Prostate Cancer- Molecular Biology

Overview

Prostate cancer is the most common malignancy found in men, incidence is highest among American Blacks and lowest in East Asian populations. Prostate specific Antigen (PSA) is an important marker in the diagnosis and monitoring of prostate cancer, and the percentage free PSA has been shown to have prognostic significance in some studies.

Androgens, which exert their effects via the androgen receptor (AR), are essential for the normal prostate. They are also required by prostate cancer cells. Therefore, androgen ablation and antiandrogen therapy are important in the treatment of the disease, though most patients go on to develop androgen-independent prostate cancer. Androgen receptor mutations are observed in late stage prostate cancer.

Caveolin-1 is overexpressed in about a quarter of human prostate cancers (Yang, 1999) . Caveolin expression is thought to induce androgen sensitivity in androgen-insensitive prostate cancer cells.

Mutations in a diverse range of other genes have been implicated in prostate cancer including PTEN, KAI1, SRD5A2, and IL6. Most of these relate to disease progression.

Hereditary prostate cancer accounts for about 9% of cases. A prostate cancer susceptibility locus (HPC1) on chromosome 1q24-25 was identified by Smith (1996). However, subsequent studies suggest that mutations in HPC1 are uncommon and are restricted to people with early onset disease. A second gene (HPC2 on chromosome 1q42.2-q43 was proposed by Berthon (1998), though again subsequent linkage studies indicate this gene could only account for a small proportion of cases. Other specific gene(s) associated with hereditary prostate cancer have yet to be identified.

See also: Prostate Cancer - clinical resources (38)

Literature Analysis

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Tag cloud generated 10 March, 2017 using data from PubMed, MeSH and CancerIndex

Mutated Genes and Abnormal Protein Expression (570)

How to use this data tableClicking on the Gene or Topic will take you to a separate more detailed page. Sort this list by clicking on a column heading e.g. 'Gene' or 'Topic'.

GeneLocationAliasesNotesTopicPapers
KLK3 19q13.41 APS, PSA, hK3, KLK2A1 Overexpression
-PSA expression in Prostate Cancer
3000
AR Xq12 KD, AIS, AR8, TFM, DHTR, SBMA, HYSP1, NR3C4, SMAX1, HUMARA -AR and Prostate Cancer
1288
PTEN 10q23.31 BZS, DEC, CWS1, GLM2, MHAM, TEP1, MMAC1, PTEN1, 10q23del -PTEN and Prostate Cancer
497
MKI67 10q26.2 KIA, MIB-, MIB-1, PPP1R105 -MKI67 and Prostate Cancer
424
TMPRSS2 21q22.3 PP9284, PRSS10 Intronic Deletion or Translocation
-ERG-TMPRSS2 Fusion in Prostate Cancer
-ETV1 translocations in Prostate Cancer
-TMPRSS2 and Prostate Cancer
336
CTNNB1 3p22.1 CTNNB, MRD19, armadillo -CTNNB1 and Prostate Cancer
371
TP53 17p13.1 P53, BCC7, LFS1, TRP53 -TP53 and Prostate Cancer
370
BRCA1 17q21.31 IRIS, PSCP, BRCAI, BRCC1, FANCS, PNCA4, RNF53, BROVCA1, PPP1R53 -BRCA1 and Prostate Cancer
210
BRCA2 13q13.1 FAD, FACD, FAD1, GLM3, BRCC2, FANCD, PNCA2, FANCD1, XRCC11, BROVCA2 -BRCA2 and Prostate Cancer
198
PROC 2q13-q14 PC, APC, PROC1, THPH3, THPH4 -PROC and Prostate Cancer
135
CDKN1A 6p21.2 P21, CIP1, SDI1, WAF1, CAP20, CDKN1, MDA-6, p21CIP1 -CDKN1A Expression in Prostate Cancer
125
NKX3-1 8p21.2 NKX3, BAPX2, NKX3A, NKX3.1 -NKX3-1 and Prostate Cancer
122
SRD5A2 2p23 -SRD5A2 and Prostate Cancer
120
SRC 20q12-q13 ASV, SRC1, c-SRC, p60-Src -SRC and Prostate Cancer
103
CD44 11p13 IN, LHR, MC56, MDU2, MDU3, MIC4, Pgp1, CDW44, CSPG8, HCELL, HUTCH-I, ECMR-III -CD44 and Prostate Cancer
102
KITLG 12q22 SF, MGF, SCF, FPH2, FPHH, KL-1, Kitl, SHEP7 -KITLG and Prostate Cancer
96
CDKN1B 12p13.1-p12 KIP1, MEN4, CDKN4, MEN1B, P27KIP1 -CDKN1B and Prostate Cancer
92
TGFB1 19q13.1 CED, LAP, DPD1, TGFB, TGFbeta -TGFB1 and Prostate Cancer
83
HIF1A 14q23.2 HIF1, MOP1, PASD8, HIF-1A, bHLHe78, HIF-1alpha, HIF1-ALPHA -HIF1A and Prostate Cancer
83
EZH2 7q35-q36 WVS, ENX1, EZH1, KMT6, WVS2, ENX-1, EZH2b, KMT6A -EZH2 and Prostate Cancer
82
CYP17A1 10q24.3 CPT7, CYP17, S17AH, P450C17 -CYP17A1 and Prostate Cancer
