Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Localized prostate cancer (CaP) can be cured using several strategies. However, the need to identify active substances in advanced tumor stages is tremendous, as the outcome in such cases is still disappointing. One approach is to deliver human tumor antigen-targeted therapy, which is recognized by T cells or antibodies. We used data mining of the Cancer Immunome Database (CID), which comprises potential immunologic targets identified by serological screening of expression libraries. Candidate antigens were screened by DNA microarrays. Genes were then validated at the protein level by tissue microarrays, representing various stages of CaP disease. Of 43 targets identified by CID, 10 showed an overexpression on the complementary DNA array in CaP metastases. The RHAMM (CD168) gene, earlier identified by our group as an immunogenic antigen in acute and chronic leukemia, also showed highly significant overexpression in CaP metastases compared with localized disease and benign prostatic hyperplasia. At the protein level, RHAMM was highest in metastatic tissue samples and significantly higher in neoplastic localized disease compared with benign tissue. High RHAMM expression was associated with clinical parameters known to be linked to better clinical outcome. Patients with high RHAMM expression in the primaries had a significantly lower risk of biochemical failure. The number of viable cells in cell cultures was reduced in blocking experiments using hormone-sensitive and hormone-insensitive metastatic CaP cell lines. Acknowledging the proven immunogenic effects of RHAMM in leukemia, this antigen is intriguing as a therapeutic target in far-advanced CaP.
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PMID:RHAMM (CD168) is overexpressed at the protein level and may constitute an immunogenic antigen in advanced prostate cancer disease. 1972 89

CYP3A5 is a cytochrome P450 superfamily member which is involved in the metabolism of drugs, steroid hormones, and other xenobiotics. Emerging evidences suggest that CYP3A5*3 (rs776746 A>G) polymorphism may play a role in the etiology of carcinogenesis and affect an individual's susceptibility to cancer in humans, but individually published studies showed inconclusive results. This meta-analysis aimed to derive a more accurate estimation of the correlation between CYP3A5*3 polymorphism and cancer risk. A literature search of PubMed, Embase, Web of Science, and China BioMedicine databases was conducted on articles published before January 1, 2013. Seventeen case-control studies were included with a total of 7,458 cancer patients and 7,166 healthy controls. The meta-analysis results showed that CYP3A5*3 polymorphism may increase the risk of cancer, especially in acute leukemia, chronic leukemia, and colorectal cancer. However, no statistically significant associations were found in prostate cancer, liver cancer, and other cancers. Further subgroup analysis by ethnicity indicated that CYP3A5*3 polymorphism was associated with an increased risk of cancer among Asian and Caucasian populations, but not among African populations. In conclusion, the current meta-analysis suggests that CYP3A5*3 polymorphism may play an important role in the development of acute and chronic leukemia and colorectal cancer, especially among Asian and Caucasian populations.
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PMID:CYP3A5*3 polymorphism and cancer risk: a meta-analysis and meta-regression. 2358 98