinase inhibitor treated CML stem cells
(Zhang B et al. Blood, Sept 2016
(epub ahead of print
 
Management of CML blast crisis
(Hehlmann R. et al. Best Pract Res Clin Haematol, September 2016)

Constitutional t(8;22) (q24;q11.2) that mimics the variant Burkitt-type translocation in Philadelphia chromosomal positiv chronic myeloid leukemia
(Kawamoto S et al. Int J Hematol, Sept 2016)
(epub ahead of print)

Identification, prevention and management of cardiovascular risk in chronic myeloid leukaemia patients candidates to ponatinib: an expert opinion
(Breccia M et al. Ann Hematol, Sept 2016)
(epub ahead of print)

Micro RNA-139-5p regulates proliferation of hematopoietic progenitors and is repressed during BCR-ABL mediated leukemogenesis
(Choi J et al. Blood, Sept. 2016
(epub ahead of print)

Dasatinib in imatinib-resistant or-intolerant chronic-phase chronic myeloid leukemia: 7-year follow-up of study CA180-034
(Shah NP et al. Am J Hematol, Sept 2016)

Molecular monitoring of chronic myeloid leukemia: present and future
(Yeung CC et al. Expert Rev Mol Diagn, Sept 2016)
(epub ahead of print

 

Ponatinib in the therapy of chronic myeloid leukemia
(Poch Martell M et al. Expert Revv Hematol, Sept)

Combined targeting of BCL-2 and BCR-ABL tyrosine kinase eradicates chronic myeloid leukemia stem cells
(
Carter BZ et al. Sci Transl Med, September 2016
August 2016

Long-term bosutinib for chronic phase myeloid leukemia after failure of imatinib plus dasatinib and/or bosutinib
(Cortes JE et al. Am J Hematol, August 2016)

(epub ahead of print)

 

The BCR-ABL/NF-kB signal transduction network: a long lasting relationship in Philadelphia positiv leukemias
(Carrà G et al. Oncotarget, August 2016)
(epub ahead of print)

 

Imatinib and polypharmacy in very old patients with chronic myeloid leukemia: effects on response rate, toxicity and outcome
(Iurlo A et al. Oncotarget, August 2016)
(epub ahead of print

Cepheid xpert monitor platform for the confirmation of BCR-ABL1 is conversion factors for the molecular monitoring of chronic myeloid leukemia
(Gerrard G. et al. Leuk Res, August 2016)

Charlson comorbidity index predicts poor outcome in CML patients treated with tyrosine kinase inhibitor
(Uemura M et al. Int J Hematol, August 2016)
(epub ahead of print)

ABCB1 overexpression is a key inhibitor of resistance to tyrosine kinase inhibitors in CML cell lines
(Eadie LN et al. PLoS one, August 2016)
In chronic myeloid leukemia patients on second-line tyrosine kinase inhibitor therapy, deep sequencing of BCR-ABL1 at the time of warning may allow sensitive detection of emerging drug-resistant mutants.
(Soverini S et al. BMC Cancer, August 2016)

MiR-124-3p/B4GALT1 axis plays an important role in SOCS3-regulated growth and chemo-sensitivity of CML
(Liu YX et al. J Hematol Oncol, August 2016)
Multiparameter analysis of off-target effects of dasatinib on bone homeostasis in patients with newly diagnosed myelogenous leukemia
(Hoehn D. et al. Clin Lymphoma Myeloma Leuk, Aug 2016)
miR-101 sensitized K562 cell line to imatinib through JAK2 downregulation and inhibition of NF-kB target genes
(Farhadi E et al. Tumour Biol, August 2016)
(epub ahead of print)

A propensity score matching analysis of dasatinib and nilotinib as a frontline therapy for patients with chronic myeloid leukemia in chronic phase
(Takahashi K et al. Cancer, Aug 2016
 
When to consider allogeneic transplantation in CML
(Radich J, Clin Lymphoma Myeloma Leuk, Aug 2016)
 
Imatinib intolerance is associated with blastic phase development in Philadelphia chromosome-positive chronic myeloid leukemia
(Ángeles-Velázquez JL. Clin Lymphoma Myeloma Leuk, August 2016)
 
