PubMed · 5811572
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R Turell. 1969. Does electrocoagulation supplant resection?. https://doi.org/10.1016/0002-9610(69)90147-0
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The molecular mechanism(s) for prostate cancer progression to androgen independence are poorly understood. We have recently shown that Foxa1 and Foxa2 proteins are differentially expressed in epithelial cells during murine prostate development, growth, and adult function. Currently, the role of Foxa proteins in prostate cancer development and progression is unknown. Foxa protein expression was investigated in the LPB-Tag LADY mouse prostate cancer models, in human prostate cancer specimens, and various prostate cancer cell lines using Western blot and immunostaining analysis. In vitro transient transfection, studies were performed to investigate Foxa/prostate-specific gene regulation. Foxa1 was strongly expressed in areas of prostatic intraepithelial neoplasia (PIN) in both the androgen dependent 12T-7f and in the metastatic, androgen independent 12T-10 LADY models. Prominent Foxa1 and Foxa2 expression was observed in 12T-10 invasive undifferentiated neuroendocrine carcinomas, in the hormone independent and metastasizing 12T-10 derived, NE-10 allograft tumors, and in all metastatic lesions isolated from 12T-10 mice. Foxa1 protein expression was always observed in human prostate carcinomas, regardless of Gleason grade score, while Foxa2 was only detected in neuroendocrine small cell carcinomas and in some high Gleason score adenocarcinomas. Foxa proteins were also differentially expressed in three prostate cancer cell lines. Importantly, in vitro functional assays demonstrated that Foxa2 could activate androgen-dependent prostate-specific genes in an androgen receptor and ligand-independent manner. These results suggest that Foxa proteins are important in prostate carcinogenesis. In particular, Foxa2 may be involved in progression of prostate cancer to androgen independence. As such, Foxa proteins may represent novel targets for therapeutic intervention.
There has been some recent work in the statistical literature for modelling the relationship between tumour biology properties and tumour progression in screening trials. While non-parametric methods have been proposed for estimation of the tumour size distribution at which metastatic transition occurs, their asymptotic properties have not been studied. In addition, no testing or regression methods are available so that potential confounders and prognostic factors can be adjusted for. We develop a unified approach to non-parametric and semi-parametric analysis of modelling tumour size-metastasis data in this article. An association between the models considered by previous authors with survival data structures is discussed. Based on this relationship, we develop non-parametric testing procedures and semi-parametric regression methodology of modelling the effect of size of tumour on the probability at which metastatic transitions occur in two situations. Asymptotic properties of these estimators are provided. The proposed methodology is applied to data from a screening study in lung cancer.
We have examined the effects of natural polysaccharides isolated from Phellinus gilvus (PG) in vitro and in vivo against gastric cancer. PG decreased cell proliferation and increased cell apoptosis in a dose-dependent manner in vitro. PG also led to a marked inhibition of tumor growth and significant decrease in the incidence of peritoneal carcinomatosis. Histological analysis of tumor confirmed dramatic increase in tumor cell apoptosis by PG, indicating reduced tumor cell proliferation. These data showed that polysaccharides isolated from PG significantly inhibited tumor growth and metastasis in an orthotopic model of human gastric adenocarcinoma, without detectable problematic adverse effects.