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Biomedical subjects

L G Wolfe

Publications and source records attributed to L G Wolfe.

76 records · Page 5Linked to original sources

Proposed mechanisms for selenium-inhibition of mammary tumorigenesis (review).

Both the reduced and oxidized forms of selenium are available at various rates through a common selenium pool for incorporation into selenoproteins, of which glutathione peroxidase is the best studied. Dietary selenium as selenite and selenomethionine decreased the incidence of rodent mammary tumorigenesis. The postulated mechanisms of this inhibition includes alterations in the level of GSHPX, membrane peroxidation, glutathione, immune functions, induction of specific selenoproteins, alterations of carcinogen metabolism, and the effect of various chemical forms of selenium. After many studies the mechanism of action of selenium in the inhibition of mammary tumorigenesis is still unknown, although studies of the role of selenoproteins appears the most promising.

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Modulation by canine interferon-gamma of major histocompatibility complex and tumor-associated antigen expression in canine mammary tumor and melanoma cell lines.

In an effort to enhance the antigenicity of canine tumor cells, canine interferon-gamma (CnIFN-gamma) was applied in vitro to seven canine mammary tumor (CMT) and two canine melanoma (CML) cell lines. Surface expression of major histocompatibility complex (MHC) antigens and tumor-associated antigens (TAA) was measured by a flow cytometric fluorescence assay using commercially available anti-MHC antibodies, and anti-canine TAA monoclonal antibodies generated against CMT and CML cell lines. Compared to constitutive antigen levels in untreated cells, treatment with CnIFN-gamma resulted in increased expression of MHC class I and II antigens (up to 19- and 167-fold, respectively) and a TAA (up to 5-fold) by CMT cell lines, and increased expression of class I antigen (131-fold) by one CML and of class II antigen (18-fold) by the other CML cell line. Expression of MHC antigens and a TAA by tumor cells was increased by Cn-IFN-gamma treatment, and such an increase may be of potential benefit in tumor cell recognition and rejection by the immune system.

Animals↗

Overexpression of c-erbB-2 and c-myc but not c-ras, in canine melanoma cell lines, is associated with metastatic potential in nude mice.

Overexpression of the proto-oncogenes c-erbB-2, c-myc, and c-ras have been associated with neoplastic transformation in a variety of tumours. We investigated expression of these oncogenes in 5 canine melanoma cell lines and 6 clonal derivatives of 1 of the cell lines, CML-6M, to determine what impact overexpression had on tumour cell growth and metastatic potential. All 11 cell lines were tumourigenic at subcutaneous inoculation sites in nude mice, but spontaneous metastasis to lung was a characteristic of only the CML-6M cell line and 3 of 6 clonal derivatives of CML-6M. Investigation of oncogene overexpression revealed no obvious pattern of expression among the 5 tumour-derived cell lines whereas overexpression of c-erbB-2 and c-myc was consistently found in the 3 clonal cell lines characterized by high metastatic potential, and in primary and metastatic mouse xenografts induced by these lines. This data suggests involvement of overexpression of these genes in development of canine melanoma and associates their overexpression with metastatic potential in nude mice.

Animals↗

Heterogenic properties of clonal cell lines derived from canine mammary carcinomas and sensitivity to tamoxifen and doxorubicin.

Five clonal cell lines were established from each of 3 cell lines derived from 3 primary malignant canine mammary tumors. The clonal lines in each series were compared with one another and to the respective parent cell line with regard to cellular morphology, growth on plastic, cloning efficiency (CE) and colony sizes in soft agar, estrogen and progesterone receptor (ER, PR) status, and response to tamoxifen or doxorubicin in clonogenic assays. The most remarkable differences observed among the cell lines were in CE, colony sizes, and sensitivity to doxorubicin. The clonal line which contained measurable ER, had a shift in colony-size distribution to smaller colonies when exposed to tamoxifen or tamoxifen with estradiol that may have been estrogen-receptor mediated.

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