July 2016
Summary of the published Indian data on chronic myeloid leukemia
(Singhal MK et al. South Asian J Cancer, Jul-Sept, 2016) 
A role for FOX01 in BCR-ABL1-independent tyrosine kinase inhibitor resistance in chronic myeloid leukemia
(Wagle M et al. Leukemia, July 2016)
Pattern of chronic myeloid leukemia in the imatinib era in a sub-Saharan African setting
(Faye BF et al. Ann Hematol, July 2016)
(epub ahead of print)
 
TP53 codon 72 polymorphism predicts chronic myeloid leukemia susceptibility and treatment outcome
(Weich N et al. Blood Celles Mol Dis, July 2016)

A safety evaluation of omacetacine mepesuccinate for the treatment of chronic myeloid leukemia
(Damlaj M et al. Expert Opin Drug Saf, July 2016) 
(epub ahead of print)

 

Cooperation of imipramine and tyrosine kinase blockade demonstrates activity against chronic myeloid leukemia
(Jorgensen KM et al. Oncotarget, July 2016)
(epub ahead of print) 
Impact of dose intensity of ponatinib on selected adverse events: Multivariate analyses from a pooled population of clinical trial patients
(Dorer DJ et al. Leuk Res, July 2016)
What are the challenges in 2016 regarding resistance to tyrosine kinase inhibitors in chronic myeloid leukemia and cancer?
(Lewis M et al. Hematol Oncol, July 2016)
(epub ahead of print)
 
Nilotinib 300 mg twice daily: an academic single-arm study of newly diagnosed chronic phase chronic myeloid leukemia
(Castagnetti F. et al. Haematologica, July 2016)
(epub ahead of print
Loss of mutL homolog-1 (MLH1) expression promotes acquisition of oncogenic and inhibitor-resistant points mutations in tyrosine kinases
(Springuel L. et al. Cell Mol Life Sci, July 2016)
(epub ahead of print
Psychological well-being and social support in chronic myeloid leukemia patients receiving lifelong targeted therapies
(Efficace F. et al. Support Care Cancer, July 2016
(epub ahead of print
Influence of CYP3A5*3 and ABCD1 C3435T on clinical outcomes and through plasma concentrations of imatinib in Nigerians with chronic myeloid leukaemia
(Adeagbo BA et al. J Clin Pharm Ther, July 2016)
(epub ahead of print)
 
Changes from imatinib mesylate to second generation tyrosine kinase inhibitors to improve renal impairment with imatinib mesylate in chronic myelogenous leukemia
(Hino A et al. Int J Hematol, July 2016)
(epub ahead of print)

The clinical significance of ABCB1 overexpression in predicting outcome of patients undergoing first-line imatinib treatment
(Eadie LN et al. Leukemia, July 2016)
(epub ahead of print)
 
Advanced phase chronic myeloid leukemia in the TKI era - a report from the Swedish CML register
(Söderlund S et al. Eur J Haematol, July 2016)
(epub ahead of print)

Measurement of BCR-ABL1 transcripts on the international scale in the United States: current status and best practices
(Arora R et al. Leuk Lymphoma, July 2016)
(epub ahead of print)

Pregnancy: part of life in chronic myelogenous leukemia
(Law AD et al. Leuk Lymphoma, July 2016)
(epub ahead of print

Impact of ABCD1 1236C> T-2677G> T-3435C> polymorphisms on the anti-proliferative activity of imatinib, nilotinib, dasatinib and ponatinib
(Dessity G et al. Sci Rep, July 2016)

 

Deep molecular reponses for treatment-free remission in chronic myeloid leukemia
(Dulucq S et al. Cancer Med, July 2016)
(epub ahead of print)

The role for FOX01 in BCR-ABL1-independent tyrosine kinase inhibitor resistance in chronic myeloid leukemia
(Wagle M et al. Leukemia, July 2016)
June 2016

Incidence of second malignancies of chronic myelid leukemia during treatment with tyrosine kinase inhibitors
(Yin XF et al. Clin Lymphoma Myeloma Leuk, June 2016)
(epub ahead of print)

Next-generation sequencing identifies major DNA methylation changes during progression of PH+ chronic myeloid leukemia
(Heller G et al. Leukemia, June 2016)

Discontinuing tyrosine kinase inhibitor therapy in chronic mylogenous leukemia: current understanding and future directions
(Bhalla S. et al. Clin Lymphoma Myeloma Leuk, June 2016) 
(epub ahead of print)

