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Following the 53rd annual meeting of the American Society of Hematology (ASH) in San Diego in December 2011, a group of clinical and laboratory investigators convened for the 6th Post-ASH International Workshop on Chronic Myeloid Leukemia (CML) and Myeloproliferative Neoplasms (MPN). The Workshop took place on 13-14 December at the Estancia, La Jolla, California, USA. This report summarizes the most recent advances in the biology and therapy of CML that were presented at the ASH meeting and discussed at the Workshop. Preclinical studies focused on the CML stem cell and its niche, and on early results of deep sequencing of CML genomes. Clinical advances include updates on second- and third-generation tyrosine kinase inhibitors (TKIs), molecular monitoring, TKI discontinuation studies and new therapeutic agents. A report summarizing the pertinent advances in MPN has been published separately.

© 2016 Ferrata Storti Foundation.With the deaths of Janet Rowley and John Goldman in December 2013, the world lost two pioneers in the field of chronic myeloid leukemia. In 1973, Janet Rowley, unraveled the cytogenetic anatomy of the Philadelphia chromosome, which subsequently led to the identification of the BCR-ABL1 fusion gene and its principal pathogenetic role in the development of chronic myeloid leukemia. This work was also of major importance to support the idea that cytogenetic changes were drivers of leukemogenesis. John Goldman originally made seminal contributions to the use of autologous and allogeneic stem cell transplantation from the late 1970s onwards. Then, in collaboration with Brian Druker, he led efforts to develop ABL1 tyrosine kinase inhibitors for the treatment of patients with chronic myeloid leukemia in the late 1990s. He also led the global efforts to develop and harmonize methodology for molecular monitoring, and was an indefatigable organizer of international conferences. These conferences brought together clinicians and scientists, and accelerated the adoption of new therapies. The abundance of praise, tributes and testimonies expressed by many serve to illustrate the indelible impressions these two passionate and affable scholars made on so many people’s lives. This tribute provides an outline of the remarkable story of chronic myeloid leukemia, and in writing it, it is clear that the historical triumph of biomedical science over this leukemia cannot be considered without appreciating the work of both Janet Rowley and John Goldman.

As a group of more than 100 experts in chronic myeloid leukemia (CML), we draw attention to the high prices of cancer drugs, with the particular focus on the prices of approved tyrosine kinase inhibitors for the treatment of CML. This editorial addresses the multiple factors involved in cancer drug pricing and their impact on individual patients and health care policies, and argues for the need to (1) lower the prices of cancer drugs to allow more patients to afford them and (2) maintain sound long-term health care policies.

Following the 53rd annual meeting of the American Society of Hematology (ASH) in San Diego in December 2011, a group of clinical and laboratory investigators convened for the 6th Post-ASH International Workshop on Chronic Myeloid Leukemia (CML) and Myeloproliferative Neoplasms (MPN). The Workshop took place on 13-14 December at the Estancia, La Jolla, California, USA. This report summarizes the most recent advances in the biology and therapy of CML that were presented at the ASH meeting and discussed at the Workshop. Preclinical studies focused on the CML stem cell and its niche, and on early results of deep sequencing of CML genomes. Clinical advances include updates on second- and third-generation tyrosine kinase inhibitors (TKIs), molecular monitoring, TKI discontinuation studies and new therapeutic agents. A report summarizing the pertinent advances in MPN has been published separately. © 2013 Informa UK, Ltd.

NIH Public Access Author Manuscript Am J Hematol. Author manuscript; available in PMC 2012 November 01. Published in final edited form as: Am J Hematol. 2011 September ; 86(9): 811–819. doi:10.1002/ajh.22097. $watermark-text Chronic Myeloid Leukemia 2011: Successes, challenges, and strategies – Proceedings of the 5 th Annual BCR-ABL1 positive and BCR-ABL1 negative myeloproliferative neoplasms workshop Tariq I Mughal 1 , Jerald P Radich 2 , Richard A. Van Etten 3 , Alfonso Quintas-Cardama 4 , Tomasz Skorski 5 , Farhad Ravandi 6 , Daniel J. DeAngelo 7 , Carlo Gambacorti-Passerini 8 , Giovanni Martinelli 9 , and Ayalew Tefferi 10 1 University of Colorado School of Medicine, Denver, USA 2 Fred Hutchinson Cancer Center, Seattle, USA 3 Tufts Medical Center, Boston, USA 4 MD Anderson Cancer Center, Houston, USA $watermark-text 5 Temple 6 MD University, Philadelphia, USA Anderson Cancer Center, Houston, USA 7 Dana Farber Cancer Center at Harvard Medical School, Boston, USA 8 University 9 Insitute 10 Mayo of Milan, Monza, Italy Le A. Seragnoli, Bologna, Italy Clinic, Rochester, MN, USA. Abstract $watermark-text This report is based on the presentations and discussions at the 5 th annual BCR-ABL1 positive and BCR-ABL1 negative myeloproliferative neoplasms (MPN) workshop, which took place immediately following the 52 nd American Society of Hematology (ASH) meeting in Orlando, Florida on December 7 th -8 th , 2011. Relevant data which was presented at the ASH meeting as well as all other recent publications were presented and discussed at the workshop. This report covers front-line therapies of BCR-ABL1-positive leukemias, in addition to addressing some topical biological, pre-clinical and clinical issues, such as new insights into genomic instability and resistance to tyrosine kinase inhibitors (TKIs), risk stratification and optimizing molecular monitoring. A report pertaining to the new therapies and other pertinent preclinical and clinical issues in the BCR-ABL1 negative MPNs is published separately. Introduction For patients with BCR-ABL1-positive leukemias, which comprise of all the Philadelphia (Ph) chromosome-positive and some Ph-negative leukemias, the introduction of the original tyrosine kinase inhibitor (TKI), imatinib mesylate (IM) into the clinics in 1998, resulted in being a classic therapeutic landmark (1,2). After 12 months of therapy with IM, 69% of Correspondence to: Tariq Mughal MD FRCP FACP 23655 Currant Drive, Golden, Colorado 80401, USA Tel +1 303 526 8586 tmughal911@hotmail.com.

none 15 No abstract available Cross N.C.; Daley G.Q.; Green A.R.; Hughes T.P.; Jamieson C.; Manley P.; Mughal T.; Perrotti D.; Radich J.; Skoda R.; Soverini S.; Vainchenker W.; Verstovsek S.; Villeval J.L.; Goldman J.M. Cross N.C.; Daley G.Q.; Green A.R.; Hughes T.P.; Jamieson C.; Manley P.; Mughal T.; Perrotti D.; Radich J.; Skoda R.; Soverini S.; Vainchenker W.; Verstovsek S.; Villeval J.L.; Goldman J.M.

Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized in 90-95% of cases by the reciprocal t(9;22)(q34;q11) chromosomal translocation, that generates a BCR-ABL fusion gene on the derivative chromosome 22 [der(22)] or Philadelphia (Ph) chromosome. The BCR-ABL gene encodes a constitutively active tyrosine kinase, which leads to the activation of multiple signaling pathways involved in cell-cycle, adhesion and apoptosis. The aim of the chapter book was to bescribe risk statification models and prognostic factors, including baseline and response-related prognostic variables, with relevant impact on the outcome of CML patients.