Expression of RNA of an Endogenous Replication-Defective Retrovirus in Rat Mammary Adenocarcinomas Induced by 7, 12-Dimethylbenz[a]anthracene

Howard A. Young; Martin L. Wenk; Dawn G. Goodman; Edward M. Scolnick

doi:10.1093/jnci/61.5.1329

Expression of RNA of an Endogenous Replication-Defective Retrovirus in Rat Mammary Adenocarcinomas Induced by 7, 12-Dimethylbenz[a]anthracene

Howard A. Young, Martin L. Wenk, Dawn G. Goodman, Edward M. Scolnick

Research output: Contribution to journal › Article › peer-review

9 Scopus citations

Abstract

An investigation into the possible relationship between chemical carcinogen Induction of rat mammary tumors and the expression of an endogenous retroviral genome was initiated. Mammary tumors were induced in female SD rats with 7, 12-dlmethylbenz[a]anthracene (DMBA). Tumors, Identified histologically as mammary adenocarcinomas, were analyzed for RNA of a replication-defective endogenous retrovirus or RNA of a helper-independent endogenous type C virus. Expression of RNA of the replication-defective virus was detected in mammary tumors weighing 0.2-2.0 g. Larger tumors, for which histologic examination revealed proportionally more fibroblastic tissue than epithelial cells, did not contain comparable concentrations of this viral RNA. RNA homologous to a helper-independent rat type C retrovirus was not detected In tumors of any size. A cell line was established from a primary DMBA-induced mammary adenocarcinoma and appeared similar to the small mammary tumors with respect to endogenous type C viral RNA expression. We discuss possible Implications of the expression of endogenous replication-defective viruses for use as markers for the effects of chemical carcinogens.—J Natl Cancer Inst 61: 1329-1337, 1978.

Original language	English (US)
Pages (from-to)	1329-1337
Number of pages	9
Journal	Journal of the National Cancer Institute
Volume	61
Issue number	5
DOIs	https://doi.org/10.1093/jnci/61.5.1329
State	Published - Nov 1978
Externally published	Yes

ASJC Scopus subject areas

Oncology
Cancer Research

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10.1093/jnci/61.5.1329

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@article{bfab127955494367b495dfe3b066a5e3,

title = "Expression of RNA of an Endogenous Replication-Defective Retrovirus in Rat Mammary Adenocarcinomas Induced by 7, 12-Dimethylbenz[a]anthracene",

abstract = "An investigation into the possible relationship between chemical carcinogen Induction of rat mammary tumors and the expression of an endogenous retroviral genome was initiated. Mammary tumors were induced in female SD rats with 7, 12-dlmethylbenz[a]anthracene (DMBA). Tumors, Identified histologically as mammary adenocarcinomas, were analyzed for RNA of a replication-defective endogenous retrovirus or RNA of a helper-independent endogenous type C virus. Expression of RNA of the replication-defective virus was detected in mammary tumors weighing 0.2-2.0 g. Larger tumors, for which histologic examination revealed proportionally more fibroblastic tissue than epithelial cells, did not contain comparable concentrations of this viral RNA. RNA homologous to a helper-independent rat type C retrovirus was not detected In tumors of any size. A cell line was established from a primary DMBA-induced mammary adenocarcinoma and appeared similar to the small mammary tumors with respect to endogenous type C viral RNA expression. We discuss possible Implications of the expression of endogenous replication-defective viruses for use as markers for the effects of chemical carcinogens.—J Natl Cancer Inst 61: 1329-1337, 1978.",

author = "Young, {Howard A.} and Wenk, {Martin L.} and Goodman, {Dawn G.} and Scolnick, {Edward M.}",

