JURČEK, Tomáš, Filip RÁZGA, Petra MAZANCOVÁ, Milena MUSILOVÁ, Dana DVOŘÁKOVÁ, Marek BORSKÝ, Daniela ŽÁČKOVÁ, Blanka DOBEŠOVÁ, Lukáš SEMERÁD, Jiří MAYER and Zdeněk RÁČIL. Prospective analysis of low-level BCR-ABL1 T315I mutation in CD34+ cells of patients with de novo chronic myeloid leukemia. LEUKEMIA & LYMPHOMA. LONDON: INFORMA HEALTHCARE, 2014, vol. 55, No 8, p. 1915-1917. ISSN 1042-8194. doi:10.3109/10428194.2013.842988.
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Basic information
Original name Prospective analysis of low-level BCR-ABL1 T315I mutation in CD34+ cells of patients with de novo chronic myeloid leukemia
Authors JURČEK, Tomáš (203 Czech Republic, guarantor), Filip RÁZGA (703 Slovakia, belonging to the institution), Petra MAZANCOVÁ (703 Slovakia, belonging to the institution), Milena MUSILOVÁ (203 Czech Republic, belonging to the institution), Dana DVOŘÁKOVÁ (203 Czech Republic, belonging to the institution), Marek BORSKÝ (203 Czech Republic), Daniela ŽÁČKOVÁ (203 Czech Republic, belonging to the institution), Blanka DOBEŠOVÁ (203 Czech Republic), Lukáš SEMERÁD (203 Czech Republic), Jiří MAYER (203 Czech Republic, belonging to the institution) and Zdeněk RÁČIL (203 Czech Republic, belonging to the institution).
Edition LEUKEMIA & LYMPHOMA, LONDON, INFORMA HEALTHCARE, 2014, 1042-8194.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 30200 3.2 Clinical medicine
Country of publisher United Kingdom of Great Britain and Northern Ireland
Confidentiality degree is not subject to a state or trade secret
Impact factor Impact factor: 2.891
RIV identification code RIV/00216224:14110/14:00078457
Organization unit Faculty of Medicine
Doi http://dx.doi.org/10.3109/10428194.2013.842988
UT WoS 000340224100035
Keywords in English BCR-ABL1; T315I; CD34+; chronic myeloid leukemia
Tags EL OK, podil
Tags International impact, Reviewed
Changed by Changed by: Ing. Mgr. Věra Pospíšilíková, učo 9005. Changed: 29. 1. 2015 12:37.
Abstract
Th e detection of BCR – ABL1 kinase domain (KD) mutations is frequently associated with resistance to tyrosine kinase inhibitors (TKIs), which results in an impaired prognosis for patients with chronic myeloid leukemia (CML) [1]. Early detection of these mutations can potentially lead to early therapeutic intervention and optimization of an ongoing treatment strategy. Considering the hematopoiesis hierar- chy, it is expected that BCR – ABL1 mutation clones expand directly from hematopoietic stem cells or early progenitor cells [2]. It has already been reported that BCR – ABL1 KD mutations were detected in these cells before they occurred in bone marrow (BM) or peripheral blood (PB) [3]. Particu- lar focus should be given to the T315I mutation, which is resistant to all approved TKIs (imatinib, nilotinib and dasa- tinib) [4,5], meaning that early detection of this key BCR – ABL1 KD mutation in “ source ” cells could have potential clinical benefits.
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