Histocompatibility Genes (the H-2 Complex) and Susceptibility to Mammary Tumor Virus in Mice2

Mühlbock, O; Dux, Anna

doi:10.1093/jnci/53.4.993

Cited by 35 publications

(12 citation statements)

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“…These data are comparable in all groups of C3H mice with those observed previously (Muhlbock and Dux, 1981;Van der Valk, 1981). All C3H foster-mothers used in the present experiments developed mammary tumors at the expected age, showing that they were a reliable source of infectious MTV.…”

Section: Ansupporting

confidence: 92%

MHC‐controlled susceptibility to C3H‐MTV‐induced mouse mammary tumors is predominantly systemic rather than local

Dux

Démant

1987

Intl Journal of Cancer

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The major histocompatibility complex (MHC) is one of the genetic factors involved in the control of susceptibility to MTV-induced mammary tumors in mice. Previously, genetic differences in mammary tumor susceptibility were shown to be mainly due to differences in susceptibility of the mammary gland itself. Such experiments, however, were carried out using inbred strains which differ in many genes. Therefore, the conclusion drawn from such experiments is not necessarily applicable to every gene involved. We tested whether in the strain C57BL/10 (B10, resistant) and the H-2 congeneic strain B10.A(5R) (5R, susceptible), which differ only at the MHC, the MHC-controlled difference in tumor susceptibility indeed resides in the mammary gland tissue itself, or is caused by systemic factors. Mammary glands of infant B10 and 5R mice were transplanted into mammary fat pads of C3H-MTV-infected mammectomized (B10 X 5R)F1 females. The hosts received a hypophyseal isograft under the kidney capsule or were subjected to force-breeding to provide hormonal stimulation necessary for mammary tumor development. Control groups of C3H-MTV-infected B10, 5R and (B10 X 5R)F1 females and (B10 X 5R)F1 females without C3H-MTV were also subjected to the 2 types of hormonal stimulation. There was no difference in susceptibility between the 5R and B10 mammary glands transplanted into C3H-MTV-infected F1 hybrid hosts. On the other hand, C3H-MTV-infected 5R and (B10 X 5R)F1 females were significantly more susceptible than the C3H-MTV-infected B10 females, when either of the 2 methods of hormonal stimulation was used. This indicates that, in the strains used, MHC-controlled susceptibility to C3H-MTV-induced mammary tumorigenesis is predominantly or exclusively controlled by systemic factors rather than by factors residing in the target tissue.

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Section: Ansupporting

confidence: 92%

MHC‐controlled susceptibility to C3H‐MTV‐induced mouse mammary tumors is predominantly systemic rather than local

Dux

Démant

1987

Intl Journal of Cancer

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“…The fact that the relative sensitivity or resistance of a given rodent strain is a heritable trait supports the premise that specific genes regulate susceptibility to tumor development. The mapping of tumor susceptibility genes that contribute to interstrain variance in development of carcinogen‐induced lung, liver, colon, mammary, kidney, hematopoietic, and skin tumors in segregating crosses of sensitive versus resistant mouse or rat strains has shown that genetic control of cancer susceptibility is complex, involving many genes [6–34]. Furthermore, Lee and Drinkwater [16] suggested that carcinogen sensitivity is determined by a combined effect of both sensitivity and resistance genes.…”

Section: Introductionmentioning

confidence: 99%

Confirmation of the mapping of a 12‐O‐tetradecanoylphorbol‐13‐acetate promotion susceptibility locus, Psl1, to distal mouse chromosome 9

Angel

Caballero

DiGiovanni

2001

Molecular Carcinogenesis

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Susceptibility to two-stage skin carcinogenesis in the mouse is affected by several genes. In addition, studies suggest that genes that modify the response of mice to skin tumor promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA) also may influence histologic changes in the skin as the result of TPA treatment. One TPA susceptibility locus, Psl1, previously was mapped to distal chromosome 9. The mapping of this locus was confirmed by marker-based genotypic selection. Furthermore, Psl1 or a gene closely linked to Psl1 influenced epidermal hyperplasia and epidermal labeling index of mice treated with TPA.

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“…Since the major histocompatibility complex (H-2D region) was shown to control resistance to mammary tumorigenesis by exogenous murine mammary-tumour viruses (Muhlbock & Dux, 1974) it was thought worth while to study the possible interaction, if it should occur, between the modulable mammary tumour virus-induced cell-surface antigens and the non-or hardly modulable antigens of the H-2K and H-2D end.…”

mentioning

confidence: 99%

Antigenic modulation of mammary tumour virus envelope antigen or GR thymic lymphoma cells in relation to expression of H-2, TL cell-surface antigens and THY1

Hilgers¹,

Sonnenberg²,

Nusse³

1980

Br J Cancer

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The MLr antigen, a mammary tumour virus-induced antigen on the surface of GR thymic lymphoma cells (GRSL) can be modulated from the cell surface upon incubation with specific antiserum for 1-2 h at 37 degrees C, followed by washing the cells. In contrast, a number of other cell-surface antigens on these GRSL cells cannot be modulated under similar conditions. These antigens include histocompatibility antigens of the H-2 complex (H-2.8 of the K-end and H-2dx(D) of the H-2dx haplotype) and two thymic markers, TL1.2 and Thy1.2. Antigenic modulation of MLr as tested by trypan-blue exclusion and by chromium51 release does not lead to a measurable change in the expression of H-2K, H-2D, TL and Thy1.2 antigens. These results could be confirmed by absorption analysis. The latter analysis showed that the number of antigenic sites per cell are about the same for MLr and the two H-2 antigens, while TL antigens are scarcer and Thy1.2 antigens are more abundant. The procedure of antigenic modulation showed that the MLr antigen resides on MTVgp52, the major protein of the envelope. There was no evidence of internal proteins, such as MTVp27, on the surface of GRSL cells.

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Histocompatibility Genes (the H-2 Complex) and Susceptibility to Mammary Tumor Virus in Mice2

Cited by 35 publications

References 0 publications

MHC‐controlled susceptibility to C3H‐MTV‐induced mouse mammary tumors is predominantly systemic rather than local

MHC‐controlled susceptibility to C3H‐MTV‐induced mouse mammary tumors is predominantly systemic rather than local

Confirmation of the mapping of a 12‐O‐tetradecanoylphorbol‐13‐acetate promotion susceptibility locus, Psl1, to distal mouse chromosome 9

Antigenic modulation of mammary tumour virus envelope antigen or GR thymic lymphoma cells in relation to expression of H-2, TL cell-surface antigens and THY1

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