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[Cancer Research 48, 2919-2922, May 15, 1988]
© 1988 American Association for Cancer Research

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No Involvement of Bovine Leukemia Virus in Childhood Acute Lymphoblastic Leukemia and Non-Hodgkin's Lymphoma1

Alan P. Bender2, Leslie L. Robison3, S. V. S. Kashmiri4, Kenneth L. McClain5, William G. Woods, W. Anthony Smithson, Ruth Heyn, Jonathan Finlay6, Leonard M. Schuman, Colleen Renier and Robert Gibson

Minnesota Department of Health, Minneapolis, Minnesota [A. P. B.]; Hematology-Oncology Division, Department of Pediatrics, University of Minnesota, Minneapolis, Minnesota [L. L. R., K. L. M., W. G. W.]; Section of Viral Oncology, University of Pennsylvania, Kennett Square, Pennsylvania [S. V. S. K.]; Department of Pediatrics, Mayo Clinic, Rochester, Minnesota [W. A. S.]; Mott Children's Hospital, Ann Arbor, Michigan [R. H.]; Wisconsin Medical School, University of Wisconsin, Madison, Wisconsin [J. F.]; and Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, Minnesota [L. M. S., C. R., R. G.]

Bovine leukemia virus (BLV) is the causative agent of enzootic bovine lymphosarcoma. Much speculation continues to be directed at the role of BLV in human leukemia. To test this hypothesis rigorously, a case-control study of childhood acute lymphoblastic leukemia and non-Hodgkin's lymphoma was conducted between December 1983 and February 1986. Cases (≤16 years at diagnosis) derived from patients diagnosed at the primary institutions and affiliated hospitals were matched (age, sex, and race) with regional population controls. DNA samples from bone marrow or peripheral blood from 157 cases (131 acute lymphoblastic leukemia, 26 non-Hodgkin's lymphoma) and peripheral blood from 136 controls were analyzed by Southern blot technique, under highly stringent conditions, using cloned BLV DNA as a probe. None of the 157 case or 136 control DNA samples hybridized with the probe. The high statistical power and specificity of this study provide the best evidence to date that genomic integration of BLV is not a factor in childhood acute lymphoblastic leukemia/non-Hodgkin's lymphoma.

1 Support was provided by the National Institute of Environmental Health Sciences (ES03417) of the Department of Health and Human Services and the University of Minnesota Children's Cancer Research Fund.

2 To whom requests for reprints should be addressed at, Chronic Disease, Minnesota Department of Health, 717 Delaware St., SE, P. O. Box 9441, Minneapolis, MN 55440.

3 Recipient of a Leukemia Society of America fellowship award.

4 Present address: Laboratory of Tumor Immunology and Biology, National Cancer Institute, Bethesda, Maryland.

5 Present address: Pediatric Hematology/Oncology, Baylor College of Medicine, Houston, Texas.

6 Present address: Division of Oncology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania.

Received 9/30/87. Revised 2/ 8/88. Accepted 2/16/88.




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Copyright © 1988 by the American Association for Cancer Research.