Development and evaluation of a secondary reference panel for BCR-ABL1 quantification on the international scale
(Cross NC et al. Leukemia, June 2016)
(epub ahead of print)

Management of pregnant chronic myeloid leukemia patients
(Abruzzese E et al. Expert Rev Hematol, June 2016)
(epub ahead of print)

A novel tubulin polymerization inhibitor, MPT0B206, downregulates BCR-ABL expression and induces apoptosis in imatinib-sensitive and imatinib-resistant CML cells
(Chen CW et al. Apoptosis, June 2016)
(epub ahed of print)

'Real-life' study of imatinib therapy in chronic-phase myeloid leukemia: A novel retrospective observational longitudinal analysis
(Merante S et al. Hematology, June 2016)
(epub ahead of print)

 

Discovery and characterization of a novel potent type II native and mutant BCR-ABL inhibitor (CHMFL-074) for chronic myeloid leukemia (CML)
(Liu F et al. Oncotarget, June 2016)
(epub ahead of print)

Life expectancy of patients with chronic myeloid leukemia approaches the life expectancy of the general population
(Bower H et al. J Clin Onol, June 2016
(epub ahead of print)
 
Drug repurposing for chronic myeloid leukemia: in silicio and in vitro investigation of DrugBank database for allosteric BCR-ABL inhibitors
(Singh VK et al. J Biomol Struct Dyn, June 2016)
(epub ahead of print)

Secondary malignancies in chronic myeloid leukemia patients after imatinib-based treatment: long-term observation in CML study IV
(Miranda et al. Leukemia, June 2016) 
A novel BCR-ABL1 fusion gene identified by next-generation sequencing in chronic myeloid leukemia
(Lyn X et al. Mol Cytogenet, June 2016)
Cardiovascular events associated with use of tyrosine kinase inhibitors in chronic myeloid leukemia: A population-based cohort study
(Dahlén T et al. Ann Intern Med, June 2016)
(epub ahead of print)
MEF2C and CEBPA: Possible co-regulators in chronic myeloid leukemia disease progression 
(Agatheeswaran S. et al. Int J Biochem Cell Biol, June 2016) 
(epub ahead of print)

Discontinuing tyrosine kinase inhibitor therapy in chronic mylogenous leukemia: current understanding and future directions
(Bhalla S. et al. Clin Lymphoma Myeloma Leuk, June 2016)

(epub ahead of print)

Dual targeting of p53 and c-MYC selectively eliminates leukaemic stem cells
(Abraham SA et al. Nature June, 2016
(epub ahead of print)

 

Incidence of second malignancies of chronic myelid leukemia during treatment with tyrosine kinase inhibitors
(Yin XF et al. Clin Lymphoma Myeloma Leuk, June 2016) 
(epub ahead of print)
 

High IL-7-levels in the bone marrow microenvironment mediate imatinib resistance and predict disease progression in chronic myeloid leukemia
(Zhang X et al. Int J. Hematol, June 2016)

European LeukemiaNet recommendations for the managment and avoidance of adverse events of treatment in chronic myeloid leukemia
(Steegmann JL et al. Leukemia, April 2017)

 

Unleashing the guardian: the targetable BCR-ABL/HAUSP/PML/PTEN network in CML
(Morotti A et al. Curr Drug Targets, June 2016)
(epub ahead of print)
 
Next-generation sequencing identifies major DNA methylation changes during progression of PH+ chronic myeloid leukemia
(Heller G et al. Leukemia, June 2016)
  Development and evaluation of a secondary reference panel for BCR-ABL1 quantification on the international scale
(Cross NC et al. Leukemia, June 2016)
(epub ahead of print
  Drug repurposing for chronic myeloid leukemia: in silicio and in vitro investigation of DrugBank database for allosteric BCR-ABL inhibitors
(Singh VK et al. J Biomol Struct Dyn, June 2016
(epub ahead of print)

  A novel BCR-ABL1 fusion gene identified by next-generation sequencing in chronic myeloid leukemia
(Lyn X et al. Mol Cytogenet, June 2016)
  A novel tubulin polymerization inhibitor, MPT0B206, downregulates BCR-ABL expression and induces apoptosis in imatinib-sensitive and imatinib-resistant CML cells
(Chen CW et al. Apoptosis, June 2016)
(epub ahed of print)

  MEF2C and CEBPA: Possible co-regulators in chronic myeloid leukemia disease progression 
(Agatheeswaran S. et al. Int J Biochem Cell Biol, June 2016
(epub ahead of print)

  Discovery and characterization of a novel potent type II native and mutant BCR-ABL inhibitor (CHMFL-074) for chronic myeloid leukemia (CML)
(Liu F et al. Oncotarget, June 2016)
(epub ahead of print)

May 2016

Optimizing the use of TKI's in the management of chronic myelogenous leukemia
(Ruiz-Cordell et al. Clin Lymphoma Myeloma Leuk, May 2016)

 

Validation of a rapid one-step high sensitivity real-time quantitative PCR system for detecting major BCR-ABL1 mRNA on an international scale
(Yoshida C et al. SpringerPlus May, 2016)

Setting global standards for stem cell research and clinical translation: The 2016 ISSCR guidelines
(Daley GQ et al. Stem Cell Reports, May 2016
(epub ahead of print)

ATG7 regulates energy metabolism, differentiation and survival of Philadelphia-chromosome positive cells
(Karvela M et al. Autophagy, May 2016)
(epub ahead of print

Dasatinib in imatinib-resistant or -intolerant chronic-phase, chronic myeloid leukemia patients: 7-year follow-up of study CA 180-034
(Shah NP et al. Am J Hematol, May 2016
(epub ahead of print)

The non-genomic loss of function of tumor suppressors: an essential role in the pathogenesis of chronic myeloid leukemia chronic phase
(Crivellaro S. et al. BMC Cancer, May 2016)

The treatment of CML at an environment with limited resources
(Gómez-Almaguer D. et al. Hematology, May 2016)

Next generation sequencing identifies major DNA methylation changes during progression of Ph+ chronic myeloid leukemia
(Heller G. et al. Leukemia, May 2016)

Final 5-year study results of DASASION: The dasatinib versus imatinib study in treatment-naive chronic myeloid leukemia patients trial
(Cortes JE et al. J Clin Oncol, May 2016)
(epub ahead of print)
The rs61764370 functional variant in the KRAS oncogene is associated with chronic myeloid leukemia risk in women
(Gutiérrez-Malacatt H. et al. Asian Pac J Cancer Prev, 2016) 
Frontline therapy with high-dose imatinib vs. 2nd generation tyrosine kinase inhibitor in patients with chronic-phase chronic myeloid leukemia - a propensity score analysis
(Sasaki K et al. Haematologica, May 2016)
(epub ahead of print)
Effect of tyrosine kinase inhibitors of stemness in normal and chronic myeloid leukemia cells
(Charaf L et al. Leukemia, May 2016
(epub ahead of print 
Management of advanced-phase chronic myelogenous leukemia
(Radich JP. J Natl. Compr Canc Netw, May 2016)
Comparison of branded and generics imatinib plasma concentrations in patients with chronic myelogenous leukemia - unicentric study
(Ostojic A. et al. Clin Lymphoma Myeloma Leuk, May2016

Chronic myeloid leukemia reminiscences and dreams
(Mughal TI et al. Haematologica, May 2016

Deregulated hedgehog pathway signaling is inhibited by the smoothened antagonist LDE225 (Sonidegib) in chronic phase chronic myeloid leukaemia
(Irvine DA et al. Sci Rep, May2016)

 Safety and efficacy of the combination of pegylated interferon-alpha2b and dasatinib in newly diagnosed chronic phase chronic myeloid leukemia patients
(Hjorth-Hansen H et al. Leukemia, May 2016
(epub ahead of print)

 
Health-related quality of life outcomes in chronic myleloid leukemia patients treated with second generation tyrosine kinase inhibitors: Do we know enough?
(Breccia M et al. Curr Med Res Opin, May 2016)
 
April 2016
Ponatinib versus imatinib for newly diagnosed chronic myeloid leukaemia: an international, randomised, open-label, phase 3 trial
(Lipton JH et al. Lancet Oncol, April 2016
(epub ahead of print) 

Identification of CD25 as STAT5 dependent growth regulator of leukemic stem cells in PH+ CML

(Sadovnik I et al. Clin Cancer Res, April 2016) 

