Literature DB >> 27488943

New hope for chronic myelogenous leukemia patients: dasatinib offers better efficacy with shorter treatment.

Kazuhito Naka1, Tatsuo Ichinohe1.   

Abstract

Although the discovery of tyrosine kinase inhibitors (TKIs) has dramatically improved the prognoses of chronic myelogenous leukemia (CML) patients, a cure has remained elusive. Unanswered questions include how long must a patient continue on TKI therapy, and how does a patient know when he/she can safely stop or finish this therapy? Imagawa et al. have carefully addressed these questions of safety and efficacy using a stop study of the second-generation TKI dasatinib. The results of a multicenter phase II trial termed the "dasatinib discontinuation" (DADI) trial indicated that 48% (30/63) of CML patients who had maintained a deep molecular response (DMR) to second-line or subsequent dasatinib therapy for at least for 1 year did not show any signs of disease relapse. Thus, even after it is stopped, dasatinib treatment may decrease the chance of disease relapse and provide a curative benefit to CML patients. This work by Imagawa et al. strongly supports the clinical utility of the second-generation TKI dasatinib for CML treatment.

Entities:  

Keywords:  Chronic myelogenous leukemia (CML); dasatinib discontinuation (DADI); deep molecular response (DMR); tyrosine kinase inhibitor (TKI) therapy

Year:  2016        PMID: 27488943      PMCID: PMC4958058          DOI: 10.21037/sci.2016.05.05

Source DB:  PubMed          Journal:  Stem Cell Investig        ISSN: 2306-9759


  21 in total

1.  Discontinuation of dasatinib in patients with chronic myeloid leukaemia who have maintained deep molecular response for longer than 1 year (DADI trial): a multicentre phase 2 trial.

Authors:  Jun Imagawa; Hideo Tanaka; Masaya Okada; Hirohisa Nakamae; Masayuki Hino; Kazunori Murai; Yoji Ishida; Takashi Kumagai; Seiichi Sato; Kazuteru Ohashi; Hisashi Sakamaki; Hisashi Wakita; Nobuhiko Uoshima; Yasunori Nakagawa; Yosuke Minami; Masahiro Ogasawara; Tomoharu Takeoka; Hiroshi Akasaka; Takahiko Utsumi; Naokuni Uike; Tsutomu Sato; Sachiko Ando; Kensuke Usuki; Satoshi Morita; Junichi Sakamoto; Shinya Kimura
Journal:  Lancet Haematol       Date:  2015-11-10       Impact factor: 18.959

2.  Poor adherence is the main reason for loss of CCyR and imatinib failure for chronic myeloid leukemia patients on long-term therapy.

Authors:  Amr R Ibrahim; Lina Eliasson; Jane F Apperley; Dragana Milojkovic; Marco Bua; Richard Szydlo; Francois-Xavier Mahon; Kasia Kozlowski; Christos Paliompeis; Letizia Foroni; Jamshid S Khorashad; Alex Bazeos; Mathieu Molimard; Alistair Reid; Katayoun Rezvani; Gareth Gerrard; John Goldman; David Marin
Journal:  Blood       Date:  2011-02-23       Impact factor: 22.113

Review 3.  Targeting survival pathways in chronic myeloid leukaemia stem cells.

Authors:  A Sinclair; A L Latif; T L Holyoake
Journal:  Br J Pharmacol       Date:  2013-08       Impact factor: 8.739

4.  Patients with chronic myeloid leukemia who maintain a complete molecular response after stopping imatinib treatment have evidence of persistent leukemia by DNA PCR.

Authors:  D M Ross; S Branford; J F Seymour; A P Schwarer; C Arthur; P A Bartley; C Slader; C Field; P Dang; R J Filshie; A K Mills; A P Grigg; J V Melo; T P Hughes
Journal:  Leukemia       Date:  2010-09-02       Impact factor: 11.528

5.  Discontinuation of imatinib in patients with chronic myeloid leukaemia who have maintained complete molecular remission for at least 2 years: the prospective, multicentre Stop Imatinib (STIM) trial.

Authors:  François-Xavier Mahon; Delphine Réa; Joëlle Guilhot; François Guilhot; Françoise Huguet; Franck Nicolini; Laurence Legros; Aude Charbonnier; Agnès Guerci; Bruno Varet; Gabriel Etienne; Josy Reiffers; Philippe Rousselot
Journal:  Lancet Oncol       Date:  2010-10-19       Impact factor: 41.316

6.  Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid leukemia after failure of imatinib therapy.

Authors:  Andreas Hochhaus; Hagop M Kantarjian; Michele Baccarani; Jeffrey H Lipton; Jane F Apperley; Brian J Druker; Thierry Facon; Stuart L Goldberg; Francisco Cervantes; Dietger Niederwieser; Richard T Silver; Richard M Stone; Timothy P Hughes; Martin C Muller; Rana Ezzeddine; Athena M Countouriotis; Neil P Shah
Journal:  Blood       Date:  2006-11-30       Impact factor: 22.113

7.  Mono/oligoclonal T and NK cells are common in chronic myeloid leukemia patients at diagnosis and expand during dasatinib therapy.

Authors:  Anna Kreutzman; Vesa Juvonen; Veli Kairisto; Marja Ekblom; Leif Stenke; Ruth Seggewiss; Kimmo Porkka; Satu Mustjoki
Journal:  Blood       Date:  2010-04-22       Impact factor: 22.113

8.  Clonal expansion of T/NK-cells during tyrosine kinase inhibitor dasatinib therapy.

Authors:  S Mustjoki; M Ekblom; T P Arstila; I Dybedal; P K Epling-Burnette; F Guilhot; H Hjorth-Hansen; M Höglund; P Kovanen; T Laurinolli; J Liesveld; R Paquette; J Pinilla-Ibarz; A Rauhala; N Shah; B Simonsson; M Sinisalo; J L Steegmann; L Stenke; K Porkka
Journal:  Leukemia       Date:  2009-03-19       Impact factor: 11.528

Review 9.  Second generation inhibitors of BCR-ABL for the treatment of imatinib-resistant chronic myeloid leukaemia.

Authors:  Ellen Weisberg; Paul W Manley; Sandra W Cowan-Jacob; Andreas Hochhaus; James D Griffin
Journal:  Nat Rev Cancer       Date:  2007-05       Impact factor: 60.716

10.  Dasatinib inhibits the proliferation and function of CD4+CD25+ regulatory T cells.

Authors:  Fei Fei; Yingzhe Yu; Anita Schmitt; Markus Thomas Rojewski; Baoan Chen; Marlies Götz; Hartmut Döhner; Donald Bunjes; Michael Schmitt
Journal:  Br J Haematol       Date:  2008-11-07       Impact factor: 6.998

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