82
PTGS2 1q25.2-q25.3 COX2, COX-2, PHS-2, PGG/HS, PGHS-2, hCox-2, GRIPGHS -PTGS2 (COX2) and Prostate Cancer
81
PPARG 3p25 GLM1, CIMT1, NR1C3, PPARG1, PPARG2, PPARgamma -PPARG and Prostate Cancer
81
PCA3 9q21.2 DD3, PCAT3, NCRNA00019 -PCA3 and Prostate Cancer
78
IGFBP3 7p12.3 IBP3, BP-53 -IGFBP3 and Prostate Cancer
77
GSTM1 1p13.3 MU, H-B, GST1, GTH4, GTM1, MU-1, GSTM1-1, GSTM1a-1a, GSTM1b-1b -GSTM1 and Prostate Cancer
77
ETV1 7p21.3 ER81 Translocation
-ETV1 translocations in Prostate Cancer
73
MSMB 10q11.2 MSP, PSP, IGBF, MSPB, PN44, PRPS, HPC13, PSP57, PSP94, PSP-94 -MSMB and Prostate Cancer
-Prostate cancer susceptibility variant (MSMB) rs10993994
45
JUN 1p32-p31 AP1, AP-1, c-Jun -c-Jun and Prostate Cancer
65
CAMP 3p21.3 LL37, CAP18, CRAMP, HSD26, CAP-18, FALL39, FALL-39 -CAMP and Prostate Cancer
61
ELAC2 17p11.2 ELC2, HPC2, COXPD17 -ELAC2 and Prostate Cancer
56
SERPINB5 18q21.33 PI5, maspin -SERPIN-B5 and Prostate Cancer
54
AMACR 5p13 RM, RACE, CBAS4, AMACRD -AMACR and Prostate Cancer
50
CD82 11p11.2 R2, 4F9, C33, IA4, ST6, GR15, KAI1, SAR2, TSPAN27 -CD82 and Prostate Cancer
50
IGF1R 15q26.3 IGFR, CD221, IGFIR, JTK13 -IGF1R and Prostate Cancer
49
IL10 1q31-q32 CSIF, TGIF, GVHDS, IL-10, IL10A -Interleukin-10 and Prostate Cancer
48
E2F1 20q11.2 RBP3, E2F-1, RBAP1, RBBP3 -E2F1 and Prostate Cancer
46
TRPM2 21q22.3 KNP3, EREG1, TRPC7, LTRPC2, NUDT9H, NUDT9L1 -TRPM2 and Prostate Cancer
46
KLK2 19q13.41 hK2, hGK-1, KLK2A2 -KLK2 and Prostate Cancer
45
FOXA1 14q21.1 HNF3A, TCF3A -FOXA1 and Prostate Cancer
44
FOS 14q24.3 p55, AP-1, C-FOS -FOS and Prostate Cancer
43
CYP3A4 7q21.1 HLP, CP33, CP34, CYP3A, NF-25, CYP3A3, P450C3, CYPIIIA3, CYPIIIA4, P450PCN1 -CYP3A4 and Prostate Cancer
43
CLU 8p21-p12 CLI, AAG4, APOJ, CLU1, CLU2, KUB1, SGP2, APO-J, SGP-2, SP-40, TRPM2, TRPM-2, NA1/NA2 -CLU and Prostate Cancer
43
PSCA 8q24.2 PRO232 -PSCA and Prostate Cancer
42
CASP9 1p36.21 MCH6, APAF3, APAF-3, PPP1R56, ICE-LAP6 -CASP9 and Prostate Cancer
41
VEGFA 6p12 VPF, VEGF, MVCD1 -VEGFA and Prostate Cancer
40
RELA 11q13.1 p65, NFKB3 -RELA and Prostate Cancer
40
MET 7q31 HGFR, AUTS9, RCCP2, c-Met -C-MET and Prostate Cancer
40
RASSF1 3p21.3 123F2, RDA32, NORE2A, RASSF1A, REH3P21 -RASSF1 and Prostate Cancer
39
CYP3A5 7q21.1 CP35, PCN3, CYPIIIA5, P450PCN3 -CYP3A5 and Prostate Cancer
39
PDLIM4 5q31.1 RIL -PDLIM4 and Prostate Cancer
38
MSR1 8p22 SRA, SR-A, CD204, phSR1, phSR2, SCARA1 -MSR1 and Prostate Cancer
38
ETV4 17q21.31 E1AF, PEA3, E1A-F, PEAS3 -ETV4 and Prostate Cancer
34
FGF2 4q26 BFGF, FGFB, FGF-2, HBGF-2 -FGF2 and Prostate Cancer
34
CAPS 19p13.3 CAPS1 -CAPS and Prostate Cancer
34
EGR1 5q31.1 TIS8, AT225, G0S30, NGFI-A, ZNF225, KROX-24, ZIF-268 -EGR1 and Prostate Cancer
34
CXCR4 2q21 FB22, HM89, LAP3, LCR1, NPYR, WHIM, CD184, LAP-3, LESTR, NPY3R, NPYRL, WHIMS, HSY3RR, NPYY3R, D2S201E -CXCR4 and Prostate Cancer
33
CHEK2 22q12.1 CDS1, CHK2, LFS2, RAD53, hCds1, HuCds1, PP1425 -CHEK2 and Prostate Cancer
30
TNFRSF11A 18q22.1 FEO, OFE, ODFR, OSTS, PDB2, RANK, CD265, OPTB7, TRANCER, LOH18CR1 -TNFRSF11A and Prostate Cancer
30
SHBG 17p13.1 ABP, SBP, TEBG -SHBG and Prostate Cancer
30
IL6 7p21 HGF, HSF, BSF2, IL-6, IFNB2 -IL6 and Prostate Cancer
29
XRCC1 19q13.2 RCC -XRCC1 and Prostate Cancer
29
ESR1 6q25.1 ER, ESR, Era, ESRA, ESTRR, NR3A1 -ESR1 and Prostate Cancer
27
CAV1 7q31.1 CGL3, PPH3, BSCL3, LCCNS, VIP21, MSTP085 -CAV1 and Prostate Cancer
27
ERBB2 17q12 NEU, NGL, HER2, TKR1, CD340, HER-2, MLN 19, HER-2/neu -ERBB2 and Prostate Cancer
27
HGF 7q21.1 SF, HGFB, HPTA, F-TCF, DFNB39 -HGF and Prostate Cancer
26
ITGB1 10p11.2 CD29, FNRB, MDF2, VLAB, GPIIA, MSK12, VLA-BETA -ITGB1 (CD29) and Prostate Cancer
25
CYP24A1 20q13 CP24, HCAI, CYP24, P450-CC24 -CYP24A1 and Prostate Cancer
24
KLF6 10p15 GBF, ZF9, BCD1, CBA1, CPBP, PAC1, ST12, COPEB -KLF6 and Prostate Cancer
24
NANOG 12p13.31 -NANOG and Prostate Cancer
23
GDF15 19p13.11 PDF, MIC1, PLAB, MIC-1, NAG-1, PTGFB, GDF-15 -GDF15 and Prostate Cancer
22
TLR4 9q33.1 TOLL, CD284, TLR-4, ARMD10 -TLR4 and Prostate Cancer
22
