Literature DB >> 19652056

Impact of baseline BCR-ABL mutations on response to nilotinib in patients with chronic myeloid leukemia in chronic phase.

Timothy Hughes1, Giuseppe Saglio, Susan Branford, Simona Soverini, Dong-Wook Kim, Martin C Müller, Giovanni Martinelli, Jorge Cortes, Lan Beppu, Enrico Gottardi, Dongho Kim, Philipp Erben, Yaping Shou, Ariful Haque, Neil Gallagher, Jerald Radich, Andreas Hochhaus.   

Abstract

PURPOSE: Nilotinib is a second-generation tyrosine kinase inhibitor indicated for the treatment of patients with chronic myeloid leukemia (CML) in chronic phase (CP; CML-CP) and accelerated phase (AP; CML-AP) who are resistant to or intolerant of prior imatinib therapy. In this subanalysis of a phase II study of nilotinib in patients with imatinib-resistant or imatinib-intolerant CML-CP, the occurrence and impact of baseline and newly detectable BCR-ABL mutations were assessed. PATIENTS AND METHODS: Baseline mutation data were assessed in 281 (88%) of 321 patients with CML-CP in the phase II nilotinib registration trial.
RESULTS: Among imatinib-resistant patients, the frequency of mutations at baseline was 55%. After 12 months of therapy, major cytogenetic response (MCyR) was achieved in 60%, complete cytogenetic response (CCyR) in 40%, and major molecular response (MMR) in 29% of patients without baseline mutations versus 49% (P = .145), 32% (P = .285), and 22% (P = .366), respectively, of patients with mutations. Responses in patients who harbored mutations with high in vitro sensitivity to nilotinib (50% inhibitory concentration [IC(50)] <or= 150 nM) or mutations with unknown nilotinib sensitivity were equivalent to those responses for patients without mutations (not significant). Patients with mutations that were less sensitive to nilotinib in vitro (IC(50) > 150 nM; Y253H, E255V/K, F359V/C) had less favorable responses, as 13%, 43%, and 9% of patients with each of these mutations, respectively, achieved MCyR; none achieved CCyR.
CONCLUSION: For most patients with imatinib resistance and with mutations, nilotinib offers a substantial probability of response. However, mutational status at baseline may influence response. Less sensitive mutations that occurred at three residues defined in this study, as well as the T315I mutation, may be associated with less favorable responses to nilotinib.

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Year:  2009        PMID: 19652056      PMCID: PMC4979230          DOI: 10.1200/JCO.2009.21.8230

Source DB:  PubMed          Journal:  J Clin Oncol        ISSN: 0732-183X            Impact factor:   44.544


  27 in total

1.  Second-line treatment with dasatinib in patients resistant to imatinib can select novel inhibitor-specific BCR-ABL mutants in Ph+ ALL.

Authors:  Simona Soverini; Giovanni Martinelli; Sabrina Colarossi; Alessandra Gnani; Michela Rondoni; Fausto Castagnetti; Stefania Paolini; Gianantonio Rosti; Michele Baccarani
Journal:  Lancet Oncol       Date:  2007-03       Impact factor: 41.316

2.  Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia.

Authors:  Brian J Druker; François Guilhot; Stephen G O'Brien; Insa Gathmann; Hagop Kantarjian; Norbert Gattermann; Michael W N Deininger; Richard T Silver; John M Goldman; Richard M Stone; Francisco Cervantes; Andreas Hochhaus; Bayard L Powell; Janice L Gabrilove; Philippe Rousselot; Josy Reiffers; Jan J Cornelissen; Timothy Hughes; Hermine Agis; Thomas Fischer; Gregor Verhoef; John Shepherd; Giuseppe Saglio; Alois Gratwohl; Johan L Nielsen; Jerald P Radich; Bengt Simonsson; Kerry Taylor; Michele Baccarani; Charlene So; Laurie Letvak; Richard A Larson
Journal:  N Engl J Med       Date:  2006-12-07       Impact factor: 91.245

3.  Several Bcr-Abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib.

Authors:  Amie S Corbin; Paul La Rosée; Eric P Stoffregen; Brian J Druker; Michael W Deininger
Journal:  Blood       Date:  2003-02-06       Impact factor: 22.113

4.  The prognosis for patients with chronic myeloid leukemia who have clonal cytogenetic abnormalities in philadelphia chromosome-negative cells.

Authors:  Michael W N Deininger; Jorge Cortes; Ron Paquette; Byung Park; Andreas Hochhaus; Michele Baccarani; Richard Stone; Thomas Fischer; Hagop Kantarjian; Dietger Niederwieser; Carlo Gambacorti-Passerini; Charlene So; Insa Gathmann; John M Goldman; Douglas Smith; Brian J Druker; François Guilhot
Journal:  Cancer       Date:  2007-10-01       Impact factor: 6.860

5.  Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl.

Authors:  Ellen Weisberg; Paul W Manley; Werner Breitenstein; Josef Brüggen; Sandra W Cowan-Jacob; Arghya Ray; Brian Huntly; Doriano Fabbro; Gabriele Fendrich; Elizabeth Hall-Meyers; Andrew L Kung; Jürgen Mestan; George Q Daley; Linda Callahan; Laurie Catley; Cara Cavazza; Mohammad Azam; Azam Mohammed; Donna Neuberg; Renee D Wright; D Gary Gilliland; James D Griffin
Journal:  Cancer Cell       Date:  2005-02       Impact factor: 31.743

6.  AMN107, a novel aminopyrimidine inhibitor of Bcr-Abl, has in vitro activity against imatinib-resistant chronic myeloid leukemia.

Authors:  Mirna Golemovic; Srdan Verstovsek; Francis Giles; Jorge Cortes; Taghi Manshouri; Paul W Manley; Jürgen Mestan; Margaret Dugan; Leila Alland; James D Griffin; Ralph B Arlinghaus; Tong Sun; Hagop Kantarjian; Miloslav Beran
Journal:  Clin Cancer Res       Date:  2005-07-01       Impact factor: 12.531

7.  Identification of BCR-ABL point mutations conferring resistance to the Abl kinase inhibitor AMN107 (nilotinib) by a random mutagenesis study.

Authors:  Arghya Ray; Sandra W Cowan-Jacob; Paul W Manley; Jürgen Mestan; James D Griffin
Journal:  Blood       Date:  2007-02-15       Impact factor: 22.113

8.  Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is active in patients with imatinib-resistant or -intolerant accelerated-phase chronic myelogenous leukemia.

Authors:  Philipp le Coutre; Oliver G Ottmann; Francis Giles; Dong-Wook Kim; Jorge Cortes; Norbert Gattermann; Jane F Apperley; Richard A Larson; Elisabetta Abruzzese; Stephen G O'Brien; Kazimierz Kuliczkowski; Andreas Hochhaus; Francois-Xavier Mahon; Giuseppe Saglio; Marco Gobbi; Yok-Lam Kwong; Michele Baccarani; Timothy Hughes; Giovanni Martinelli; Jerald P Radich; Ming Zheng; Yaping Shou; Hagop Kantarjian
Journal:  Blood       Date:  2007-11-29       Impact factor: 22.113

9.  Evidence that resistance to nilotinib may be due to BCR-ABL, Pgp, or Src kinase overexpression.

Authors:  François-Xavier Mahon; Sandrine Hayette; Valérie Lagarde; Francis Belloc; Béatrice Turcq; Franck Nicolini; Coralie Belanger; Paul W Manley; Cédric Leroy; Gabriel Etienne; Serge Roche; Jean-Max Pasquet
Journal:  Cancer Res       Date:  2008-12-01       Impact factor: 12.701

10.  Sequential ABL kinase inhibitor therapy selects for compound drug-resistant BCR-ABL mutations with altered oncogenic potency.

Authors:  Neil P Shah; Brian J Skaggs; Susan Branford; Timothy P Hughes; John M Nicoll; Ronald L Paquette; Charles L Sawyers
Journal:  J Clin Invest       Date:  2007-09       Impact factor: 14.808

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  107 in total

1.  PF-114, a potent and selective inhibitor of native and mutated BCR/ABL is active against Philadelphia chromosome-positive (Ph+) leukemias harboring the T315I mutation.

Authors:  A A Mian; A Rafiei; I Haberbosch; A Zeifman; I Titov; V Stroylov; A Metodieva; O Stroganov; F Novikov; B Brill; G Chilov; D Hoelzer; O G Ottmann; M Ruthardt
Journal:  Leukemia       Date:  2014-11-14       Impact factor: 11.528

2.  Major molecular response in CML patients treated with tyrosine kinase inhibitors: the paradigm for monitoring targeted cancer therapy.

Authors:  Richard D Press
Journal:  Oncologist       Date:  2010-06-21

Review 3.  The influence of subclonal resistance mutations on targeted cancer therapy.

Authors:  Michael W Schmitt; Lawrence A Loeb; Jesse J Salk
Journal:  Nat Rev Clin Oncol       Date:  2015-10-20       Impact factor: 66.675

Review 4.  Molecular resistance: an early indicator for treatment change?

Authors:  Carmen Fava; Hagop Kantarjian; Jorge Cortes
Journal:  Clin Lymphoma Myeloma Leuk       Date:  2012-01-28

Review 5.  Stem cell transplant for chronic myeloid leukemia in the imatinib era.

Authors:  Jerald Radich
Journal:  Semin Hematol       Date:  2010-10       Impact factor: 3.851

6.  The BCR-ABLT315I mutation compromises survival in chronic phase chronic myelogenous leukemia patients resistant to tyrosine kinase inhibitors, in a matched pair analysis.

Authors:  Franck E Nicolini; Amr R Ibrahim; Simona Soverini; Giovanni Martinelli; Martin C Müller; Andreas Hochhaus; Inge H Dufva; Dong-Wook Kim; Jorge Cortes; Michael J Mauro; Charles Chuah; Hélène Labussière; Stéphane Morisset; Catherine Roche-Lestienne; Eric Lippert; Sandrine Hayette; Senaka Peter; Wei Zhou; Véronique Maguer-Satta; Mauricette Michallet; John Goldman; Jane F Apperley; François-Xavier Mahon; David Marin; Gabriel Etienne
Journal:  Haematologica       Date:  2013-05-28       Impact factor: 9.941

7.  Incidence of Bcr-Abl kinase domain mutations in imatinib refractory chronic myeloid leukemia patients from South India.

Authors:  Sailaja Kagita; Srihari Uppalapati; Sangeeta Jiwatani; Vijay Gandhi Linga; Sadasivudu Gundeti; Narayana Nagesh; Raghunadharao Digumarti
Journal:  Tumour Biol       Date:  2014-04-26

8.  Mutant BCR-ABL clones in chronic myeloid leukemia.

Authors:  Michael S Mathisen; Hagop M Kantarjian; Jorge Cortes; Elias Jabbour
Journal:  Haematologica       Date:  2011-03       Impact factor: 9.941

Review 9.  Current developments in molecular monitoring in chronic myeloid leukemia.

Authors:  Justine Ellen Marum; Susan Branford
Journal:  Ther Adv Hematol       Date:  2016-07-15

10.  Dasatinib treatment of chronic-phase chronic myeloid leukemia: analysis of responses according to preexisting BCR-ABL mutations.

Authors:  Martin C Müller; Jorge E Cortes; Dong-Wook Kim; Brian J Druker; Philipp Erben; Ricardo Pasquini; Susan Branford; Timothy P Hughes; Jerald P Radich; Lynn Ploughman; Jaydip Mukhopadhyay; Andreas Hochhaus
Journal:  Blood       Date:  2009-09-24       Impact factor: 22.113

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