NOMENCLATURE OF Genes in Prostate cancers    
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The CRBCM does not have a significant laboratory. fOR ANY RESEARCH WORK, we have to contract with our local university (UTEP) and we intend to do so.  The gene discussed here in are easily found in the literature  What we bring to the discussion is our unique perspective that most of the time is still to be proven but appears sound based on available evidence.  We provide this opinion anyway in order to tease researchers around the world to prove us wrong or right.  We do not make up stuff.  We offer an interpretation of facts.   When you look at the genes involved in the pathogenesis of Prostate cancer

1. HPC1.
controversy has marred this one but it is found in several familial Prostate cancer.  Some has advocated this gene as a screening tool for familial Prostate cancer.  Clearly it is not the only one! 

"RNase L is now implicated in protecting the central nervous system against viral-induced demyelination. A role in tumor suppression was inferred by mapping of the RNase L gene to the hereditary prostate cancer 1 (HPC1) gene,
It encodes a ribonuclease that mediates the antiviral and apoptotic activities of interferons." (wikipedia)

2.CAPB

 "Perlecan is a proteoglycan that regulates extracellular and stromal accessibility to growth factors such as SHH, thus allowing for the maintenance of SHH signaling under growth factor limiting conditions. This proteoglycan represents an important central regulator of SHH activity and presents an ideal drug target for blocking SHH effects."
This open the door to use of anti Hedgehog agent such as the one used in Basal cell skin cancer in the treatment of prostate cancer!?

3.BRCA 1,2

" The protein encoded by the BRCA1 gene combines with other tumor suppressors, DNA damage sensors, and signal transducers to form a large multi-subunit protein complex known as the BRCA1-associated genome surveillance complex (BASC).^[9] The BRCA1 protein associates with RNA polymerase II, and through the C-terminal domain, also interacts with histone deacetylase complexes. Thus, this protein plays a role in transcription, DNA repair of double-stranded breaks^[8] ubiquitination, transcriptional regulation as well as other functions.^[10]The BARD1/BRCA1 interaction is disrupted by tumorigenic amino acid substitutions in BRCA1, implying that the formation of a stable complex between these proteins may be an essential aspect of BRCA1 tumor suppression.^[19] The ring domain is an important element of ubiquitin E3 ligases which catalyse protein ubiquitination2. Ubiquitin is a small regulatory protein

  BRCA1 interacts with the NELF-B (COBRA1) subunit of the NELF complex.^[29]

  the BRCA1 protein interacts with RAD51 during repair of DNA double-strand breaks.[26
Wikipedia and related sources
sources have reported that one form of aggressive prostate cancer was characterized by Mutated BRCA2.
DOES THIS OPEN THE DOOR TO PLATINUM AS THE ANSWER TO THESE TYPE OF CANCERS LIKE IN BREAST CANCER?


^{4. Androgen Receptor genes}

"The androgen receptor (AR), also known as NR3C4 (nuclear receptor subfamily 3, group C, member 4), is a type of nuclear receptor^[6] that is activated by binding of either of the androgenic hormones testosterone or dihydrotestosterone ^[7] in the cytoplasm and then translocating into the nucleus. The androgen receptor is most closely related to the progesterone receptor, and progestins in higher dosages can block the androgen receptor.^[8][9]
The main function of the androgen receptor is as a DNA-binding transcription factor that regulates gene expression;^[10] however, the androgen receptor has other functions as well.^[11] Androgen regulated genes are critical for the development and maintenance of the male sexual phenotype.

testosterone is converted by 5-alpha-reductase to dihydrotestosterone, an even more potent agonist for androgen receptor activation.^[12]

  normal male sexual development
 receptors allow the body to respond appropriately to these hormones." WIKIPEDIA AND RELATED SOURCE

ANDROGEN DEPRIVATION IS OF COURSE THE MAIN SOURCE.  REFRACTORINESS IS SEEN IN ADVANCED CANCER WITH ASSOCIATED MUTATIONS TO THE AR  GENE.  BYPASSING THE RECEPTOR AND ACTING ON THE SUBSTRATE OF THESE RECEPTOR IS BEING LOOKED AT.  FOR THE AR TO WORK IT HAS TO BE TRANSFERRED TO THE NUCLEUS,  CYTOPLASMIC MISLOCATION OF THESE AR IS BEING LOOKED AT AS A WAY TO IMPROVE ON ANTI ANDROGEN  (HERE GNB2L1 IS A TARGET)

GOOD CONTROVERSY
 " a DNA segment known as CAG is repeated multiple times. This CAG segment is called a triplet or trinucleotide repeat. In most people, the number of CAG repeats in the AR gene ranges from fewer than 10 to about 36.Researchers have considered a possible relationship between the length of the CAG repeat region in the AR gene and a woman's chance of developing breast cancer. The results of research studies have been mixed. Some studies have suggested that a long CAG repeat region is associated with an increased risk of breast cancer in women,
 Some studies have shown an increased risk of prostate cancer in men with a short CAG repeat region in the AR gene;

Transcriptional activity is enhanced by binding to RANBP9.
The level of tyrosine phosphorylation may serve as a diagnostic tool to predict patient outcome in response to hormone-ablation therapy. Inhibition of tyrosine phosphorylation may be an effective intervention target for hormone-refractory prostate cancer."

PLENTY OF TARGETS!!!

(SIMILARITY FOR AR )  Belongs to the nuclear hormone receptor family. NR3 subfamily.
Contains 1 nuclear receptor DNA-binding domain.
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Related AND UNDER THE THUMBS OF THE AR gene are the TMPRSS-ERG, and ETS,ETV1,  TMPRSS-ERG fusion  (WE DISCUSSED THESE EARLIER)

5.ELAC2
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6. ERG
7.PSA:  strategy here is to use this prominent protein to selectively deliver a powerful chemotherapy drug like in the T-DM1 experience
8.chrXq27.3
9.PCAP
10.MRS1
11.GALACTIN-1
12.SNP
13TGFB1
15NCOA1
16HIPK3
17ZIPK/DAPK3
18GNB2L1
19EFCAB6/DJBP
20NR0B2 AND PELP1

Underclinical investigation you find more the HER-2, Bcl-2, VEGF, Endothelin receptor gene, and the PSA

(several quotes are left intact here to tell you we don't make this stuff up!)