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Sentences for "carcinogenesis "
Results Wnt-1 TG mice have been used to assess the functions of a number of genetic lesions in breast carcinogenesis because tumors appear with predictable kinetics.
They include metaplasia, dysplasia, and carcinoma in situ (CIS), which are thought to represent progressive histologic correlates of carcinogenesis for squamous cell carcinoma [ 6].
It has also been documented that prostate epithelial cells exhibited squamous metaplastic phenotype during vitamin A deficiency [ 7 ] , and prostate cell carcinogenesis could be prevented by retinoic acid (RA) and its analogs in vitro [ 8 9 10 ] .
Gastric carcinogenesis is considered as a multistage progressive process.
However, the information for the mechanism of gastric carcinogenesis is very limited.
We hypothesized that alterations of p53, iNOS and VEGF expression may contribute to gastric carcinogenesis and influence the clinical behavior of GC via angiogenesis.
Thus, the high coincidental expression of iNOS and VEGF and p53 protein accumulation may be important events to enhance gastric carcinogenesis and poorly clinical features and may be useful biomarkers to assess risk for the development of GC.
Black tea has been shown to have a preventative effect against skin carcinogenesis in animal models [ 4 5 6 7 8 9 ] .
These data therefore suggest that 5p genetic alterations occur early in cervical carcinogenesis and they may be critical to the development of invasive cancer.
In the present study we used a carcinogen-induced rat mammary carcinogenesis model to test the hypothesis that chemoprevention by tamoxifen and retinoids is associated with local upregulation of TGF-ßs in the mammary gland, and that TGF-ßs might therefore be useful as potential surrogate end-point biomarkers of chemopreventive efficacy in clinical trials.
In the present study, we used a carcinogen-induced rat model of mammary carcinogenesis to test whether chemoprevention by tamoxifen and by two different retinoids (4-HPR, also known as fenretinide, and 9-cRA) is associated with local upregulation of TGF-ßs in the initiated mammary gland.
Materials and method Mammary carcinogenesis studies A standard protocol for induction of breast cancer in female Sprague-Dawley rats was used [ 4, 18], with initiation induced by a single intravenous dose of NMU (50 mg/kg body weight) at 8 weeks of age.
However, here we used the NMU-induced rat model of mammary carcinogenesis to show that the chemopreventive effect of tamoxifen and two retinoids is not associated with any consistent changes in TGF-ß levels, at least as determined immunohistochemically.
Limitations of the NMU-induced rat model of mammary carcinogenesis The NMU-induced rat model of mammary tumorigenesis is widely used for chemoprevention studies and yields rapid development of hormonally responsive mammary tumors with 100% incidence [ 2, 4, 18].
Expression patterns for selected genes of known interest in breast cancer Differences in gene expression for specific genes that are implicated in breast carcinogenesis were examined.
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