Literature DB >> 21252655

Navigating the road toward optimal initial therapy for chronic myeloid leukemia.

Ross A Okimoto1, Richard A Van Etten.   

Abstract

PURPOSE OF REVIEW: Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment of chronic myeloid leukemia (CML) and are now widely accepted as the initial therapy of choice in this disease, supplanting interferon and allogeneic stem cell transplantation. There are currently three drugs approved by the US Food and Drug Administration (FDA) for front-line treatment of CML: imatinib, nilotinib, and dasatinib. A fourth drug, bosutinib, may also win FDA approval in 2011. The goal of this review is to summarize the most recent information on initial treatment of CML and to aid clinicians in managing newly diagnosed CML patients. RECENT
FINDINGS: Phase III studies comparing imatinib with nilotinib or dasatinib in newly diagnosed CML were published in June 2010, leading to accelerated FDA approval for both of these 'second-generation' TKIs for initial therapy of CML. There are significant differences between the agents in terms of frequency and rate of responses, progression-free survival, and side-effects. However, the follow-up period on these trials is short, and there are as yet no significant differences in overall survival. Guidelines for monitoring CML patients on TKI therapy have been recently revised.
SUMMARY: Management of newly diagnosed CML patients in the coming decade will begin to resemble antibiotic treatment of infection, with therapy individualized based on patient risk factors, co-morbidities, and tolerability. In addition, the cost of therapy will emerge as an important consideration as generic imatinib becomes available in 2015. In this context, clinical trials to guide decision-making in newly diagnosed CML patients are needed.

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Year:  2011        PMID: 21252655      PMCID: PMC3496274          DOI: 10.1097/MOH.0b013e32834399a5

Source DB:  PubMed          Journal:  Curr Opin Hematol        ISSN: 1065-6251            Impact factor:   3.284


  54 in total

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Authors:  Janice M Mueller
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2.  Effective targeting of quiescent chronic myelogenous leukemia stem cells by histone deacetylase inhibitors in combination with imatinib mesylate.

Authors:  Bin Zhang; Adam C Strauss; Su Chu; Min Li; Yinwei Ho; Keh-Dong Shiang; David S Snyder; Claudia S Huettner; Leonard Shultz; Tessa Holyoake; Ravi Bhatia
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3.  Sustained molecular response with interferon alfa maintenance after induction therapy with imatinib plus interferon alfa in patients with chronic myeloid leukemia.

Authors:  Andreas Burchert; Martin C Müller; Philippe Kostrewa; Philipp Erben; Tilman Bostel; Simone Liebler; Rüdiger Hehlmann; Andreas Neubauer; Andreas Hochhaus
Journal:  J Clin Oncol       Date:  2010-02-08       Impact factor: 44.544

4.  Current event-free survival after sequential tyrosine kinase inhibitor therapy for chronic myeloid leukemia.

Authors:  Aref Al-Kali; Hagop Kantarjian; Jianqin Shan; Roland Bassett; Alfonso Quintás-Cardama; Gautam Borthakur; Elias Jabbour; Srdan Verstovsek; Susan O'Brien; Jorge Cortes
Journal:  Cancer       Date:  2010-09-15       Impact factor: 6.860

5.  Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia.

Authors:  B J Druker; M Talpaz; D J Resta; B Peng; E Buchdunger; J M Ford; N B Lydon; H Kantarjian; R Capdeville; S Ohno-Jones; C L Sawyers
Journal:  N Engl J Med       Date:  2001-04-05       Impact factor: 91.245

Review 6.  Initial treatment for patients with CML.

Authors:  John M Goldman
Journal:  Hematology Am Soc Hematol Educ Program       Date:  2009

7.  Results of dasatinib therapy in patients with early chronic-phase chronic myeloid leukemia.

Authors:  Jorge E Cortes; Dan Jones; Susan O'Brien; Elias Jabbour; Farhad Ravandi; Charles Koller; Gautam Borthakur; Brenda Walker; Weiqiang Zhao; Jianqin Shan; Hagop Kantarjian
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8.  Cytogenetic and molecular responses to standard-dose imatinib in chronic myeloid leukemia are correlated with Sokal risk scores and duration of therapy but not trough imatinib plasma levels.

Authors:  Donna L Forrest; Shannon Trainor; Ryan R Brinkman; Michael J Barnett; Donna E Hogge; Thomas J Nevill; John D Shepherd; Stephen H Nantel; Cynthia L Toze; Heather J Sutherland; Kevin W Song; Julye C Lavoie; Maryse M Power; Yasser Abou-Mourad; Clayton A Smith
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9.  Imatinib for newly diagnosed patients with chronic myeloid leukemia: incidence of sustained responses in an intention-to-treat analysis.

Authors:  Hugues de Lavallade; Jane F Apperley; Jamshid S Khorashad; Dragana Milojkovic; Alistair G Reid; Marco Bua; Richard Szydlo; Eduardo Olavarria; Jaspal Kaeda; John M Goldman; David Marin
Journal:  J Clin Oncol       Date:  2008-06-02       Impact factor: 44.544

10.  Nilotinib in imatinib-resistant CML and Philadelphia chromosome-positive ALL.

Authors:  Hagop Kantarjian; Francis Giles; Lydia Wunderle; Kapil Bhalla; Susan O'Brien; Barbara Wassmann; Chiaki Tanaka; Paul Manley; Patricia Rae; William Mietlowski; Kathy Bochinski; Andreas Hochhaus; James D Griffin; Dieter Hoelzer; Maher Albitar; Margaret Dugan; Jorge Cortes; Leila Alland; Oliver G Ottmann
Journal:  N Engl J Med       Date:  2006-06-15       Impact factor: 91.245

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Journal:  Am J Hematol       Date:  2011-09       Impact factor: 10.047

Review 2.  Contemporary insights into the pathogenesis and treatment of chronic myeloproliferative neoplasms.

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Review 7.  Advances in the biology and therapy of chronic myeloid leukemia: proceedings from the 6th Post-ASH International Chronic Myeloid Leukemia and Myeloproliferative Neoplasms Workshop.

Authors:  Richard A Van Etten; Michael Mauro; Jerald P Radich; John M Goldman; Giuseppe Saglio; Catriona Jamieson; Simona Soverini; Carlo Gambacorti-Passerini; Rüdiger Hehlmann; Giovanni Martinelli; Danilo Perrotti; David T Scadden; Tomasz Skorski; Ayalew Tefferi; Tariq I Mughal
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Review 8.  Signal transduction in the chronic leukemias: implications for targeted therapies.

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Journal:  Curr Hematol Malig Rep       Date:  2013-03       Impact factor: 3.952

9.  Phosphorylation events during viral infections provide potential therapeutic targets.

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10.  Stat5 signaling specifies basal versus stress erythropoietic responses through distinct binary and graded dynamic modalities.

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