RUNX2 6p21 CCD, AML3, CCD1, CLCD, OSF2, CBFA1, OSF-2, PEA2aA, PEBP2aA, CBF-alpha-1 -RUNX2 and Prostate Cancer
22
HPCX Xq27-q28 -HPCX and Prostate Cancer
22
SLC45A3 1q32.1 PRST, IPCA6, IPCA-2, IPCA-6, IPCA-8, PCANAP2, PCANAP6, PCANAP8 -SLC45A3 and Prostate Cancer
22
HNF1B 17q12 FJHN, HNF2, LFB3, TCF2, HPC11, LF-B3, MODY5, TCF-2, VHNF1, HNF-1B, HNF1beta, HNF-1-beta -HNF1B and Prostate Cancer
21
CYP27B1 12q14.1 VDR, CP2B, CYP1, PDDR, VDD1, VDDR, VDDRI, CYP27B, P450c1, CYP1alpha -CYP27B1 and Prostate Cancer
21
TNFSF11 13q14 ODF, OPGL, sOdf, CD254, OPTB2, RANKL, TRANCE, hRANKL2 -TNFSF11 and Prostate Cancer
21
TNFRSF10B 8p22-p21 DR5, CD262, KILLER, TRICK2, TRICKB, ZTNFR9, TRAILR2, TRICK2A, TRICK2B, TRAIL-R2, KILLER/DR5 -TNFRSF10B and Prostate Cancer
21
SKP2 5p13 p45, FBL1, FLB1, FBXL1 -SKP2 and Prostate Cancer
20
UGT2B17 4q13 BMND12, UDPGT2B17 -UGT2B17 and Prostate Cancer
19
IKBKB 8p11.2 IKK2, IKKB, IMD15, NFKBIKB, IKK-beta -IKBKB and Prostate Cancer
19
LOX 5q23.2 -LOX and Prostate Cancer
19
NCOA4 10q11.2 RFG, ELE1, PTC3, ARA70 -NCOA4 and Prostate Cancer
19
NDRG1 8q24.3 GC4, RTP, DRG1, NDR1, NMSL, TDD5, CAP43, CMT4D, DRG-1, HMSNL, RIT42, TARG1, PROXY1 -NDRG1 and Prostate Cancer
19
TTPA 8q12.3 ATTP, AVED, TTP1, alphaTTP -TTPA and Prostate Cancer
18
GPX1 3p21.3 GPXD, GSHPX1 -GPX1 and Prostate Cancer
18
SOD2 6q25.3 IPOB, MNSOD, MVCD6 -SOD2 and Prostate Cancer
18
FGF8 10q24 HH6, AIGF, KAL6, FGF-8, HBGF-8 -FGF8 and Prostate Cancer
18
TRPM8 2q37.1 TRPP8, LTRPC6 -TRPM8 and Prostate Cancer
18
UGT2B15 4q13 HLUG4, UGT2B8, UDPGTH3, UDPGT 2B8, UDPGT2B15 -UGT2B15 and Prostate Cancer
17
SPINK1 5q32 TCP, PCTT, PSTI, TATI, Spink3 -SPINK1 and Prostate Cancer
17
SLC2A1 1p34.2 PED, DYT9, GLUT, DYT17, DYT18, EIG12, GLUT1, HTLVR, GLUT-1, GLUT1DS -GLUT1 expression in Prostate Cancer
17
TIMP2 17q25 DDC8, CSC-21K -TIMP2 and Prostate Cancer
17
SOX9 17q24.3 CMD1, SRA1, CMPD1, SRXX2, SRXY10 -SOX9 and Prostate Cancer
17
PIM1 6p21.2 PIM -PIM1 and Prostate Cancer
17
CCL2 17q11.2-q12 HC11, MCAF, MCP1, MCP-1, SCYA2, GDCF-2, SMC-CF, HSMCR30 -CCL2 and Prostate Cancer
16
MCAM 11q23.3 CD146, MUC18 -MCAM and Prostate Cancer
16
TNFRSF11B 8q24 OPG, TR1, OCIF -TNFRSF11B and Prostate Cancer
16
NCOA2 8q13.3 SRC2, TIF2, GRIP1, KAT13C, NCoA-2, bHLHe75 -NCOA2 and Prostate Cancer
16
ETV5 3q28 ERM -ETV5 and Prostate Cancer
15
SIRT1 10q21.3 SIR2, hSIR2, SIR2L1 -SIRT1 and Prostate Cancer
15
CCK 3p22.1 -CCK and Prostate Cancer
15
JUND 19p13.2 AP-1 -JUND and Prostate Cancer
15
FLCN 17p11.2 BHD, FLCL -FLCN and Prostate Cancer
15
FASN 17q25 FAS, OA-519, SDR27X1 -FASN and Prostate Cancer
14
HSD17B2 16q24.1-q24.2 HSD17, SDR9C2, EDH17B2 -HSD17B2 and Prostate Cancer
14
VEGFC 4q34.3 VRP, Flt4-L, LMPH1D -VEGFC and Prostate Cancer
14
GADD45A 1p31.2 DDIT1, GADD45 -GADD45A and Prostate Cancer
14
AKR1C3 10p15-p14 DD3, DDX, PGFS, HAKRB, HAKRe, HA1753, HSD17B5, hluPGFS -AKR1C3 and Prostate Cancer
14
EDNRB 13q22 ETB, ET-B, ETB1, ETBR, ETRB, HSCR, WS4A, ABCDS, ET-BR, HSCR2 -EDNRB and Prostate Cancer
13
COMT 22q11.21 HEL-S-98n -COMT and Prostate Cancer
13
PITX2 4q25 RS, RGS, ARP1, Brx1, IDG2, IGDS, IHG2, PTX2, RIEG, IGDS2, IRID2, Otlx2, RIEG1 -PITX2 and Prostate Cancer
13
NOS3 7q36 eNOS, ECNOS -NOS3 and Prostate Cancer
13
SRD5A1 5p15 S5AR 1 -SRD5A1 and Prostate Cancer
13
KLK4 19q13.41 ARM1, EMSP, PSTS, AI2A1, EMSP1, KLK-L1, PRSS17, kallikrein -KLK4 and Prostate Cancer
13
SPDEF 6p21.3 PDEF, bA375E1.3 -SPDEF and Prostate Cancer
13
IGFBP2 2q35 IBP2, IGF-BP53 -IGFBP2 and Prostate Cancer
13
RFX6 6q22.1 MTFS, MTCHRS, RFXDC1, dJ955L16.1 -rs339331 Polymorphism and Prostate Cancer susceptibility
-RFX6 and Prostate Cancer
6
DKK3 11p15.3 RIG, REIC -DKK3 and Prostate Cancer
12
SREBF1 17p11.2 SREBP1, bHLHd1, SREBP-1c -SREBF1 and Prostate Cancer
12
RARB 3p24.2 HAP, RRB2, NR1B2, MCOPS12 -RARB and Prostate Cancer
12
AGR2 7p21.3 AG2, GOB-4, HAG-2, XAG-2, PDIA17, HEL-S-116 -AGR2 and Prostate Cancer
12
HSPB1 7q11.23 CMT2F, HMN2B, HSP27, HSP28, Hsp25, SRP27, HS.76067, HEL-S-102 -HSPB1 and Prostate Cancer
12
CD24 6q21 CD24A -CD24 and Prostate Cancer
12
MXI1 10q24-q25 MXI, MAD2, MXD2, bHLHc11 -MXI1 and Prostate Cancer
12
