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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.