note = "Funding Information: 1 Received March 16. 1978; accepted June 15. 1978. 2 Supported in part by Public Health Service contracts from the Division of Cancer Cause and Prevention (DCCP). National Cancer Institute (NCI): NOl·CP43236 (Virus Cancer Program) to Meloy Laboratories. Rockville. Md .. and NOl·CP02199 to Microbiological Associates. Bethesda. Md. ! Laboratory of Tumor Virus Genetics. DCCP. NCI. National Institutes of Health. Public Health Service. U.S. Department of Health. Education. and Welfare. Bethesda. Md. 20014. • Microbiological Associates. Bethesda. Md. 5 Tumor Pathology Branch. DCCP. NCI. 6 We acknowledge the technical assistance of John Vere. Jr.. and Robert Shores.",

year = "1978",

month = nov,

doi = "10.1093/jnci/61.5.1329",

language = "English (US)",

volume = "61",

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journal = "Journal of the National Cancer Institute",

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AU - Young, Howard A.

AU - Wenk, Martin L.

AU - Goodman, Dawn G.

AU - Scolnick, Edward M.

N1 - Funding Information: 1 Received March 16. 1978; accepted June 15. 1978. 2 Supported in part by Public Health Service contracts from the Division of Cancer Cause and Prevention (DCCP). National Cancer Institute (NCI): NOl·CP43236 (Virus Cancer Program) to Meloy Laboratories. Rockville. Md .. and NOl·CP02199 to Microbiological Associates. Bethesda. Md. ! Laboratory of Tumor Virus Genetics. DCCP. NCI. National Institutes of Health. Public Health Service. U.S. Department of Health. Education. and Welfare. Bethesda. Md. 20014. • Microbiological Associates. Bethesda. Md. 5 Tumor Pathology Branch. DCCP. NCI. 6 We acknowledge the technical assistance of John Vere. Jr.. and Robert Shores.

PY - 1978/11

Y1 - 1978/11

N2 - An investigation into the possible relationship between chemical carcinogen Induction of rat mammary tumors and the expression of an endogenous retroviral genome was initiated. Mammary tumors were induced in female SD rats with 7, 12-dlmethylbenz[a]anthracene (DMBA). Tumors, Identified histologically as mammary adenocarcinomas, were analyzed for RNA of a replication-defective endogenous retrovirus or RNA of a helper-independent endogenous type C virus. Expression of RNA of the replication-defective virus was detected in mammary tumors weighing 0.2-2.0 g. Larger tumors, for which histologic examination revealed proportionally more fibroblastic tissue than epithelial cells, did not contain comparable concentrations of this viral RNA. RNA homologous to a helper-independent rat type C retrovirus was not detected In tumors of any size. A cell line was established from a primary DMBA-induced mammary adenocarcinoma and appeared similar to the small mammary tumors with respect to endogenous type C viral RNA expression. We discuss possible Implications of the expression of endogenous replication-defective viruses for use as markers for the effects of chemical carcinogens.—J Natl Cancer Inst 61: 1329-1337, 1978.

AB - An investigation into the possible relationship between chemical carcinogen Induction of rat mammary tumors and the expression of an endogenous retroviral genome was initiated. Mammary tumors were induced in female SD rats with 7, 12-dlmethylbenz[a]anthracene (DMBA). Tumors, Identified histologically as mammary adenocarcinomas, were analyzed for RNA of a replication-defective endogenous retrovirus or RNA of a helper-independent endogenous type C virus. Expression of RNA of the replication-defective virus was detected in mammary tumors weighing 0.2-2.0 g. Larger tumors, for which histologic examination revealed proportionally more fibroblastic tissue than epithelial cells, did not contain comparable concentrations of this viral RNA. RNA homologous to a helper-independent rat type C retrovirus was not detected In tumors of any size. A cell line was established from a primary DMBA-induced mammary adenocarcinoma and appeared similar to the small mammary tumors with respect to endogenous type C viral RNA expression. We discuss possible Implications of the expression of endogenous replication-defective viruses for use as markers for the effects of chemical carcinogens.—J Natl Cancer Inst 61: 1329-1337, 1978.

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Expression of RNA of an Endogenous Replication-Defective Retrovirus in Rat Mammary Adenocarcinomas Induced by 7, 12-Dimethylbenz[a]anthracene

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