Mammary tumors, plaques, and hyperplastic alveolar nodules in various combinations of mouse inbred strains and the different lines of the mammary tumor virus

Heston, W. E.; Vlahakis, George

doi:10.1002/ijc.2910070116

Cited by 50 publications

(32 citation statements)

References 8 publications

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“…Several dominant agouti alleles (e.g., Ay, An, Asy, AiY) cause a predominantly yellow pelage (1), as well as a number of additional effects that include a non-insulin-dependent diabetic-like condition, pronounced obesity, and a marked increase in the incidence of spontaneous and induced tumors (1,(8)(9)(10)(11). Assessment of the physiology of these mutants revealed that their diabetic/obesity condition has a notable similarity to non-insulin-dependent diabetes in humans (11,12).…”

mentioning

confidence: 99%

Molecular structure and chromosomal mapping of the human homolog of the agouti gene.

Kwon

Bultman

Löffler

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

154

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The agouti (a) locus in mouse chromosome 2 normally regulates coat color pigmentation. The mouse agouti gene was recently cloned and shown to encode a distinctive 131-amino acid protein with a consensus signal peptide. Here we describe the cloning of the human homolog of the mouse agouti gene using an interspecies DNA-hybridization approach. Sequence analysis revealed that the coding region of the human agouti gene is 85% identical to the mouse gene and has the potential to encode a protein of 132 amino acids with a consensus signal peptide. Chromosomal assignment using somatic-cell-hybrid mapping panels and fluorescence in situ hybridization demonstrated that the human agouti gene maps to chromosome band 20q11.2. This result revealed that the human agouti gene is closely linked to several traits, including a locus called MODY (for maturity onset diabetes of the young) and another region that is associated with the development of myeloid leukemia. Initial expression studies with RNA from several adult human tissues showed that the human agouti gene is expressed in adipose tissue and testis.

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mentioning

confidence: 99%

Molecular structure and chromosomal mapping of the human homolog of the agouti gene.

Kwon

Bultman

Löffler

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

154

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“…HANs, and less frequently plaques, may eventually progress to overt mammary tumors (13). During this progression a number of genes may become activated including the putative mammary oncogenes, int-1 (14), int-2 (15), int-3 (16) and int-H (17).…”

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confidence: 99%

Expression of the oncogenes mil and ras abolishes the in vivo differentiation of mammary epithelial cells

et al. 1988

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Three carcinoma-associated oncogenes, two of which have been strongly implicated in human mammary tumorigenesis, have been introduced into a novel mouse mammary epithelial cell line, EF43, that retains many differentiated functions. The effect of oncogene expression upon classical transformation parameters as well as parameters specific for mammary epithelial cells such as growth in three-dimensional collagen matrices and the ability to repopulate the cleared mammary fat pad and to form alveolar structures in vivo has been investigated. Expression of \-myc in EF43 cells results in no obvious phenotypk changes, and does not confer tumorigenic potential upon the cells. Expression of v-Ha-ras confers upon EF43 cells the ability to grow rapidly, grow in an anchorageindependent manner, results in tumor formation in nude and syngeneic animals, abolishes their ability to repopulate the mammary gland and, instead, results in rapid induction of anaplastic tumors. The v-mil oncogene, an avian homolog of the mouse \-mht and human c-raf oncogenes, previously thought to be non-transforming in the absence of a cooperating oncogene, transforms EF43 cells, allowing them to grow in an anchorage-independent manner, form tumors in nude mice and abolishes their ability to repopulate the cleared mammary fat pad. In contrast to v-ras, however, the tumors arising from \-mil expression have a differentiated morphology, typical of adenocarcinomas. Thus, different oncogenes show varying degrees of inhibition of the differentiation of mammary epithelial cells in vivo. IntroductionNeoplastic transformation of the mammary gland proceeds via a multistep pathway involving the tumorigenic conversion of one or a number of mammary cell types. The identity of the cell types involved in this process, their interaction during the conversion and the identity of the cellular genes which are deregulated is open both to speculation and investigation.Transfection of DNA from the human mammary tumor derived cell line MCF-7 into NIH/3T3 fibroblasts has identified potential mammary oncogenes (1). Additionally, the Ha-ras oncogene has been found activated or overexpressed in some human mammary•Abbreviations: EGF, epidermal growth factor, HANs, hyperplastic alveolar nodules.tumors (2 -4) and a human mammary tumor cell line (5,6). Two erb-B related genes, the human epidermal growth factor (EGF*) receptor gene (7,8) and the neu oncogene (9) have been found amplified in human mammary carcinoma derived cell lines. More recently, the neu oncogene has been shown to be amplified in primary mammary tumors (10). Similarly, the c-myc gene has been found to be amplified (11) and overexpressed in some human primary breast carcinomas (12).In the mouse, depending upon strain, either plaques or hyperplastic alveolar nodules (HANs) represent the first visible preneoplastic lesion. HANs, and less frequently plaques, may eventually progress to overt mammary tumors (13). During this progression a number of genes may become activated including the putative mammary oncogenes, in...

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“…There is not only an increase in the number of lesions, but the y develop more rapidly in the hybrid than in C3H mice (Heston et al, 1960;Heston and Vlahakis, 1961; and Heston, 1966). …”

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Morphologic and Biologic Correlation of Hyperplastic and Neoplastic Hepatic Lesions Occurring “Spontaneously” in C3H × Y Hybrid Mice

Reuber¹

1971

Br J Cancer

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(Reuber and Firminger, 1963; Reuber, 1966).The purpose of the present study was to see if there was a biologic and morphologic correlation for lesilons of the liver developing " spontaneously " in C3H x Y hybrid mice. There is not only an increase in the number of lesions, but the y develop more rapidly in the hybrid than in C3H mice (Heston et al., 1960;Heston and Vlahakis, 1961; and Heston, 1966). MATERIALS AND METHODSC3H x Y hybrid micet were given National Cancer Institute pellets (Heston et al., 1960). They were divided into five groups of 15 animals each. Laparotomy and liver biopsy were performed on different groups at 12, 24, 36, 48, and 64 weeks of age. Additional groups of 15 to 25 male mice were killed at the same time

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Mammary tumors, plaques, and hyperplastic alveolar nodules in various combinations of mouse inbred strains and the different lines of the mammary tumor virus

Cited by 50 publications

References 8 publications

Molecular structure and chromosomal mapping of the human homolog of the agouti gene.

Molecular structure and chromosomal mapping of the human homolog of the agouti gene.

Expression of the oncogenes mil and ras abolishes the in vivo differentiation of mammary epithelial cells

Morphologic and Biologic Correlation of Hyperplastic and Neoplastic Hepatic Lesions Occurring “Spontaneously” in C3H × Y Hybrid Mice

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