Detailed Information on Publication Record
2012
Analysis of Mutations in the BCR-ABL1 Kinase Domain, Using Direct Sequencing Detection of the T315I Mutation in Bone Marrow CD34+Cells of a Patient with Chronic Myelogenous Leukemia 6 Months Prior to its Emergence in Peripheral Blood
RÁZGA, Filip, Tomáš JURČEK, Ivana JEZISKOVA, Daniela ŽÁČKOVÁ, Dana DVOŘÁKOVÁ et. al.Basic information
Original name
Analysis of Mutations in the BCR-ABL1 Kinase Domain, Using Direct Sequencing Detection of the T315I Mutation in Bone Marrow CD34+Cells of a Patient with Chronic Myelogenous Leukemia 6 Months Prior to its Emergence in Peripheral Blood
Authors
RÁZGA, Filip (703 Slovakia, guarantor, belonging to the institution), Tomáš JURČEK (203 Czech Republic, belonging to the institution), Ivana JEZISKOVA (203 Czech Republic), Daniela ŽÁČKOVÁ (203 Czech Republic, belonging to the institution), Dana DVOŘÁKOVÁ (203 Czech Republic, belonging to the institution), Marek BORSKÝ (203 Czech Republic, belonging to the institution), Jiří MAYER (203 Czech Republic, belonging to the institution) and Zdeněk RÁČIL (203 Czech Republic, belonging to the institution)
Edition
Molecular Diagnosis & Therapy, AUCKLAND, ADIS INT LTD, 2012, 1177-1062
Other information
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
30200 3.2 Clinical medicine
Country of publisher
New Zealand
Confidentiality degree
není předmětem státního či obchodního tajemství
References:
Impact factor
Impact factor: 1.692
RIV identification code
RIV/00216224:14740/12:00060675
Organization unit
Central European Institute of Technology
UT WoS
000305442900004
Keywords in English
CHRONIC MYELOID-LEUKEMIA; IMATINIB RESISTANCE; ABL MUTATIONS; TRANSCRIPTS; PROGENITORS; INHIBITOR; ASSAY
Tags
International impact, Reviewed
Změněno: 23/4/2013 07:49, Olga Křížová
Abstract
V originále
Background and Objective: It has been shown that the occurrence of the BCR-ABL1 T315I mutation leads to a very poor therapeutic outcome in chronic myelogenous leukemia (CM L) patients treated with tyrosine kinase inhibitors. Therefore, early detection of this mutation could potentially lead to early therapeutic intervention and a better prognosis with the ongoing treatment regimen. Methods: The detection of BCR-ABL1 kinase domain (KID) mutations was performed by direct sequencing of peripheral blood (PB), total bone marrow (BM), and BM CD34+ cells from a reported CML patient. Results: In this patient, the T315I mutation was detected in BM CD34+ cells 6 months prior to its emergence in PB, suggesting evolution and expansion of the T315I mutation clone, which most likely originated from more primitive CML cells. Conclusion: Our finding reflects the natural development of a T315I mutation within the hematopoietic system of the reported patient and indicates the importance of BCR-ABL1 mutation monitoring in more primitive cell populations. Considering the natural history of T315I development in this reported CM L case, we hypothesize that BCR-ABL1 KD mutations may be pre-concentrated in more primitive CM L cells, which subsequently expand into the PB. These findings may have future implications for the strategy used for detecting BCR-ABL1 mutations.
Links
MSM0021622430, plan (intention) |
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