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Secondary Acute Myelogenous Leukemia in Patients Previously Treated for Childhood Renal Tumors: A Report From the National Wilms Tumor Study Group

 

作者: Patricia Shearer,   Gauri Kapoor,   J. Beckwith,   J. Takashima,   N. Breslow,   D. Green,  

 

期刊: Journal of Pediatric Hematology/Oncology  (OVID Available online 2001)
卷期: Volume 23, issue 2  

页码: 109-111

 

ISSN:1077-4114

 

年代: 2001

 

出版商: OVID

 

关键词: Wilms tumor;Secondary malignant neoplasms;Acute myelogenous leukemia;WT1;Doxorubicin;Epipodophyllotoxin;Radiation

 

数据来源: OVID

 

摘要:

PurposeThis review characterized cases of secondary acute myelogenous leukemia (AML) occurring after treatment of renal neoplasms on protocols of the National Wilms Tumor Study Group (NWTSG) between October 1969 and December 1991.Patients and MethodsThe NWTSG database was reviewed for cases of secondary AML and forWT1status of the affected patients. Referring institutions were contacted by a confidential letter requesting pathology reports, results of immunophenotyping, cytogenetic, and molecular analyses, and details concerning treatment of AML.ResultsOf the 5,278 patients treated during the study period, 43 had second malignant neoplasms, and 7 of these 43 had AML. At the time of diagnosis of Wilms tumor, the median age of the seven patients (4 boys) was 3.2 years. Five of the seven renal neoplasms had favorable histologic characteristics. The most common French-American-British morphology was M5. One patient had bilateral tumors, and two were treated for recurrent Wilms tumor. All patients received chemotherapy regimens that included doxorubicin (6) or etoposide (1), and six were treated with infradiaphragmatic irradiation. The median latency period from initial diagnosis of the renal neoplasm to development of secondary AML was 3 years (range, 1.2–4 yrs). One patient had the translocationt(9;11)(p22;q23);WT1status was not noted for any of the seven patients.ConclusionsThe development of secondary AML in this subset of patients after treatment of renal neoplasms may reflect the interaction of the effects of treatment and possible genetic predisposition toward cancer.

 

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