Abstract: |
A 69-year-old woman developed microgranular acute promyelocytic leukemia (APL-M3) 10 months after receiving adjuvant cyclophosphamide, doxorubicin, and paclitaxel for breast cancer. Replicate bone marrow aspirate karyotypes contained a translocation between the long arms of chromosomes 15 and 17, but not at breakpoints typical for APL. Fluorescence in situ hybridization paints and RARα/PML cosmid probes verified that the breakpoints on chromosomes 15 and 17 were proximal to both the PML and RARα genes; t(15;17)(q13;12). Although the patient received induction chemotherapy and a several month trial of all-trans retinoic acid (ATRA), there was no clinical improvement or hematological remission. We suspect that this patient developed postchemotherapy secondary APL with an atypical t(15;17), which rendered her leukemic cells unresponsive to ATRA therapy. © 2002 Elsevier Science Inc. All rights reserved. |
Keywords: |
adult; aged; treatment failure; hydroxyurea; case report; doxorubicin; cancer combination chemotherapy; paclitaxel; cancer adjuvant therapy; cytarabine; gene; in situ hybridization, fluorescence; breast cancer; bone marrow; cyclophosphamide; dexamethasone; drug resistance, neoplasm; breast neoplasms; cancer resistance; coughing; dyspnea; leukemia, promyelocytic, acute; cancer regression; fluorescence in situ hybridization; bone marrow biopsy; leukemia cell; promyelocytic leukemia; tamoxifen; chromosome breakage; chromosome translocation; translocation, genetic; gene probe; idarubicin; chromosome analysis; karyotype; retinoic acid; chromosome 17; amifostine; chromosomes, human, pair 17; chromosomes, human, pair 15; codeine; tretinoin; receptors, retinoic acid; chromosome 15; retinoic acid syndrome; pml gene; humans; human; female; priority journal; article; cosmid; raralpha gene; pomacanthus maculosus
|