Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:O76050 (neu)
 3,969 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four murine cellular tumor models expressing various combinations of oncogenes (SV40 large T and v-Ha-ras, SV40 large T and v-src, SV40 large T and neu, adenovirus EIA and v-Ha-ras) induce sarcoma when they are inoculated s.c. into the DBA/2 syngenic mice. The metastatic patterns, distribution and fate of these tumor cells transplanted by two different routes into syngenic DBA/2 mice have been studied. All the tumor cell lines except EIA-ras, induce massive overt artificial metastases principally in the lung after i.v. injection. In s.c. tumor-bearing mice, a few resting cells colonize the lung as micrometastases. When removed from this tissue context and injected s.c. these cells regain their proliferative potential and grow as local tumors which again give rise to occult pulmonary micrometastases.
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PMID:Metastatic phenotype of murine tumor cells expressing different cooperating oncogenes. 131 11

CBA, C3HA, C57Bl, Balb/c and DBA female mice received 20 subcutaneous weekly injections of 1,2-dimethylhydrazine in the dose of 8 mg/kg body weight. Estrous cycles were studied in vaginal smears taken 5, 10, 15 and 20 weeks after the 1st DMH injection. In CBA strain susceptible to DMH induction of uterine sarcomas a persistent estrus was observed in 50% of mice after 5 to 10 DMH injections. In C3HA, C57B1, Balb/c and DBA strains resistant to the DNH induction of uterine sarcomas persistent estrus was not observed; the majority of these mice retained a normal estrus cycle. Persistent diestrus which was absent in susceptible CBA mice was found in these resistant strains. No CBA females with a normal estrous cycle were observed after the beginning of DMH treatment. The differences in the estrous cycle found in the mouse strains treated with DMH may partly explain the observed strain differences in the susceptibility to the DMH induction of uterine sarcomas.
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PMID:[Effect of 1,2-dimethylhydrazine on the estrous cycle in different strains of mice]. 380 85

The occurrence of different components of the cell growth regulation pathway as expressed in experimental skin carcinogenesis in haired carcinogen-sensitive NMRI, in haired carcinogen resistant DBA/2 mice and in hairless SKH/1 mice was studied by morphological and immunohistochemical methods. The results were compared with respect to neoplastic response, number of tumors, tumor behaviour and to the inducing agent (UV irradiation or chemical carcinogen), in order to increase our understanding of specific alterations in neoplastic development caused by extraneous agents and to determine their possible usefulness as indicators of carcinogen exposure. The expression of growth factors (transforming growth factor alpha and epidermal growth factor), growth factor receptors (epidermal growth factor receptor/c-erbB-1 and c-erbB-2/neu), cell signalling component c-myc, the nuclear transcription factor Harvey-Ras and the tumor suppressor gene p53, were studied in carcinogen- and UV-induced tumor formation in mouse. The results showed increased oncogene expression as well as growth factor expression in the skin during tumor development appearing early in neoplastic and premalignant conditions and becoming more distinct during neoplastic progression. Efforts to delineate specifically initiated cells prior to the appearance of morphologically detectable alterations including dysplasia, papilloma formation and squamous cell carcinomas, were unsuccessful. Increased staining by antibodies to growth factors and oncogenes were also observed in DBA/2 animals resistant to tumor formation. It is concluded that oncogene expression and growth factor protein deposits are associated with carcinogenic effects, partly explaining the mechanism of action of these agents, but the applicability, as such, for the analysis of potential hazardous agents needs further studies.
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PMID:Oncogenes and growth factors as indicators of carcinogen exposure. 867 68

In this study we established a HER2/neu expressing mouse tumor model using hepatoma MH-22a cell line tumorigenic in DBA mice. G10 clone with high level of HER2/neu expression was obtained by stable transfection and cloning. Solid tumors induced by subcutaneous injection of G10 cells into immunocompetent mice retain the expression of human receptor for at least three weeks. Treatment with trastuzumab results in statistically significant inhibition of tumor growth. This model can be used to evaluate in vivo efficiency of novel anti-HER2/neu antibodies and to test antibody-based conjugates for diagnostics.
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PMID:[Creation of a model of HER2/neu-positive transplantable tumor on the immunocompetent mice]. 3044 91