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Human Mammary Tumor Virus (HMTV) in Endometrial Carcinoma
  1. Liane Deligdisch, MD*,,
  2. Tania Marin, MS,
  3. Anna T. Lee, MS,
  4. Polly Etkind, PhD,
  5. James F. Holland, MD,
  6. Stella Melana, PhD and
  7. Beatriz G.T. Pogo, MD,§
  1. *Departments of Pathology,
  2. Obstetrics, Gynecology and Reproductive Science,
  3. Medicine, Division of Hematology/Oncology, and
  4. §Microbiology, Mount Sinai School of Medicine, New York, NY.
  1. Address correspondence and reprint requests to Stella Melana, PhD, Division of Hematology/Oncology, Department of Medicine. Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1079, New York, N.Y. 10029. E-mail:


Objective Human mammary tumor virus (HMTV) is 90% to 98% homologous to mouse mammary tumor virus, the etiological agent of mammary tumors in mice. Human mammary tumor virus sequences were found in 40% of the breast cancers studied in both American and Australian women. In addition, 10% of endometrial carcinomas studied in Australian women also contained HMTV sequences. We have explored the possibility that endometrial cancer of American women may also contain HMTV.

Methods/Materials Nested polymerase chain reactions, radioactive internal probing, and sequencing were used to establish the presence of unique nucleotide sequences of HMTV in human genomic DNA. The genomic DNAs were tested to guarantee that they were free of murine DNA. Immunohistochemistry with a monoclonal antibody specific for HMTV envelope protein demonstrated that HMTV sequences were translated.

Results Thirteen (23.2%) of 56 of the endometrial cancers studied contained HMTV sequences and proteins. Human mammary tumor virus sequences and protein were not detected in the 33 normal endometria studied.

Conclusion Human mammary tumor virus, an agent with high homology to mouse mammary tumor virus, was found in 23.2% of the endometrial cancers studied, thus opening the possibility of a pathogenic role.

  • Endometrial carcinoma
  • HMTV
  • Retrovirus
  • Virus
  • Cancer

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  • This work was supported by the TJ Martell Foundation for Leukemia, Cancer and AIDS Research, the Faith Lynn Price Kash Family Foundation, the Myra Shaw Cancer Foundation, and The Susan Komen for the Cure Foundation.

  • Presented in part at the American Association for Cancer Research, Proc AACR 51:2302, 2010.

  • The authors declare no conflicts of interest.