Molecular monitoring of tyrosine kinase inhibitor therapy of chronic myeloid leukemia in China
(Jiang Q et al. J Cancer Res Clin Oncol, April 2016)
(epub ahead of print) 

Early BCR-ABL reduction is predictive of better event-free survival in patients with newly diagnosed chronic myeloid leukemia treated with any tyrosine kinase inhibitor
(Fava C et al. Clin Lymphoma Myeloma Leuk, April 2016)
(epub ahead of print)

Health-related quality of life during bosutinib (SKI-606) therapy in patients with advanced chronic myeloid leukemia after imatinib failure
(Whitely J et al. Curr Med Res Opin, April 2016
(epub ahead of print) 

Modeling BCR-ABL and MLL-AF9 leukemia in a human bone marrow-like scaffold based xenograft model
(Sontakke P et al. Leukemia, April 2016
(epub ahead of print)

Monitoring disease burden in chronic myeloid leukemia: past, present, and future
(Egan D. et al. Am J Hematol, April 2016) 
(epub ahead of print
Quantitative analysis of mutant subclones in chronic myeloid leukemia: comparison of different methodological approaches
(Preuner S. et al. Int J Mol Sci, April)

 

 

Quantitative assessment of the CD26+ leukemic stem cell compartment in chronic myeloid leukemia: patient-subgroups, prognostic impact, and technical aspects
Culen M et al. Oncotarget, April 2016
(epub ahead of print)

 

Mtss1 is a critical epigenetically regulated tumor suppressor in CML
(Schemionek M et al. Leukemia, April 2016)

 

The impact of multiple low-level BCR-ABL1 mutations on response to Ponatinib
(Parker WT et al. Blood, April 2016)

Combined population dynamics and entropy modelling supports patients stratification in chronic myeloid leukemia
(Brehme M et al. Sci Rep, April 2016
March 2016
Cross-intolerance with dasatinib among imatinib-intolerant patients with chronic phase myeloid leukemia

(Khoury HJ et al. Clin Lymphoma Myeloma Leuk, March 2016)
(epub ahead of print)

Risk stratification of chromosomal abnormalities in chronic myelogenous leukemia in the era of tyrosine kinase inhibitor therapy
(Wang W et al. Blood, March 2016)
(epub ahead of print 
Hyperhomocysteinemia and high doses of nilotinib favor cardiovascular events in chronic phae chronic myelogenous leukemia patients
(Fossard G. et al. Haematologica, March 2016)
Leukemic stem cell quantification in newly diagnosed chronic myeloid leukamia patients predict response to nilotinib therapy
(Thielen N et al. Clin Cancer Res, March 2016
(epub ahead of print

Increased prevalance of prior malignancies and autoimmune diseases in patients diagnosed with chronic myeloid leukemia
(Gunnarson N et al. Leukemia, March 2016
(epub ahead of print)

A role for FOXO1 in BCR-ABL-1 independent tyrosine kinase inhibitor resistance in chronic myeloid leukemia
(Wagle M et al. Leukemia, March 2016
(epub ahead of print)

Next generation sequencing for sensitive detection of BCR-ABL1 mutations relevant to tyrosine kinase inhibitor choice in imatinib-resistant patients
(
Soverini S. et al. Oncotarget, March 2016
(epub ahead of print)
The role of Fas-associatd phosphotase 1 in leukemia stem cell persistence during tyrosine kinase inhibitor treatment of chronic myeloid leukemia 
(Huang W et al. Leukemia, March 2016)
(epub ahead of print)

Lymphocytosis after treatment with dasatinib in chronic myeloid leukemia: Effects on response and toxicity
(Schiffer CA et al. Cancer, March 2016
(epub ahead of print)

Timosaponin A-III reverses multi-drug resistance in human chronic myelogenous leukemia K562/ADM cells via downregulation of MDR1 and MRP1 expression by inhibiting PI3K/Akt signaling pathway
(Chen JR et al. Int. J Oncol, March 2016
(epub ahead of print)

Long-term evaluation of cardiac and vascular toxicity in patients with philadelphia chromosome positive leukemias treated with Bosutinib 
(Cortes JE et al. Am J Hematol, March 2016
(epub ahead of print)

Characteristics of BCR-ABL kinase domain mutations in chronic myeloid leukemia from India: not just missense mutations but insertions and deletions are also associated with TKI resistance
(Patkar N et al. Leuk Lymphoma, March 2016
(epub ahead of print)

