A common mouse mammary tumor virus integration site in chemically induced precancerous mammary hyperplasias |
| |
| Authors: | D A Gray C M McGrath R F Jones V L Morris |
| |
| Affiliation: | 1. Division of Medical Zoology, Department of Microbiology and Immunology, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago, Tottori 683-8503, Japan;2. Division of Malaria Research, Proteo-Science Center, Ehime University, Matsuyama, Ehime 790-8577, Japan;3. Department of Molecular and Clinical Diagnosis, School of Pharmacy, Shujitsu University, Okayama 703-8516, Japan;4. Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, United States;5. Department of Biology, Faculty of Science, Burapha University, Chonburi 20131, Thailand;6. Malaria Research and Training Centre, Faculty of Medicine, Pharmacy and Odonto-stomatology, University of Sciences, Techniques, and Technologies of Bamako, Point G, BP 1805, Mali;7. Mahidol Vivax Research Unit, Faculty of Tropical Medicine, Mahidol University, Bangkok 10400, Thailand;8. Center for Research and Innovation, Faculty of Medical Technology, Mahidol University, Salaya, Nakhosn Pathom, 73170, Thailand;9. Division of Global Infectious Diseases, Department of Public Health, Kobe University Graduate School of Health Sciences, 7-10-2 Tomogaoka, Suma-ku, Kobe, Hyogo 654-0142, Japan;10. Division of Molecular Parasitology, Proteo-Science Center, Ehime University, Toon Ehime, 791-0295, Japan |
| |
| Abstract: | ![]()
Mammary carcinomas can be induced by chemical and hormonal as well as viral carcinogens. Irrespective of the class of inducer, these tumors develop in discrete stages, of which alveolar hyperplasia is one of the earliest identifiable. Since carcinogenesis by the mammary tumor virus is now thought to involve proviral activation of adjacent cell genes at specific loci, we sought to determine if a similar mechanism also played a role in chemical and hormonal carcinogenesis and if its role was stage specific. Three high-tumor-incidence BALB/c hyperplastic alveolar nodule outgrowths of two different etiologies were found to have exogenous mouse mammary tumor virus proviruses integrated at the same site in the genome. This common site of integration is not within the bounds of the int-1 and int-2 loci into which proviruses detected at these loci are clustered in MMTV-induced mammary tumors. All three HANs are commonly impaired in end-point differentiation. We propose that mouse mammary tumor virus integration at this site is responsible for a specific abnormality in differentiation associated with the preneoplastic phenotype. |
| |
| Keywords: | |
| 本文献已被 ScienceDirect 等数据库收录！ |
|
