Genetic control of radiation leukemia virus-induced tumorigenesis. I. Role of the major murine histocompatibility complex, H-2.

Meruelo, Daniel; Leiberman, M; Ginzton, Nancy; Deak, Beverly D.; McDevitt, H O

doi:10.1084/jem.146.4.1079

Cited by 69 publications

(14 citation statements)

References 22 publications

(18 reference statements)

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“…In adult animals, F-MuLV strain of radiation leukemia virus, the alleles for susceptibility and resist ance are opposite from those for FV (20). In adult animals, F-MuLV strain of radiation leukemia virus, the alleles for susceptibility and resist ance are opposite from those for FV (20).…”

Section: Introductionmentioning

confidence: 95%

Host Genetic Control of Spontaneous and Induced Immunity to Friend Murine Retrovirus Infection

Chesebro

Miyazawa²,

Britt³

1990

Annu. Rev. Immunol.

118

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Section: Introductionmentioning

confidence: 95%

Host Genetic Control of Spontaneous and Induced Immunity to Friend Murine Retrovirus Infection

Chesebro

Miyazawa²,

Britt³

1990

Annu. Rev. Immunol.

118

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“…We first became interested in the relationship between viral and lymphocyte differentiation loci while investigating the mechanism by which genes of the major murine histocompatibility complex, H-2, influenced susceptibility to leukemia induction by the Kaplan strain of radiation leukemia virus (RadLV) (4)(5)(6). RadLV infection or transformation has profound effects on the expression of H-2-encoded antigens.…”

mentioning

confidence: 99%

Association of endogenous viral loci with genes encoding murine histocompatibility and lymphocyte differentiation antigens.

Meruelo¹,

Rossomando²,

Offer³

et al. 1983

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

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Several polymorphic DNA restriction endonuclease fragments hybridizing with xenotropic and ecotropic envelope virus probes map adjacent to minor histocompatibility and lymphocyte (H/Ly) antigen-encoding loci. Viral DNA restriction fragments are associated with Ly-17 on chromosome 1, H-30, H-3, and H-13 on chromosome 2, Ly-21 on chromosome 7, H-28 on chromosome 3, and H-38 (chromosomal location as yet undetermined). In each case no recombinant can be found between the H/Ly locus in question and the virus-related restriction fragment, suggesting that linkage is very tight. Although some viral loci map to locations where no H/Ly has yet been mapped, the frequency and tightness of linkage in the seven instances described, coupled with the large number of as yet unmapped H/Ly loci, suggests that the associations found are significant.

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“…There is experimental as well as clinical evidence that susceptibility to certain neoplastic diseases may be partly under genetic control (Heston, 1976;Lilly and Mayer, 1980). The genes involved may be expressed at different levels, determining for instance high susceptibility to DNA-damage (Robbins et al, 1974), "permissiveness" for replication and recombination of certain oncogenic viruses (Lilly and Mayer, 1980) genetic differences in the susceptibility of the target tissue to undergo neoplastic transformation, or defects in immune mechanisms which normally contribute to control of neoplasia (Lonai and Haran-Ghera, 1977;Meruelo et al, 1977Meruelo et al, , 1980Purtilo, 1980;Klein, G.O. et al, 1978).…”

mentioning

confidence: 99%

Incidence and type of tumors induced in C57BL bg/bg mice and +/bg littermates by oral administration of DMBA

Argov

Cochran

Kärre

et al. 1981

Intl Journal of Cancer

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As an attempt to study the effect of the beige (bg) mutation on chemical carcinogenesis, 65 C57Bl/bg/bg mice and 83 +/bg littermate controls received DMBA in five weekly intragastric doses. The incidence of tumors of different histological types was monitored through observation periods ranging between 165 and 500 days. By 165 days after the first DMBA feeding, 18% of the +/bg and 31% of the bg/bg mice had developed tumors. The beige mice had a higher incidence of epithelial and non-epithelial tumors arising in cutaneous or subcutaneous sites than the controls. The total incidence of lymphomas was similar in the two groups. However, lymphomas appeared somewhat earlier in beige than in control mice. Altogether 33 +/bg and 27 bg/bg mice were followed for 500 days. By this time, 73% of the +/bg and 78% of the bg/bg mice had developed tumors. The beige group showed a higher incidence of non-thymic lymphomas than the controls. In contrast, the incidence of thymic lymphoma, cutaneous epithelial tumors and bile-duct adenomas was similar in the two groups or higher in +/bg that in bg/bg mice. The results suggest that the bg mutation causes a certain defect in a mechanism that may prevent or delay the onset of non-thymic lymphomas and of epithelial and non-epithelial cutaneous tumors in DMBA-treated mice. The differences between the two groups were smaller than those previously reported in relation to the increased susceptibility of beige mice to certain transplanted tumors, attributed to the known defect in natural killer (NK) activity in the beige mice. The reduced differential in the DMBA system may be due to the partial reduction of NK activity, induced by the carcinogen, as reported previously (Ehrlich et al., 1980) and confirmed in the present study.

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Genetic control of radiation leukemia virus-induced tumorigenesis. I. Role of the major murine histocompatibility complex, H-2.

Cited by 69 publications

References 22 publications

Host Genetic Control of Spontaneous and Induced Immunity to Friend Murine Retrovirus Infection

Host Genetic Control of Spontaneous and Induced Immunity to Friend Murine Retrovirus Infection

Association of endogenous viral loci with genes encoding murine histocompatibility and lymphocyte differentiation antigens.

Incidence and type of tumors induced in C57BL bg/bg mice and +/bg littermates by oral administration of DMBA

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