HSD3B2 1p13.1 HSDB, HSD3B, SDR11E2 -HSD3B2 and Prostate Cancer
11
STAT5A 17q11.2 MGF, STAT5 -STAT5A and Prostate Cancer
11
PTER 10p12 HPHRP, RPR-1 -PTER and Prostate Cancer
11
FGFR4 5q35.2 TKF, JTK2, CD334 -FGFR4 and Prostate Cancer
11
E2F3 6p22 E2F-3 -E2F3 and Prostate Cancer
11
EPHB2 1p36.1-p35 DRT, EK5, ERK, CAPB, Hek5, PCBC, EPHT3, Tyro5 -EPHB2 and Prostate Cancer
11
DAB2IP 9q33.1-q33.3 AIP1, AIP-1, AF9Q34, DIP1/2 -DAB2IP and Prostate Cancer
11
CRP 1q23.2 PTX1 -CRP and Prostate Cancer
11
ELK1 Xp11.2 -ELK1 and Prostate Cancer
11
HMOX1 22q13.1 HO-1, HSP32, HMOX1D, bK286B10 -HMOX1 and Prostate Cancer
11
JAZF1 7p15.2-p15.1 TIP27, ZNF802 -JAZF1 and Prostate Cancer
11
CTNNA1 5q31.2 CAP102 -CTNNA1 and Prostate Cancer
11
NCOA1 2p23 SRC1, KAT13A, RIP160, F-SRC-1, bHLHe42, bHLHe74 -NCOA1 and Prostate Cancer
11
FGF1 5q31 AFGF, ECGF, FGFA, ECGFA, ECGFB, FGF-1, HBGF1, HBGF-1, GLIO703, ECGF-beta, FGF-alpha -FGF1 and Prostate Cancer
11
CASP1 11q22.3 ICE, P45, IL1BC -CASP1 and Prostate Cancer
11
RECK 9p13.3 ST15 -RECK and Prostate Cancer
11
WNT5A 3p21-p14 hWNT5A -WNT5A and Prostate Cancer
10
GPX3 5q33.1 GPx-P, GSHPx-3, GSHPx-P -GPX3 and Prostate Cancer
10
SMAD1 4q31 BSP1, JV41, BSP-1, JV4-1, MADH1, MADR1 -SMAD1 and Prostate Cancer
10
NBN 8q21 ATV, NBS, P95, NBS1, AT-V1, AT-V2 -NBN and Prostate Cancer
10
MBD2 18q21 DMTase, NY-CO-41 -MBD2 and Prostate Cancer
10
ANXA2 15q22.2 P36, ANX2, LIP2, LPC2, CAL1H, LPC2D, ANX2L4, PAP-IV, HEL-S-270 -ANXA2 and Prostate Cancer
10
TACSTD2 1p32 EGP1, GP50, M1S1, EGP-1, TROP2, GA7331, GA733-1 -TACSTD2 and Prostate Cancer
10
MIRLET7C 21q21.1 LET7C, let-7c, MIRNLET7C, hsa-let-7c -MicroRNA let-7c and Prostate Cancer
10
DLC1 8p22 HP, ARHGAP7, STARD12, p122-RhoGAP -DLC1 and Prostate Cancer
10
FYN 6q21 SLK, SYN, p59-FYN -FYN and Prostate Cancer
10
TMEFF2 2q32.3 TR, HPP1, TPEF, TR-2, TENB2, CT120.2 -TMEFF2 and Prostate Cancer
10
IGFBP1 7p12.3 AFBP, IBP1, PP12, IGF-BP25, hIGFBP-1 -IGFBP1 and Prostate Cancer
10
KLF4 9q31 EZF, GKLF -KLF4 and Prostate Cancer
10
ERBB4 2q33.3-q34 HER4, ALS19, p180erbB4 -ERBB4 and Prostate Cancer
10
GATA2 3q21.3 DCML, IMD21, NFE1B, MONOMAC -GATA2 and Prostate Cancer
10
FGF7 15q21.2 KGF, HBGF-7 -FGF7 and Prostate Cancer
10
IRS1 2q36 HIRS-1 -IRS1 and Prostate Cancer
10
NCOA3 20q12 ACTR, AIB1, RAC3, SRC3, pCIP, AIB-1, CTG26, SRC-3, CAGH16, KAT13B, TNRC14, TNRC16, TRAM-1, bHLHe42 -NCOA3 and Prostate Cancer
10
ESR2 14q23.2 Erb, ESRB, ESTRB, NR3A2, ER-BETA, ESR-BETA -ESR2 and Prostate Cancer
10
TPD52 8q21.13 D52, N8L, PC-1, PrLZ, hD52 -TPD52 and Prostate Cancer
10
IGFBP5 2q35 IBP5 -IGFBP5 and Prostate Cancer
10
VIP 6q25 PHM27 -VIP and Prostate Cancer
10
HSD3B1 1p13.1 I, HSD3B, HSDB3, HSDB3A, SDR11E1, 3BETAHSD -HSD3B1 and Prostate Cancer
10
ELK4 1q32 SAP1 -ELK4 and Prostate Cancer
10
SUZ12 17q11.2 CHET9, JJAZ1 -SUZ12 and Prostate Cancer
9
EEF1A1 6q14.1 CCS3, EF1A, PTI1, CCS-3, EE1A1, EEF-1, EEF1A, EF-Tu, LENG7, eEF1A-1, GRAF-1EF, HNGC:16303 -EEF1A1 and Prostate Cancer
9
MIF 22q11.23 GIF, GLIF, MMIF -MIF and Prostate Cancer
9
MAF 16q22-q23 CCA4, AYGRP, c-MAF, CTRCT21 -MAF and Prostate Cancer
9
CREB1 2q34 CREB -CREB1 and Prostate Cancer
9
CCR5 3p21.31 CKR5, CCR-5, CD195, CKR-5, CCCKR5, CMKBR5, IDDM22, CC-CKR-5 -CCR5 and Prostate Cancer
9
NCOR1 17p11.2 N-CoR, TRAC1, N-CoR1, hN-CoR, PPP1R109 -NCOR1 and Prostate Cancer
9
CCNA2 4q27 CCN1, CCNA -CCNA2 and Prostate Cancer
9
KLF5 13q22.1 CKLF, IKLF, BTEB2 -KLF5 and Prostate Cancer
9
BNIP3 10q26.3 NIP3 -BNIP3 and Prostate Cancer
9
BMP7 20q13 OP-1 -BMP7 and Prostate Cancer
9
CCR2 3p21.31 CKR2, CCR-2, CCR2A, CCR2B, CD192, CKR2A, CKR2B, CMKBR2, MCP-1-R, CC-CKR-2 -CCR2 and Prostate Cancer
9
CDC25C 5q31 CDC25, PPP1R60 -CDC25C and Prostate Cancer
9
HMGB1 13q12 HMG1, HMG3, SBP-1 -HMGB1 and Prostate Cancer
9
ALOX15 17p13.3 12-LOX, 15LOX-1, 15-LOX-1 -ALOX15 and Prostate Cancer
9
EIF3E 8q22-q23 INT6, EIF3S6, EIF3-P48, eIF3-p46 -EIF3E and Prostate Cancer
9
KDM1A 1p36.12 AOF2, KDM1, LSD1, BHC110 -KDM1A and Prostate Cancer
8
CDC6 17q21.3 CDC18L, HsCDC6, HsCDC18 -CDC6 and Prostate Cancer
8
PGK1 Xq13.3 PGKA, MIG10, HEL-S-68p -PGK1 and Prostate Cancer
8
PLAU 10q22.2 ATF, QPD, UPA, URK, u-PA, BDPLT5 -PLAU and Prostate Cancer
8
CYP11A1 15q23-q24 CYP11A, CYPXIA1, P450SCC -CYP11A1 and Prostate Cancer
8
PWAR1 15q11.2 PAR1, PAR-1, D15S227E -PAR1 and Prostate Cancer
8
RELB 19q13.32 IREL, I-REL, REL-B -RELB and Prostate Cancer
8
KLK5 19q13.33 SCTE, KLKL2, KLK-L2 -KLK5 and Prostate Cancer
8
COL18A1 21q22.3 KS, KNO, KNO1 -COL18A1 and Prostate Cancer
8
MCM7 7q21.3-q22.1 MCM2, CDC47, P85MCM, P1CDC47, PNAS146, PPP1R104, P1.1-MCM3 -MCM7 and Prostate Cancer
8
TLR9 3p21.3 CD289 -TLR9 and Prostate Cancer
8
FOXP3 Xp11.23 JM2, AIID, IPEX, PIDX, XPID, DIETER -FOXP3 and Prostate Cancer
8
UBE2C 20q13.12 UBCH10, dJ447F3.2 -UBE2C and Prostate Cancer
8
PHIP 6q14 ndrp, BRWD2, WDR11, DCAF14 -PHIP and Prostate Cancer
8
MECP2 Xq28 RS, RTS, RTT, PPMX, MRX16, MRX79, MRXSL, AUTSX3, MRXS13 -MECP2 and Prostate Cancer
8
CAST 5q15 BS-17, PLACK -CAST and Prostate Cancer
8
MED1 17q12 PBP, CRSP1, RB18A, TRIP2, PPARBP, CRSP200, DRIP205, DRIP230, PPARGBP, TRAP220 -MED1 and Prostate Cancer
8
ETS2 21q22.2 ETS2IT1 -ETS2 and Prostate Cancer
8
ASAH1 8p22 AC, PHP, ASAH, PHP32, ACDase, SMAPME -ASAH1 and Prostate Cancer
8
PLAUR 19q13 CD87, UPAR, URKR, U-PAR -PLAUR and Prostate Cancer
8
SOX4 6p22.3 EVI16 -SOX4 and Prostate Cancer
8
CYR61 1p22.3 CCN1, GIG1, IGFBP10 -CYR61 and Prostate Cancer
8
CHIA 1p13.2 CHIT2, AMCASE, TSA1902 -CHIA and Prostate Cancer
8
NEFL 8p21 NFL, NF-L, NF68, CMT1F, CMT2E, PPP1R110 -NEFL and Prostate Cancer
8
SOX11 2p25 MRD27 -SOX11 and Prostate Cancer
7
CKAP4 12q23.3 p63, CLIMP-63, ERGIC-63 -CKAP4 and Prostate Cancer
7
HOXA4 7p15.2 HOX1, HOX1D -HOXA4 and Prostate Cancer
7
PON1 7q21.3 ESA, PON, MVCD5 -PON1 and Prostate Cancer
7
TLR6 4p14 CD286 -TLR6 and Prostate Cancer
7
TSG101 11p15.1 TSG10, VPS23 -TSG101 and Prostate Cancer
7
GLIPR1 12q21.2 GLIPR, RTVP1, CRISP7 -GLIPR1 and Prostate Cancer
7
CDH2 18q11.2 CDHN, NCAD, CD325, CDw325 -CDH2 and Prostate Cancer
7
ADAM9 8p11.22 MCMP, MDC9, CORD9, Mltng -ADAM9 and Prostate Cancer
7
FLNC 7q32-q35 ABPA, ABPL, FLN2, MFM5, MPD4, ABP-280, ABP280A -FLNC and Prostate Cancer
7
BMP2 20p12 BDA2, BMP2A -BMP2 and Prostate Cancer
7
AGO2 8q24 Q10, EIF2C2 -AGO2 and Prostate Cancer
7
HOXC6 12q13.3 CP25, HOX3, HOX3C, HHO.C8 -HOXC6 and Prostate Cancer
7
AKT3 1q44 MPPH, PKBG, MPPH2, PRKBG, STK-2, PKB-GAMMA, RAC-gamma, RAC-PK-gamma -AKT3 and Prostate Cancer
7
CD14 5q31.1 -CD14 and Prostate Cancer
7
FOXA2 20p11 HNF3B, TCF3B -FOXA2 and Prostate Cancer
7
MAP2K4 17p12 JNKK, MEK4, MKK4, SEK1, SKK1, JNKK1, SERK1, MAPKK4, PRKMK4, SAPKK1, SAPKK-1 -MAP2K4 and Prostate Cancer
7
CTAG1B Xq28 CTAG, ESO1, CT6.1, CTAG1, LAGE-2, LAGE2B, NY-ESO-1 -CTAG1B and Prostate Cancer
7
GAS6 13q34 AXSF, AXLLG -GAS6 and Prostate Cancer
7
ALOX5 10q11.2 5-LO, 5LPG, LOG5, 5-LOX -ALOX5 and Prostate Cancer
7
SNAI2 8q11 SLUG, WS2D, SLUGH1, SNAIL2 -SNAI2 and Prostate Cancer
6
HOXB13 17q21.2 PSGD Germline
-Germline mutations of HOXB13 in Familiar Prostate Cancer?
-rs339331 Polymorphism and Prostate Cancer susceptibility
6
BCAR1 16q23.1 CAS, CAS1, CASS1, CRKAS, P130Cas -BCAR1 and Prostate Cancer
6
AIDA 1q41 C1orf80 -AIDA and Prostate Cancer
6
BAG1 9p12 HAP, BAG-1, RAP46 Overexpression
-BAG1 overexpression in Prostate Cancer
6
OGG1 3p26.2 HMMH, MUTM, OGH1, HOGG1 -OGG1 and Prostate Cancer
6
LIG4 13q33-q34 LIG4S -LIG4 and Prostate Cancer
6
SOD1 21q22.11 ALS, SOD, ALS1, IPOA, hSod1, HEL-S-44, homodimer -SOD1 and Prostate Cancer
6
ACPP 3q22.1 ACP3, 5'-NT, ACP-3 Prognostic
-ACPP expression in Prostate Cancer
6
MST1 3p21 MSP, HGFL, NF15S2, D3F15S2, DNF15S2 -MST1 and Prostate Cancer
6
CXCR2 2q35 CD182, IL8R2, IL8RA, IL8RB, CMKAR2, CDw128b -CXCR2 and Prostate Cancer
6
KLK14 19q13.3-q13.4 KLK-L6 -KLK14 and Prostate Cancer
6
SSTR5 16p13.3 SS-5-R -SSTR5 and Prostate Cancer
6
SEPP1 5q31 SeP, SELP, SEPP -SEPP1 and Prostate Cancer
6
CDH13 16q23.3 CDHH, P105 -CDH13 and Prostate Cancer
6
NFKB2 10q24 p52, p100, H2TF1, LYT10, CVID10, LYT-10, NF-kB2 -NFKB2 and Prostate Cancer
6
IRS2 13q34 IRS-2 -IRS2 and Prostate Cancer
6
CXCL5 4q13.3 SCYB5, ENA-78 -CXCL5 and Prostate Cancer
6
PDGFD 11q22.3 IEGF, SCDGFB, MSTP036, SCDGF-B -PDGFD and Prostate Cancer
6
TXNRD1 12q23-q24.1 TR, TR1, TXNR, TRXR1, GRIM-12 -TXNRD1 and Prostate Cancer
6
IL1B 2q14 IL-1, IL1F2, IL1-BETA -IL1B and Prostate Cancer
6
FHL2 2q12.2 DRAL, AAG11, FHL-2, SLIM3, SLIM-3 -FHL2 and Prostate Cancer
6
BMP6 6p24-p23 VGR, VGR1 -BMP6 and Prostate Cancer
6
SOCS3 17q25.3 CIS3, SSI3, ATOD4, Cish3, SSI-3, SOCS-3 -SOCS3 and Prostate Cancer
6
BMPR1A 10q22.3 ALK3, SKR5, CD292, ACVRLK3, 10q23del -BMPR1A and Prostate Cancer
6
KAT5 11q13.1 TIP, ESA1, PLIP, TIP60, cPLA2, HTATIP, ZC2HC5, HTATIP1 -KAT5 and Prostate Cancer
6
SGK1 6q23 SGK -SGK1 and Prostate Cancer
6
CSK 15q24.1 -CSK and Prostate Cancer
6
BMPR2 2q33-q34 BMR2, PPH1, BMPR3, BRK-3, POVD1, T-ALK, BMPR-II -BMPR2 and Prostate Cancer
6
S100P 4p16 MIG9 -S100P and Prostate Cancer
6
ARNT 1q21 HIF1B, TANGO, bHLHe2, HIF1BETA, HIF-1beta, HIF1-beta, HIF-1-beta -ARNT and Prostate Cancer
6
RARRES1 3q25.32 LXNL, TIG1, PERG-1 -RARRES1 and Prostate Cancer
6
RICTOR 5p13.1 PIA, AVO3, hAVO3 -RICTOR and Prostate Cancer
6
NCOR2 12q24 SMRT, TRAC, CTG26, SMRTE, TRAC1, N-CoR2, TNRC14, TRAC-1, SMAP270, SMRTE-tau -NCOR2 and Prostate Cancer
6
DAB2 5p13.1 DOC2, DOC-2 -DAB2 and Prostate Cancer
6
TFF3 21q22.3 ITF, P1B, TFI -TFF3 and Prostate Cancer
6
HBEGF 5q23 DTR, DTS, DTSF, HEGFL -HBEGF and Prostate Cancer
6
CEACAM1 19q13.2 BGP, BGP1, BGPI -CEACAM1 and Prostate Cancer
6
ATF3 1q32.3 -ATF3 and Prostate Cancer
6
STAT6 12q13 STAT6B, STAT6C, D12S1644, IL-4-STAT -STAT6 and Prostate Cancer
6
CCNB2 15q22.2 HsT17299 -CCNB2 and Prostate Cancer
6
PDK1 2q31.1 -PDK1 and Prostate Cancer
6
THRB 3p24.2 GRTH, PRTH, THR1, ERBA2, NR1A2, THRB1, THRB2, C-ERBA-2, C-ERBA-BETA -THRB and Prostate Cancer
5
HRK 12q24.22 DP5, HARAKIRI -HRK and Prostate Cancer
5
CHUK 10q24-q25 IKK1, IKKA, IKBKA, TCF16, NFKBIKA, IKK-alpha -CHUK and Prostate Cancer
5
SLCO1B3 12p12 LST3, HBLRR, LST-2, OATP8, OATP-8, OATP1B3, SLC21A8, LST-3TM13 -SLCO1B3 and Prostate Cancer
5
TRAF6 11p12 RNF85, MGC:3310 -TRAF6 and Prostate Cancer
5
GSTA1 6p12.1 GST2, GTH1, GSTA1-1 -GSTA1 and Prostate Cancer
5
KLK10 19q13 NES1, PRSSL1 -KLK10 and Prostate Cancer
5
GREB1 2p25.1 -GREB1 and Prostate Cancer
5
CXCL14 5q31 KEC, KS1, BMAC, BRAK, NJAC, MIP2G, MIP-2g, SCYB14 -CXCL14 and Prostate Cancer
5
AKR1C2 10p15-p14 DD, DD2, TDD, BABP, DD-2, DDH2, HBAB, HAKRD, MCDR2, SRXY8, DD/BABP, AKR1C-pseudo -AKR1C2 and Prostate Cancer
5
XAF1 17p13.1 BIRC4BP, XIAPAF1, HSXIAPAF1 -XAF1 and Prostate Cancer
5
PARK7 1p36.23 DJ1, DJ-1, HEL-S-67p -PARK7 and Prostate Cancer
5
PEBP1 12q24.23 PBP, HCNP, PEBP, RKIP, HCNPpp, PEBP-1, HEL-210, HEL-S-34 -PEBP1 and Prostate Cancer
5
HIP1 7q11.23 SHON, HIP-I, ILWEQ, SHONbeta, SHONgamma -HIP1 and Prostate Cancer
5
ROCK1 18q11.1 ROCK-I, P160ROCK -ROCK1 and Prostate Cancer
5
CLMP 11q24.1 ACAM, ASAM, CSBM, CSBS -CLMP and Prostate Cancer
5
TLR2 4q32 TIL4, CD282 -TLR2 and Prostate Cancer
5
IL18 11q23.1 IGIF, IL-18, IL-1g, IL1F4 -IL18 and Prostate Cancer
5
KPNA2 17q24.2 QIP2, RCH1, IPOA1, SRP1alpha -KPNA2 and Prostate Cancer
5
UGT1A1 2q37 GNT1, UGT1, UDPGT, UGT1A, HUG-BR1, BILIQTL1, UDPGT 1-1 -UGT1A1 and Prostate Cancer
5
CXCR1 2q35 C-C, CD128, CD181, CKR-1, IL8R1, IL8RA, CMKAR1, IL8RBA, CDw128a, C-C-CKR-1 -CXCR1 and Prostate Cancer
5
CASR 3q13 CAR, FHH, FIH, HHC, EIG8, HHC1, NSHPT, PCAR1, GPRC2A, HYPOC1 -CASR and Prostate Cancer
5
CUL1 7q36.1 -CUL1 and Prostate Cancer
5
CYP1A2 15q24.1 CP12, P3-450, P450(PA) -CYP1A2 and Prostate Cancer
5
B2M 15q21.1 -B2M and Prostate Cancer
5
ADIPOQ 3q27 ACDC, ADPN, APM1, APM-1, GBP28, ACRP30, ADIPQTL1 -ADIPOQ and Prostate Cancer
5
PHLPP1 18q21.33 SCOP, PHLPP, PLEKHE1 -PHLPP1 and Prostate Cancer
5
MYBL2 20q13.1 BMYB, B-MYB -MYBL2 and Prostate Cancer
5
TAGLN 11q23.3 SM22, SMCC, TAGLN1, WS3-10 -TAGLN and Prostate Cancer
5
MUC6 11p15.5 MUC-6 -MUC6 and Prostate Cancer
5
TLR1 4p14 TIL, CD281, rsc786, TIL. LPRS5 -TLR1 and Prostate Cancer
5
DUSP1 5q34 HVH1, MKP1, CL100, MKP-1, PTPN10 -DUSP1 and Prostate Cancer
5
TP53BP1 15q15-q21 p202, 53BP1 -TP53BP1 and Prostate Cancer
5
PPIA 7p13 CYPA, CYPH, HEL-S-69p -PPIA and Prostate Cancer
5