Splenic irradication before hematopoietic stem cell transplantation for chronic myeloid leukemia: long-term follow-up of a prospective randomized study
(Gratwohl A et al. Ann Hematol, March 2016)
(epub ahead of print)

Micro RNAs mediated regulation of MAPK signaling pathways in chronic myeloid leukemia
(Chakraborty C. et al. Oncotarget, March 2016)
(epub ahead of print)

Rotation of nilotinib and imatinib for first-line treatment of chronic myeloid leukemia
(Gugliotta G. Am J Hematol, March 2016
(epub ahead of print)

Overexpression of RPS27a contributes to enhanced chemoresistance of CML cells to imatinib by the transactivated STAT3
(Wang H et al. Oncotarget, March 2016)
(epub ahead of print)
Cost-effectiveness of tyrosine kinase inhibitor treatment strategies for chronic myeloid leukemia in chronic phase after generic entry of imatinib in the United States
(
Padula WV et al. J Natl Cancer Inst., March 2016
(epub ahead of print
NUMB inactivation confers resistance to imatinib in chronic myeloid leukemia cells
(Garcia-Alegría E et al. Cancer Lett, March 2016)
(epub ahead of print) 

New methodologies in the molecular monitoring of CML
(Yeung CC et al. Curr Hematol Malig Rep, March 2016
(epub ahead of print)

c-MYB is a transcriptional regulator of ESPL1/separase in BCR-ABL-positive chronic myeloid leukemia
(Prinzhorn W et al. Biomark Res, March 2016) 
(epub ahead of print

Clinical safety and efficacy of nilotinib or dasatinib in patients with newly diagnosed chronic-phase chronic myelogenous leukemia and pre-existing liver and/or renal dysfunction
(Sasaki K et al. Clin Lymphoma Myeloma Leuk, March 2016)

Next generation sequencing-assisted DNA-based digital PCR for a personalized approach to the detection and quantification of residual disease in chronic myeloid leukemia patients
(Alikian M et al. J Mol Diagn, March 2016)

Present and future of molecular monitoring in chronic myloid leukaemia
(
Soverini S et al. Br J Haematol, March 2016) 
(epub ahead of print)
Next generation sequencing-assisted DNA-based digital PCR for a personalized approach to the detection and quantification of residual disease in chronic myeloid leukemia patients
(Alikian M et al. J Mol Diagn, March 2016)
Is cure for chronic myeloid leukemia possible in the tyrosine kinase inhibitors era?
(Bansal A et al. Curr Opin Hematol, March 2016)
(epub ahead of print)

 

 

Long-term benefits and risks of frontline nilotinib vs imatinib for chronic myeloid leukemia in chronic phase: 5-year update of the randomized ENESTnd trial
(Hochhaus A et al. Leukemia, April 2017)

 
February 2016
Evaluating the impact of a switch to nilotinib on imatinib-related chronic low-grade adverse events in patients with CML-CP: The ENRICH study
(Cortes JE et al. Clin Lymphoma Myeloma Leuk, February 2016) 
(epub ahead of print) 
High CIP2A levels correlates with an antiapoptoic phenotype that can be overcome by targeting BCL-XL in chronic meyloid leukemia
(Lucas CM et al. Leukemia, February 2016)
(epub ahead of print)
Long-term side effects of tyrosine kinase inhibitors in chronic myeloid leukemia
(Caldemeyer L et al. Curr Hematol Malig Rep, February 2016) 
(epub ahead of print)

Inhibition of protein kinase CK2 by CX-5011 counteracts imatinib resistance preventing rpS6 phosphorylation in chronic meyloid leukaemia cells: new combined therapeutic strategies
(Salizzato V et al. Oncotarget, February 2016
(epub ahead of print)

Hematologic malignancies in pregnancy: Management guidelines from an international consensus
(Lishner M et al. J Clin Oncol, February 2016
BCR-ABL1 expression, RT-qPCR and treatment decisions in chronic myeloid leukemia
(Latham S et al. J Clin Pathol, February 2016
(epub ahead of print) 

Quality of life and long-term therapy in patients with chronic myeloid leukemia
(Flynn KE et al. Curr Hematol Malig Rep, 
February 2016
)
(epub ahead of print

