Exogenous and Endogenous Mouse Mammary Tumor Viruses: Replication and Cell Transformation

Slagle, Betty L.; Butel, Janet S.

doi:10.1007/978-1-4613-0943-7_16

Cited by 8 publications

(5 citation statements)

References 208 publications

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“…One of the most frequent allelic deletions in HCC has been found at chromosome 17p where the tumor suppressor gene p53 is located (Fujimori et al, 1991;Murakami et al, 1991;Slagle et al, 1991). The frequency of p53 mutations varies largely among HCC samples, depending on the geographic location in the world, and a hot spot mutation at codon 249 was observed in HCCs from regions with high levels of dietary a¯atoxins and high prevalence of HBV infection (Bressac et al, 1991;Buetow et al, 1992;Hsu et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Comprehensive allelotyping of human hepatocellular carcinoma

et al. 1997

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Hepatocellular carcinoma (HCC) is one of the most common cancers in many parts of the world, however the molecular mechanisms underlying liver cell transformation remain obscure. A genome-wide scan of loss of heterozygosity (LOH) in tumors provides a powerful tool to search for genes involved in neoplastic processes. To identify recurrent genetic alterations in liver tumors, we examined DNAs isolated from 120 HCCs and their adjacent non tumorous parts for LOH using a collection of 195 microsatellite markers located roughly every 20 cM throughout 39 autosomal arms. The mean heterozygosity was 73%. Our ®ndings provide additional support that LOH for loci on chromosomal arms 1p, 4q, 6q, 8p, 13q and 16p is signi®cantly elevated in HCC. The highest percentage of LOH is found for a locus in 8p23 (42% of informative csaes). This corresponds to one of the most common genetic abnormalities reported to date in these tumors. In addition, high ratio of LOH (535%) is observed on chromosome arms which had not been implicated in previous studies, notably on 1q, 2q and 9q. No correlation was found between LOH of speci®c chromosomal regions and etiologic factors such as chronic infections with hepatitis B or C viruses. This ®rst report of an extensive allelotypic analysis of HCC should help in identifying new genes whose loss of function contributes to the development of liver cancer.

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Section: Introductionmentioning

confidence: 99%

Comprehensive allelotyping of human hepatocellular carcinoma

et al. 1997

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“…Such a correlation could occur in two ways: either the random integration of the HBV DNA into the host cell genome may have a small probability of causing a relevant phenotypic transformation, or the transformation could occur by a mutation of the infected cell DNA during cell division. Both the absence of an essential cofactor and the observation that viral DNA integration, random in nontumor cells, is nonrandom in malignant cells (25) would suggest the former scenario to be more likely. The infected S cells could also be potentially tumorigenic, but their limited capacity for cell division means that their role in the promotion of PHC would not be significant.…”

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confidence: 99%

The dynamics of hepatitis B virus infection.

Payne¹,

Nowak²,

Blumberg³

1996

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

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We consider a cellular model of infection by the hepatitis B virus and describe how it may be used to account for two important features of the disease, namely (i) the wide variety of manifestations of infection and the age dependence thereof, and (ii) the typically long delay before the development of virus-induced liver cancer (primary hepatocellular carcinoma). The model is based on the assumption that the liver is comprised of both immature and mature hepatocytes, with these two subpopulations of cells responding contrastingly upon infection by the virus.

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“…M ouse mammary tumor viruses (MMTV) are milk-borne . retroviruses that are infectious and tumorigenic in mice (1). The natural history of these viruses, including the mechanism by which milk-borne transmission leads to host infection and the role of the immune system in this process, is poorly understood.…”

mentioning

confidence: 99%

“…The natural history of these viruses, including the mechanism by which milk-borne transmission leads to host infection and the role of the immune system in this process, is poorly understood. Most mice also express a number of ge-nomicaUy integrated mammary tumor proviruses, the majority of which are defective and do not encode infectious virus (1). Recently, it was demonstrated that the open reading frame (ORF) of the MMTV 3' LTR encodes a superantigenic product which is recognized by T cells expressing an appropriate Tcr VB product (2)(3)(4)(5)(6)(7).…”

mentioning

confidence: 99%

Expression of a MHC class II transgene determines both superantigenicity and susceptibility to mammary tumor virus infection.

Pucillo

Cepeda

Hodes

1993

The Journal of Experimental Medicine

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SummaryMilk-borne mouse mammary tumor virus (MMTV) is a type B retrovirus that induces mammary carcinoma. Infectious MMTV, as well as genomically integrated mouse mammary proviruses, encode superantigens that are recognized by T cells that express appropriate T cell receptor VB products. To determine the relationship between the superantigenic property of milk-borne MMTV and its in vivo infectivity, mice which were either positive or negative for expression of a transgeneencoded E~EB class II major histocompatibility complex (MHC) product were exposed to milk borne C3H MMTV. Superantigen-mediated deletion of VB14-expressing T cells occurred only in Eot transgene-positive mice, indicating that the deletion was Ec~EB dependent. When mice were analyzed for viral infection by assaying viral p28 in the milk of recipient females, significant p28 levels were found only in E~E~ transgene-positive mice. Similarly, the presence of C3H MMTV LTR mRNA in mammary glands, as detected by PCR, paralleled p28 levels. These findings indicate that Ec~ expression or the E~-dependent T cell response to viral superantigen is causally related to susceptibility to MMTV infection, and that lack of a permissive class II product can protect mice from virus infection.

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Exogenous and Endogenous Mouse Mammary Tumor Viruses: Replication and Cell Transformation

Cited by 8 publications

References 208 publications

Comprehensive allelotyping of human hepatocellular carcinoma

Comprehensive allelotyping of human hepatocellular carcinoma

The dynamics of hepatitis B virus infection.

Expression of a MHC class II transgene determines both superantigenicity and susceptibility to mammary tumor virus infection.

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