Premium
Clonal cytogenetic abnormalities after tyrosine kinase inhibitor therapy in Ph+ all resolution after decitabine therapy
Author(s) -
Lockhart Sharon,
McDonald Lisa,
Rytting Michael,
Chan Ka Wah
Publication year - 2012
Publication title -
pediatric blood and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.116
H-Index - 105
eISSN - 1545-5017
pISSN - 1545-5009
DOI - 10.1002/pbc.23318
Subject(s) - medicine , decitabine , myeloid leukemia , philadelphia chromosome , tyrosine kinase inhibitor , tyrosine kinase , cancer research , leukemia , minimal residual disease , population , dasatinib , abl , imatinib , oncology , immunology , cancer , chromosomal translocation , dna methylation , genetics , biology , gene , receptor , gene expression , environmental health
Mixed chimerism and presence of minimal residual disease after stem cell transplantation (SCT) usually predict leukemia recurrence. In Philadelphia chromosome positive (Ph+) leukemia tyrosine kinase inhibitors can restore remission. These agents can induce clonal cytogenetic abnormalities in the Philadelphia negative cell population (CCA/Ph−), which may rarely progress to acute myeloid leukemia. A child with Ph+ acute lymphoblastic leukemia showed mixed donor chimerism and persistent bcr‐abl transcripts after a matched sibling SCT. There was no response to tyrosine kinase inhibitor (TKI) therapy, but she has remained hematologically normal for more than 5 years. CCA/Ph− was detected but resolved with hypomethylating therapy. Pediatr Blood Cancer 2012;59:573–575. © 2011 Wiley Periodicals, Inc.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom