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)

The p53 gene is known to be one of the frequently altered tumor suppressor genes, involved in the oncogenesis of a wide spectrum of human malignant tumors. We investigated mutational events of the p53 gene in 18 clinically untreated prostate cancers. Direct sequencing analysis demonstrated that 1 of 18 cases harbored point mutation in the highly conserved transcript region. The case showed CAT at codon 273 instead of wild-type CGT, substituting the encoded amino acid form histidine to arginine. The case had previously revealed homozygous loci on 17p, including the p53 locus, by restriction fragment length polymorphism analysis. The other 17 cases harbored neither mutation nor small deletion. It is concluded that point mutation of the p53 gene is a infrequent event in the oncogenesis of untreated prostate cancer.
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PMID:Point mutation of the p53 gene is an infrequent event in untreated prostate cancer. 876 16

Hydrogen sulfide (H2S) was originally considered toxic at elevated levels; however just in the past decade H2S has been proposed to be an important gasotransmitter with various physiological and pathophysiological roles in the body. H2S can be generated endogenously from L-cysteine by multiple enzymes, including cystathionine gamma-lyase, cystathionine beta-synthase, and 3-mercaptopyruvate sulfurtransferase in combination with cysteine aminotransferase. Prostate cancer is a major health concern and no effective treatment for prostate cancers is available. H2S has been shown to inhibit cell survival of androgen-independent, androgen-dependent, and antiandrogen-resistant prostate cancer cells through different mechanisms. Various H2S-releasing compounds, including sulfide salts, diallyl disulfide, diallyl trisulfide, sulforaphane, and other polysulfides, also have been shown to inhibit prostate cancer growth and metastasis. The expression of H2S-producing enzyme was reduced in both human prostate cancer tissues and prostate cancer cells. Androgen receptor (AR) signaling is indispensable for the development of castration resistant prostate cancer, and H2S was shown to inhibit AR transactivation and contributes to antiandrogen-resistant status. In this review, we summarized the current knowledge of H2S signaling in prostate cancer and described the molecular alterations, which may bring this gasotransmitter into the clinic in the near future for developing novel pharmacological and therapeutic interventions for prostate cancer.
Prostate Cancer 2016
PMID:Hydrogen Sulfide Signaling Axis as a Target for Prostate Cancer Therapeutics. 2701 51