Hsp90 inhibitor, BIIBo21, induces apoptosis and authopagy by regulating mTOR-UIIK1 pathway in imatinib-sensitive and-resistant chronic myeloid leukemic cells
(He W et al. Int J Oncol, February 2016) 

Omacetaxine Mepesuccinate for chronic myeloid leukemia
(Rosshandler Y et al. Expert Rev Hematol, February 2016) 

Normal ABL1 is a tumour suppressor and therapeutic target in human and mouse leukemias expressing oncogeneic ABL1 kinase
(Dasgupta Y et al. Blood, February 2016
Analysis of 2013 European LeukemiaNET (ELN) responses in chronic phase CML across four frontline TKI modalities and impact on clinical outcome
(Jain P et al. Br. J Hematol, February 2016)
Heterogeneity of leukemia-initiating capacity of chronic meylogenous leukemic stem cells
(Zhang B et al. J Clin Invest, February 2016)
(epub ahead of print)
Chronic Myeloid Leukemia: 2016 update on diagnosis, therapy and monitoring
(Jabbour E et al. Am J Hematol, February 2016)
Compound mutations in BCR-ABL1 are not major drivers of primary or secondary resistance to ponatinib in CP-CML patients
(Deiniger MW et al. Blood, February 2015)
Association between BCR-ABL tyrosine kinase inhibitors for chronic myeloid leukemia and cardiovascular events, major molecular response and overall survival: A systemic review and meta-analysis
(Douxfils J et al. JAMA Oncol, February 2016)
(epub ahead of print)
The role of microRNAs in the pathogenesis and drug resistance of chronic myelogenous leukemia (Review
(Di Stefano C et al. Oncol Rep, February 2016)
The reality of cancer treatment in a developing country: the effects of delayed TKI treatment on survival, cytogenetic and molecular responses in chronic myeloid leukaemia patients
(Kurtovic-Kozaric A et al. Br J Haematol, 
February 2016

(epub ahead of print
 
Allogeneic transplantation for CML in the TKI era: striking the right balance
(Innes AJ et al. Nat Rev Clin Oncol, 
February 
2016
 
January 2016
Conditional survival with chronic myeloid leukemia in chronic phase in the era of tyrosine kinase inhibitors
(Sasaki K et al. Cancer, January 2016)
The impact of multiple low-level BCR-ABL1 mutations on response to ponatinib
(Parker WT et al. Blood, January 2016) 
(epub ahead of print)
Management of the cardiovascular disease risk during nilotinib treatment in chronic myeloid leukemia: 2015 recommendations from the France intergroup des leucémies myéloides chroniques
(Rea D et al. Bull Cancer, January 2016)
Imatinib reduces bone marrow fibrosis and overwhelms the adverse prognostic impact of reticulin formation in patients with chronic myeloid leukaemia
(Tanrikulu Simsek E et al. J Clin Pathol, January 2016)
Dasatinib first-line: Multicentric Italian experience outside clinical trials
(Breccia M et al. Leuk Res, January 2016)

Impact of BCR-ABL transcript type on response and survival in patients with chronic phase chronic myeloid leukemia treated with tyrosine kinase inhibitors
(Jain P et al. Blood, January 2016

(epub ahead of print)

Prognosis of long-term survival considering disease-specific death in patients with chronic myeloid leukemia
(Pfirrmann M et al. Leukemia, January 2016)
 

Identification and characterization of tyrosine kinase nonreceptor 2 mutations in leukemia through integration of kinase inhibitor screening and genomic analysis

(Maxson JE et al. Cancer Res, January 2016)

Factors influencing long-term efficacy and tolerability of bosutinib in chronic phase myeloid leukaemia resistant or intolerant to imatinib
(Brümmendorf TH et al. Br J Haematol, 
January 2016
)
(epub ahead of print 
In silico identifcation of inhibitors against mutated BCR-ABL protein screening and molecular dynamics simultation study
(Kumar H et al. J Biomol Struct Dyn, January 2016)
(epub ahead of print) 
Conditioned survival in patients with chronic myeloid leukemia in chronic phase in the era of tyrosine kinase inhibitors
(Sasaki K et al. Cancer, January 2015 
 
Considering baseline factors and early response rates to optimize therapy for chronic myeloid leukemia in chronic phase
(Akard LP et al. Leuk Lymphoma, January 2016)
(epub ahead of print)
 


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