Complete Remission by Imatinib Mesylate (Glivec) in a Child Relapsing with Philadelphia Chromosome Positive Acute Lymphoblastic Leukemia (Ph (+) ALL) after Unrelated Donor Stem Cell Transplantation.
- Author:
Young Yeui KIM
1
;
Young Kyoung YOO
;
Sun Young KIM
;
Pil Sang JANG
;
Nak Gyun CHUNG
;
Bin CHO
;
Dae Chul JEONG
;
Soon Ju LEE
;
Hack Ki KIM
Author Information
1. Department of Pediatrics, The Catholic University of Korea College of Medicine, Seoul, Korea. cngped@catholic.ac.kr
- Publication Type:Case Report
- Keywords:
Philadelphia chromosome;
Acute lymphoblastic leukemia;
BCR/ABL;
Imatinib mesylate;
Stem cell transplantation
- MeSH:
Child*;
Chimerism;
Cyclosporine;
Cytogenetics;
Graft vs Host Disease;
Humans;
Hydrogen-Ion Concentration;
Male;
Mesylates*;
Neutropenia;
Philadelphia Chromosome*;
Precursor Cell Lymphoblastic Leukemia-Lymphoma*;
Prognosis;
Protein-Tyrosine Kinases;
Stem Cell Transplantation*;
Stem Cells*;
Thrombocytopenia;
Tissue Donors;
Unrelated Donors*;
Imatinib Mesylate
- From:Korean Journal of Pediatric Hematology-Oncology
2003;10(1):110-114
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The prognosis of patients with Philadelphia chromosome positive acute lymphoblastic leukemia (Ph ALL) who relapsed after allogeneic stem cell transplantation (allo-SCT) is poor. Imatinib mesylate (Glivec (R) ) is an inhibitor of the ABL tyrosine kinase with potent antileukemic activity in advanced Ph ALL. The clinical effects of imatinib on Ph ALL recurring after allo-SCT have not been established. We describe the clinical activity of imatinib in a 7 year-old boy with Ph ALL relapsing after unrelated donor stem cell transplantation. Imatinib as a single agent resulted in rapid elimination of leukemic cells with ensuing prolonged neutropenia and thrombocytopenia. Subsequent hematological recovery by donor-derived cells was associated with grade 3 graft-versus-host disease (GvHD), which responded to cyclosporine A and steroid. Imatinib successfully induced hematologic, cytogenetic and molecular remission of Ph ALL, and restored complete donor chimerism, along with controllable GvHD.
