We shortlist and discuss the most significant over-expressed genes in prostate cancer and PIN, and highlight expression differences between malignant and benign samples.
This group of high-risk patients includes men with a family history of prostate cancer and various histologic features such as PIN and ASAP identified on an initial biopsy.
Prolonged treatment of adult rodents with estrogens along with androgens also leads to epithelial metaplasia, PIN-like lesions and even adenocarcinoma of prostate speaking for the role of estrogen in prostate cancer development.
Statistically significant differential SCD expression between normal and cancerous epithelium was determined at the p=0.001 level, and between PIN and prostate carcinoma at the p=0.03 level.
Strong immunostaining for CRISP-3 is common in HG-PIN and preserved in most PCa specimens, which warrant further immunohistochemical studies of CRISP-3 in PCa.
No association was found for correlation of PCA3 score change with age >65 years (p=0.975), family history of prostate cancer (p=0.796), positive DRE (p=0.179), use of 5-alpha-reductase inhibitors (p=0.793) and BPH/prostatitis/HG-PIN/ASAP diagnosis (p=0.428).
The prostate-specific G-protein coupled receptor (PSGR, or OR51E2) is an olfactory receptor family member with highly specific expression in human prostate epithelium that is highly overexpressed in PIN and prostate cancer.
We are interested in understanding the inhibitory mechanism of metformin on tumor-associated inflammation in prostate cancer.<b>Experimental Design:</b> By using a transgenic adenocarcinoma of the mouse prostate (TRAMP) mouse model, <i>in vitro</i> macrophage migration assays, and patient samples, we examined the effect of metformin on tumor-associated inflammation during the initiation and after androgen deprivation therapy of prostate cancer.<b>Results:</b> Treating TRAMP mice with metformin delays prostate cancer progression from low-grade prostatic intraepithelial neoplasia to high-grade PIN, undifferentiated to well-differentiated, and PIN to adenocarcinoma with concurrent inhibition of inflammatory infiltration evidenced by reduced recruitment of macrophages.