ABCA1 9q31.1 TGD, ABC1, CERP, ABC-1, HDLDT1 -ABCA1 and Prostate Cancer
5
CD151 11p15.5 GP27, MER2, RAPH, SFA1, PETA-3, TSPAN24 -CD151 and Prostate Cancer
5
NEDD4 15q RPF1, NEDD4-1 -NEDD4 and Prostate Cancer
5
SKP1 5q31 OCP2, p19A, EMC19, SKP1A, OCP-II, TCEB1L -SKP1 and Prostate Cancer
5
KDM4C 9p24.1 GASC1, JHDM3C, JMJD2C, TDRD14C -KDM4C and Prostate Cancer
5
BTG2 1q32 PC3, TIS21 -BTG2 and Prostate Cancer
5
WEE1 11p15.4 WEE1A, WEE1hu -WEE1 and Prostate Cancer
5
GHRH 20q11.2 GRF, INN, GHRF -GHRH and Prostate Cancer
5
ZBTB7A 19p13.3 LRF, FBI1, FBI-1, ZBTB7, ZNF857A, pokemon -ZBTB7A and Prostate Cancer
5
SPRY2 13q31.1 hSPRY2 -SPRY2 and Prostate Cancer
5
TRPS1 8q24.12 GC79, LGCR -TRPS1 and Prostate Cancer
5
SPRY1 4q28.1 hSPRY1 -SPRY1 and Prostate Cancer
5
SHMT1 17p11.2 SHMT, CSHMT -SHMT1 and Prostate Cancer
4
LTA 6p21.3 LT, TNFB, TNFSF1 -LTA and Prostate Cancer
4
TNFRSF10D 8p21 DCR2, CD264, TRUNDD, TRAILR4, TRAIL-R4 -TNFRSF10D and Prostate Cancer
4
DAXX 6p21.3 DAP6, EAP1, BING2 -DAXX and Prostate Cancer
4
MUC2 11p15.5 MLP, SMUC, MUC-2 -MUC2 and Prostate Cancer
4
DDX5 17q21 p68, HLR1, G17P1, HUMP68 -DDX5 and Prostate Cancer
4
HSD17B1 17q11-q21 HSD17, EDHB17, EDH17B2, SDR28C1 -HSD17B1 and Prostate Cancer
4
MBD4 3q21.3 MED1 -MBD4 and Prostate Cancer
4
ADAM17 2p25 CSVP, TACE, NISBD, ADAM18, CD156B, NISBD1 -ADAM17 and Prostate Cancer
4
GPRC6A 6q22.1 GPCR, bA86F4.3 -GPRC6A and Prostate Cancer
4
ADAMTS1 21q21.2 C3-C5, METH1 -ADAMTS1 and Prostate Cancer
4
BTG1 12q22 -BTG1 and Prostate Cancer
4
PER1 17p13.1 PER, hPER, RIGUI -PER1 and Prostate Cancer
4
UCP2 11q13.4 UCPH, BMIQ4, SLC25A8 -UCP2 and Prostate Cancer
4
MED12 Xq13 OKS, FGS1, HOPA, OPA1, OHDOX, ARC240, CAGH45, MED12S, TNRC11, TRAP230 -MED12 and Prostate Cancer
4
IL11 19q13.3-q13.4 AGIF, IL-11 -IL11 and Prostate Cancer
4
TES 7q31.2 TESS, TESS-2 -TES and Prostate Cancer
4
TGFBR3 1p33-p32 BGCAN, betaglycan -TGFBR3 and Prostate Cancer
4
PRLR 5p13.2 HPRL, MFAB, hPRLrI -PRLR and Prostate Cancer
4
IL16 15q26.3 LCF, NIL16, PRIL16, prIL-16 -IL16 and Prostate Cancer
4
YBX1 1p34 YB1, BP-8, CSDB, DBPB, YB-1, CSDA2, NSEP1, NSEP-1, MDR-NF1 -YBX1 and Prostate Cancer
4
MBD1 18q21 RFT, PCM1, CXXC3 -MBD1 and Prostate Cancer
4
STK4 20q11.2-q13.2 KRS2, MST1, YSK3, TIIAC -STK4 and Prostate Cancer
4
GAS1 9q21.3-q22 -GAS1 and Prostate Cancer
4
ST14 11q24.3 HAI, MTSP1, SNC19, ARCI11, MT-SP1, PRSS14, TADG15, TMPRSS14 -ST14 and Prostate Cancer
4
LZTS1 8p22 F37, FEZ1 -LZTS1 and Prostate Cancer
4
SOCS2 12q CIS2, SSI2, Cish2, SSI-2, SOCS-2, STATI2 -SOCS2 and Prostate Cancer
4
IKBKE 1q32.1 IKKE, IKKI, IKK-E, IKK-i -IKBKE and Prostate Cancer
4
MT2A 16q13 MT2 -MT2A and Prostate Cancer
4
TGFB3 14q24 ARVD, RNHF, ARVD1, TGF-beta3 -TGFB3 and Prostate Cancer
4
CHGA 14q32 CGA -CHGA and Prostate Cancer
4
GADD45B 19p13.3 MYD118, GADD45BETA -GADD45B and Prostate Cancer
4
PKD1 16p13.3 PBP, Pc-1, TRPP1 -PKD1 and Prostate Cancer
4
HLA-DRB1 6p21.3 SS1, DRB1, DRw10, HLA-DRB, HLA-DR1B -HLA-DRB1 and Prostate Cancer
4
GNL3 3p21.1 NS, E2IG3, NNP47, C77032 -GNL3 and Prostate Cancer
4
CARS 11p15.4 CARS1, CYSRS, MGC:11246 -CARS and Prostate Cancer
4
ELF3 1q32.2 ERT, ESX, EPR-1, ESE-1 -ELF3 and Prostate Cancer
4
NGFR 17q21-q22 CD271, p75NTR, TNFRSF16, p75(NTR), Gp80-LNGFR -NGFR and Prostate Cancer
4
CTBP1 4p16 BARS -CTBP1 and Prostate Cancer
4
ADRB2 5q31-q32 BAR, B2AR, ADRBR, ADRB2R, BETA2AR -ADRB2 and Prostate Cancer
4
TNFRSF25 1p36.2 DR3, TR3, DDR3, LARD, APO-3, TRAMP, WSL-1, WSL-LR, TNFRSF12 -TNFRSF25 and Prostate Cancer
4
ANXA7 10q22.2 SNX, ANX7, SYNEXIN -ANXA7 and Prostate Cancer
4
INHA 2q35 -INHA and Prostate Cancer
4
NKX2-5 5q34 CSX, CSX1, VSD3, CHNG5, HLHS2, NKX2E, NKX2.5, NKX4-1 -NKX2-5 and Prostate Cancer
4
FGF10 5p13-p12 -FGF10 and Prostate Cancer
4
BIRC7 20q13.3 KIAP, LIVIN, MLIAP, RNF50, ML-IAP -BIRC7 and Prostate Cancer
4
AMFR 16q21 GP78, RNF45 -AMFR and Prostate Cancer
4
YWHAZ 8q23.1 HEL4, YWHAD, KCIP-1, HEL-S-3, 14-3-3-zeta -YWHAZ and Prostate Cancer
4
HNRNPA2B1 7p15 RNPA2, HNRPA2, HNRPB1, SNRPB1, HNRNPA2, HNRNPB1, IBMPFD2, HNRPA2B1 -HNRNPA2B1 and Prostate Cancer
4
