Genetic analysis of dasatinib-treated chronic myeloid leukemia rapidly developing into acute myeloid leukemia with monosomy 7 in Philadelphia-negative cells.
Larsson, Nina LU ; Billström, Rolf ; Lilljebjörn, Henrik LU
; Lassen, Carin
LU
; Richter, Johan
LU
; Ekblom, Marja
LU
and Fioretos, Thoas
LU
(2010)
In Cancer Genetics and Cytogenetics
199(2).
p.89-95
- Abstract
- Despite the recent success of tyrosine kinase inhibitors (TKIs) in the treatment of chronic myeloid leukemia (CML), approximately 2-17% of patients develop clonal cytogenetic changes in the Philadelphia-negative (Ph(-)) cell population. A fraction of these patients, in particular those displaying trisomy 8 or monosomy 7, are at risk of developing a myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML). Consequently, there is a need to characterize the clinical features of such cases and to increase our understanding of the pathogenetic mechanisms underlying the emergence of clonal cytogenetic changes in Ph(-) cells. To date, most cases reported have received treatment with imatinib. Here we describe the case of a patient with CML... (More)
- Despite the recent success of tyrosine kinase inhibitors (TKIs) in the treatment of chronic myeloid leukemia (CML), approximately 2-17% of patients develop clonal cytogenetic changes in the Philadelphia-negative (Ph(-)) cell population. A fraction of these patients, in particular those displaying trisomy 8 or monosomy 7, are at risk of developing a myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML). Consequently, there is a need to characterize the clinical features of such cases and to increase our understanding of the pathogenetic mechanisms underlying the emergence of clonal cytogenetic changes in Ph(-) cells. To date, most cases reported have received treatment with imatinib. Here we describe the case of a patient with CML who developed monosomy 7 in Ph(-) cells during dasatinib therapy. At 20 months after dasatinib initiation, the patient developed MDS, which rapidly progressed into AML. Genome-wide 500K SNP array analysis of the monosomy 7 clone revealed no acquired submicroscopic copy number changes. Given the strong association between monosomy 7 and mutation of genes involved in the RAS pathway in juvenile myelomonocytic leukemia, we also screened for pathogenetic variants in KRAS, NRAS, and PTPN11, but did not detect any changes. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1610215
- author
- Larsson, Nina
LU
; Billström, Rolf
; Lilljebjörn, Henrik
LU
; Lassen, Carin
LU
; Richter, Johan
LU
; Ekblom, Marja
LU
and Fioretos, Thoas
LU
- organization
- publishing date
- 2010
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Cancer Genetics and Cytogenetics
- volume
- 199
- issue
- 2
- pages
- 89 - 95
- publisher
- Elsevier
- external identifiers
-
- wos:000278156100004
- pmid:20471511
- scopus:77952772669
- pmid:20471511
- ISSN
- 0165-4608
- DOI
- 10.1016/j.cancergencyto.2010.02.005
- language
- English
- LU publication?
- yes
- id
- d628734a-a83a-4cf9-bbb0-dc1683bf51c8 (old id 1610215)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/20471511?dopt=Abstract
- date added to LUP
- 2016-04-04 09:37:11
- date last changed
- 2025-04-04 13:54:06
@article{d628734a-a83a-4cf9-bbb0-dc1683bf51c8,
abstract = {{Despite the recent success of tyrosine kinase inhibitors (TKIs) in the treatment of chronic myeloid leukemia (CML), approximately 2-17% of patients develop clonal cytogenetic changes in the Philadelphia-negative (Ph(-)) cell population. A fraction of these patients, in particular those displaying trisomy 8 or monosomy 7, are at risk of developing a myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML). Consequently, there is a need to characterize the clinical features of such cases and to increase our understanding of the pathogenetic mechanisms underlying the emergence of clonal cytogenetic changes in Ph(-) cells. To date, most cases reported have received treatment with imatinib. Here we describe the case of a patient with CML who developed monosomy 7 in Ph(-) cells during dasatinib therapy. At 20 months after dasatinib initiation, the patient developed MDS, which rapidly progressed into AML. Genome-wide 500K SNP array analysis of the monosomy 7 clone revealed no acquired submicroscopic copy number changes. Given the strong association between monosomy 7 and mutation of genes involved in the RAS pathway in juvenile myelomonocytic leukemia, we also screened for pathogenetic variants in KRAS, NRAS, and PTPN11, but did not detect any changes.}},
author = {{Larsson, Nina and Billström, Rolf and Lilljebjörn, Henrik and Lassen, Carin and Richter, Johan and Ekblom, Marja and Fioretos, Thoas}},
issn = {{0165-4608}},
language = {{eng}},
number = {{2}},
pages = {{89--95}},
publisher = {{Elsevier}},
series = {{Cancer Genetics and Cytogenetics}},
title = {{Genetic analysis of dasatinib-treated chronic myeloid leukemia rapidly developing into acute myeloid leukemia with monosomy 7 in Philadelphia-negative cells.}},
url = {{https://lup.lub.lu.se/search/files/5372542/1637382.pdf}},
doi = {{10.1016/j.cancergencyto.2010.02.005}},
volume = {{199}},
year = {{2010}},
}