Correlation between selected environmental exposures and karyotype in acute myelocytic leukemia.

Journal Article (Journal Article)

Many bone marrow cytogenetic abnormalities in acute myelogenous leukemia (AML) are tumor specific, clonal, nonrandom, and related to prognosis; it has been hypothesized that they may be markers of exposure to etiological agents. A previous report from our institution revealed several such associations; the purpose of the current study was to determine whether previous findings were present in a new group of patients. Subjects included 84 newly diagnosed AML patients (French-American-British M1 and M2); exposure data were gathered using self-report questionnaires at the time of registration. Two sets of comparisons were made: (a) patients with all (AA) or some (AN) cytogenetically abnormal cells versus those with normal karyotypes (NN) and (b) patients with specific abnormalities [-5/5q-, -7/7q-, +8, t(8;21)] versus all others. Odds ratios (ORs) were 4.64 for the association between prior cytotoxic therapy and -5/5q- and 6.38 for the association with -7/7q-, but were <1.00 for +8 and t(8;21). There were no ORs > 2.0 for specific abnormalities in any of the other exposures evaluated (cigarette smoking, alcohol use, occupational exposure to organic chemicals, paints, or pesticides/herbicides), with the exception of exposure to paints and -7/7q- (OR, 7.50). The ORs for AA/AN versus NN patients were 1.43 and 3.81 for smoking and alcohol use, and weak dose-response trends were present. The most consistent positive associations between the two series were for prior cytotoxic therapy (-5/5q-; -7/7q-), cigarette smoking (AA/AN versus NN) and alcohol use (AA/AN versus NN). Reasoning from the known association between prior cytotoxic therapy and -7/7q-, we would have predicted relatively high ORs (> 4.0) if specific abnormalities acted as markers for the exposures assessed, but none were present. However, in both series, AA/AN patients were more likely to smoke and use alcohol than were NN patients, and weak dose-response patterns were present for both. This finding suggests that both smoking and alcohol use may play a role in the pathogenesis of cytogenetic abnormalities in AML-M1/M2; however, the mechanism by which they work and whether they are involved in the etiology of these diseases remain unclear.

Full Text

Duke Authors

Cited Authors

  • Crane, MM; Strom, SS; Halabi, S; Berman, EL; Fueger, JJ; Spitz, MR; Keating, MJ

Published Date

  • August 1996

Published In

Volume / Issue

  • 5 / 8

Start / End Page

  • 639 - 644

PubMed ID

  • 8824367

International Standard Serial Number (ISSN)

  • 1055-9965


  • eng

Conference Location

  • United States