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Daniel C. McFarland, Heather Polizzi, John Mascarenhas, Marina Kremyanskaya, Jimmie Holland and Ronald Hoffman

Background The prevalence of distress, anxiety, and depressive symptoms has not been assessed by standard measures in patients with BCR-ABL–negative myeloproliferative neoplasms (MPNs). This is perhaps surprising given the large symptom burden

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Susan O'Brien, Ellin Berman, Joseph O. Moore, Javier Pinilla-Ibarz, Jerald P. Radich, Paul J. Shami, B. Douglas Smith, David S. Snyder, Hema M. Sundar, Moshe Talpaz and Meir Wetzler

head to tail fusion of the breakpoint cluster region ( BCR ) gene on chromosome 22 at band q11 and the Abelson murine leukemia ( ABL ) gene located on chromosome 9 at band q34. 1 The fusion gene, BCR-ABL , encodes a protein (p210 BCR-ABL ) with

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Michael Deininger

achieving a molecular response . Blood 2004 ; 104 : 2204 – 2205 . 10 Kim Y-J Kim D-W Lee S . Monitoring of BCR-ABL transcript levels after discontinuation of imatinib therapy in chronic myelogenous leukemia patients achieving complete

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Michael W. Deininger, Neil P. Shah, Jessica K. Altman, Ellin Berman, Ravi Bhatia, Bhavana Bhatnagar, Daniel J. DeAngelo, Jason Gotlib, Gabriela Hobbs, Lori Maness, Monica Mead, Leland Metheny, Sanjay Mohan, Joseph O. Moore, Kiran Naqvi, Vivian Oehler, Arnel M. Pallera, Mrinal Patnaik, Keith Pratz, Iskra Pusic, Michal G. Rose, B. Douglas Smith, David S. Snyder, Kendra L. Sweet, Moshe Talpaz, James Thompson, David T. Yang, Kristina M. Gregory and Hema Sundar

;22] that gives rise to a BCR-ABL1 fusion gene. 2 In most patients, the chromosomal break points are located in intron 13 or 14 of the BCR gene on chromosome 22 (major break point cluster region; M-BCR ); in the ABL1 gene they are located between the

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Jerald P. Radich

agent used, it is important to give initial therapy a fair trial before considering it ineffective, he added. The first milestone is the 3-month BCR-ABL/ABL percentage. According to the NCCN Guidelines, if the BCR-ABL/ABL is less than 10% (indicative

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Ellin Berman

nilotinib based on results of phase I and II trials that showed greater than 70% major cytogenetic response rates in heavily pretreated patients. 1 , 2 Ponatinib was also approved for patients with the T315I BCR-ABL1 mutation, with similar response rates

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Susan O’Brien, Jerald P. Radich, Camille N. Abboud, Mojtaba Akhtari, Jessica K. Altman, Ellin Berman, Daniel J. DeAngelo, Michael Deininger, Steven Devine, Amir T. Fathi, Jason Gotlib, Madan Jagasia, Patricia Kropf, Joseph O. Moore, Arnel Pallera, Javier Pinilla-Ibarz, Vishnu VB. Reddy, Neil P. Shah, B. Douglas Smith, David S. Snyder, Meir Wetzler, Kristina Gregory and Hema Sundar

cluster region ( BCR) gene on chromosome 22 and the Abelson murine leukemia ( ABL1 ) gene located on chromosome 9. 1 The product of the BCR-ABL fusion gene, the p210 fusion protein with deregulated tyrosine kinase activity, plays a central role in the

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Giuseppe Saglio and Carmen Fava

Chronic myelogenous leukemia (CML) is a clonal stem cell disease characterized by the presence of the BCR-ABL oncogene, whose endowed and constitutively activated tyrosine kinase activity leads to increased proliferation and genomic instability of

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Paul J. Shami

Chronic myelogenous leukemia (CML) is a myeloproliferative disorder resulting from a translocation between chromosomes 9 and 22 (t(9;22) or Philadelphia chromosome) leading to an abnormal fusion protein (BCR-ABL) with dysregulated tyrosine kinase activity

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Javier Pinilla-Ibarz and Alfonso Quintás-Cardama

tyrosine kinase on the growth of Bcr-Abl positive cells . Nat Med 1996 ; 2 : 561 – 566 . 4 O’Brien SG Guilhot F Larson RA . Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukemia