Literature DB >> 24382642

Drug resistance and BCR-ABL kinase domain mutations in Philadelphia chromosome-positive acute lymphoblastic leukemia from the imatinib to the second-generation tyrosine kinase inhibitor era: The main changes are in the type of mutations, but not in the frequency of mutation involvement.

Simona Soverini1, Caterina De Benedittis, Cristina Papayannidis, Stefania Paolini, Claudia Venturi, Ilaria Iacobucci, Mario Luppi, Paola Bresciani, Marzia Salvucci, Domenico Russo, Simona Sica, Ester Orlandi, Tamara Intermesoli, Antonella Gozzini, Massimiliano Bonifacio, Gian Matteo Rigolin, Fabrizio Pane, Michele Baccarani, Michele Cavo, Giovanni Martinelli.   

Abstract

BACKGROUND: Patients with Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL) frequently relapse on imatinib with acquisition of BCR-ABL kinase domain (KD) mutations. To analyze the changes that second-generation tyrosine kinase inhibitors (TKIs) have brought in mutation frequency and type, a database review was undertaken of the results of all the BCR-ABL KD mutation analyses performed in the authors' laboratory from January 2004 to January 2013.
METHODS: Interrogation of the database retrieved 450 mutation analyses in 272 patients with Ph+ ALL. Prescreening of samples was performed with denaturing high-performance liquid chromatography (D-HPLC), followed by direct sequencing of D-HPLC-positive cases.
RESULTS: BCR-ABL KD mutations were detected in 70% of imatinib-resistant patients, with T315I, E255K, and Y253H mutations accounting for 75% of cases. Seventy-eight percent of the patients reported to be resistant to second-generation TKIs after imatinib failure were positive for mutations, and 58% of them had multiple mutations. Analysis of patients relapsing on dasatinib revealed a newly acquired T315I mutation in almost two-thirds of the cases. Direct sequencing detected no mutations at diagnosis, even in patients who relapsed after a few months.
CONCLUSIONS: Second-generation TKIs ensure a more rapid debulking of the leukemic clone and have much fewer insensitive mutations, but long-term disease control remains a problem, and the T315I mutation is revealed to be an even more frequent enemy. BCR-ABL KD mutation screening of patients with Ph+ ALL who are receiving imatinib or second-generation TKIs would be a precious ally for timely treatment optimization. In contrast, the clinical usefulness of conventional direct sequencing at diagnosis seems to be very low. American Cancer Society.
© 2013 American Cancer Society.

Entities:  

Keywords:  BCR-ABL mutations; acute lymphoblastic leukemia; dasatinib; imatinib; resistance

Mesh:

Substances:

Year:  2013        PMID: 24382642     DOI: 10.1002/cncr.28522

Source DB:  PubMed          Journal:  Cancer        ISSN: 0008-543X            Impact factor:   6.860


  51 in total

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4.  Allogeneic haematopoietic stem cell transplantation improves outcome of adults with relapsed/refractory Philadelphia chromosome-positive acute lymphoblastic leukemia entering remission following CD19 chimeric antigen receptor T cells.

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5.  Single-Molecule Sequencing Reveals Patterns of Preexisting Drug Resistance That Suggest Treatment Strategies in Philadelphia-Positive Leukemias.

Authors:  Michael W Schmitt; Justin R Pritchard; Scott M Leighow; Bella I Aminov; Lan Beppu; Daniel S Kim; J Graeme Hodgson; Victor M Rivera; Lawrence A Loeb; Jerald P Radich
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6.  Targeting STAT5 or STAT5-Regulated Pathways Suppresses Leukemogenesis of Ph+ Acute Lymphoblastic Leukemia.

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Review 8.  Treatment of Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia.

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9.  Clinical impact of low-burden BCR-ABL1 mutations detectable by amplicon deep sequencing in Philadelphia-positive acute lymphoblastic leukemia patients.

Authors:  S Soverini; C De Benedittis; C Papayannidis; K Machova Polakova; C Venturi; D Russo; P Bresciani; A Iurlo; M Mancini; A Vitale; S Chiaretti; R Foà; E Abruzzese; F Sorà; A Kohlmann; T Haferlach; M Baccarani; M Cavo; G Martinelli
Journal:  Leukemia       Date:  2016-02-12       Impact factor: 11.528

10.  Janus kinase inhibition by ruxolitinib extends dasatinib- and dexamethasone-induced remissions in a mouse model of Ph+ ALL.

Authors:  Iris Appelmann; Cory D Rillahan; Elisa de Stanchina; Gregory Carbonetti; Chong Chen; Scott W Lowe; Charles J Sherr
Journal:  Blood       Date:  2014-12-12       Impact factor: 22.113

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