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AttributesValues
rdf:type
rdfs:label
  • Prostate Cancer Pathway
rdfs:subClassOf
Semantic_Type
  • Functional Concept
Preferred_Name
  • Prostate Cancer Pathway
UMLS_CUI
  • C2984325
KEGG_ID
  • hsa05215
ALT_DEFINITION
  • The identification of key molecular alterations in prostate-cancer cells implicates carcinogen defenses (GSTP1), growth-factor-signaling pathways (NKX3.1, PTEN, and p27), and androgens (AR) as critical determinants of the phenotype of prostate-cancer cells. Glutathione S-transferases (GSTP1) are detoxifying enzymes that catalyze conjunction of glutathione with harmful, electrophilic molecules, thereby protecting cells from carcinogenic factors. Cells of prostatic intraepithelial neoplasia, devoid of GSTP1, undergo genomic damage mediated by such carcinogens. NKX3.1, PTEN, and p27 regulate the growth and survival of prostate cells in the normal prostate. Inadequate levels of PTEN and NKX3.1 lead to a reduction in p27 levels and to increased proliferation and decreased apoptosis. After therapeutic reduction in the levels of testosterone and dihydrotestosterone, the emergence of androgen-independent prostate cancer has been associated with mutations in the androgen receptor (AR) that permit receptor activation by other ligands, increased expression of androgen receptors accompanying AR amplification, and ligand-independent androgen-receptor activation.KEGG
FULL_SYN
  • Prostate Cancer PathwayPTNCI
  • Prostate cancerPTKEGG
code
  • C91517
is someValuesFrom of
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