MX1 21q22.3 MX, MxA, IFI78, IFI-78K -MX1 and Prostate Cancer
4
KRT18 12q13 K18, CK-18, CYK18 -KRT18 and Prostate Cancer
4
CEBPD 8p11.2-p11.1 CELF, CRP3, C/EBP-delta, NF-IL6-beta -CEBPD and Prostate Cancer
4
LCN2 9q34 24p3, MSFI, NGAL -LCN2 and Prostate Cancer
4
AIFM1 Xq26.1 AIF, CMT2D, CMTX4, COWCK, NADMR, NAMSD, PDCD8, COXPD6 -AIFM1 and Prostate Cancer
3
RAC3 17q25.3 -RAC3 and Prostate Cancer
3
AKR1C1 10p15-p14 C9, DD1, DDH, DDH1, H-37, HBAB, MBAB, HAKRC, DD1/DD2, 2-ALPHA-HSD, 20-ALPHA-HSD -AKR1C1 and Prostate Cancer
3
CAV2 7q31.1 CAV -CAV2 and Prostate Cancer
3
ENO1 1p36.2 NNE, PPH, MPB1, ENO1L1 -ENO1 and Prostate Cancer
3
KDM6A Xp11.2 UTX, KABUK2, bA386N14.2 -KDM6A and Prostate Cancer
3
PDPK1 16p13.3 PDK1, PDPK2, PDPK2P, PRO0461 -PDPK1 and Prostate Cancer
3
PIAS3 1q21 ZMIZ5 -PIAS3 and Prostate Cancer
3
WNT11 11q13.5 HWNT11 -WNT11 and Prostate Cancer
3
BAG3 10q25.2-q26.2 BIS, MFM6, BAG-3, CAIR-1 -BAG3 and Prostate Cancer
3
MUC4 3q29 ASGP, MUC-4, HSA276359 -MUC4 and Prostate Cancer
3
NR3C1 5q31.3 GR, GCR, GRL, GCCR, GCRST -NR3C1 and Prostate Cancer
3
SMAD5 5q31 DWFC, JV5-1, MADH5 -SMAD5 and Prostate Cancer
3
CCNE2 8q22.1 CYCE2 -CCNE2 and Prostate Cancer
3
PER3 1p36.23 GIG13 -PER3 and Prostate Cancer
3
SEMA3A 7p12.1 HH16, SemD, COLL1, SEMA1, SEMAD, SEMAL, coll-1, Hsema-I, SEMAIII, Hsema-III -SEMA3A and Prostate Cancer
3
CTSB 8p22 APPS, CPSB -CTSB and Prostate Cancer
3
PTK6 20q13.3 BRK -PTK6 and Prostate Cancer
3
CARM1 19p13.2 PRMT4 -CARM1 and Prostate Cancer
3
CDT1 16q24.3 DUP, RIS2 -CDT1 and Prostate Cancer
3
MUC5AC 11p15.5 TBM, leB, MUC5, mucin -MUC5AC and Prostate Cancer
3
NRP1 10p12 NP1, NRP, BDCA4, CD304, VEGF165R -NRP1 and Prostate Cancer
3
REG4 1p13.1-p12 GISP, RELP, REG-IV -REG4 and Prostate Cancer
3
IL27 16p11 p28, IL30, IL-27, IL27A, IL-27A, IL27p28 -IL27 and Prostate Cancer
3
RALBP1 18p11.3 RIP1, RLIP1, RLIP76 -RALBP1 and Prostate Cancer
3
UPRT Xq13.3 UPP, FUR1 -UPRT and Prostate Cancer
3
PRDX1 1p34.1 PAG, PAGA, PAGB, PRX1, PRXI, MSP23, NKEFA, TDPX2, NKEF-A -PRDX1 and Prostate Cancer
3
LAMB3 1q32 AI1A, LAM5, LAMNB1, BM600-125KDA -LAMB3 and Prostate Cancer
3
KRT8 12q13 K8, KO, CK8, CK-8, CYK8, K2C8, CARD2 -KRT8 and Prostate Cancer
3
CUL3 2q36.2 CUL-3, PHA2E -CUL3 and Prostate Cancer
3
CMBL 5p15.2 JS-1 -CMBL and Prostate Cancer
3
PPARGC1A 4p15.1 LEM6, PGC1, PGC1A, PGC-1v, PPARGC1, PGC-1(alpha) -PPARGC1A and Prostate Cancer
3
RXRA 9q34.3 NR2B1 -RXRA and Prostate Cancer
3
GNAS 20q13.3 AHO, GSA, GSP, POH, GPSA, NESP, SCG6, SgVI, GNAS1, C20orf45 -GNAS and Prostate Cancer
3
LRP1 12q13.3 APR, LRP, A2MR, CD91, APOER, LRP1A, TGFBR5, IGFBP3R -LRP1 and Prostate Cancer
3
ITGB3 17q21.32 GT, CD61, GP3A, BDPLT2, GPIIIa, BDPLT16 -ITGB3 and Prostate Cancer
3
CXCL16 17p13 SRPSOX, CXCLG16, SR-PSOX -CXCL16 and Prostate Cancer
3
ADIPOR1 1q32.1 CGI45, PAQR1, ACDCR1, CGI-45, TESBP1A -ADIPOR1 and Prostate Cancer
3
STEAP2 7q21.13 STMP, IPCA1, PUMPCn, STAMP1, PCANAP1 -STEAP2 and Prostate Cancer
3
SSTR1 14q13 SS1R, SS1-R, SRIF-2, SS-1-R -SSTR1 and Prostate Cancer
3
NBL1 1p36.13 NB, DAN, NO3, DAND1, D1S1733E -NBL1 and Prostate Cancer
3
AGTR2 Xq22-q23 AT2, ATGR2, MRX88 -AGTR2 and Prostate Cancer
3
CKS2 9q22 CKSHS2 -CKS2 and Prostate Cancer
3
MTSS1 8p22 MIM, MIMA, MIMB -MTSS1 and Prostate Cancer
3
FABP5 8q21.13 EFABP, KFABP, E-FABP, PAFABP, PA-FABP -FABP5 and Prostate Cancer
3
LDLR 19p13.2 FH, FHC, LDLCQ2 -LDLR and Prostate Cancer
3
LEPR 1p31 OBR, OB-R, CD295, LEP-R, LEPRD -LEPR and Prostate Cancer
3
KLK6 19q13.3 hK6, Bssp, Klk7, SP59, PRSS9, PRSS18 -KLK6 and Prostate Cancer
3
ARL11 13q14.2 ARLTS1 -ARL11 and Prostate Cancer
3
DDIT4 10q22.1 Dig2, REDD1, REDD-1 -DDIT4 and Prostate Cancer
3
IRAK2 3p25.3 IRAK-2 -IRAK2 and Prostate Cancer
3
SERPINB2 18q21.3 PAI, PAI2, PAI-2, PLANH2, HsT1201 -SERPINB2 and Prostate Cancer
3
TNFRSF10C 8p22-p21 LIT, DCR1, TRID, CD263, TRAILR3, TRAIL-R3, DCR1-TNFR -TNFRSF10C and Prostate Cancer
3
PLAGL1 6q24-q25 ZAC, LOT1, ZAC1 -PLAGL1 and Prostate Cancer
3
IL13RA1 Xq24 NR4, CT19, CD213A1, IL-13Ra -IL13RA1 and Prostate Cancer
3
CRY2 11p11.2 HCRY2, PHLL2 -CRY2 and Prostate Cancer
3
APOD 3q29 -APOD and Prostate Cancer
3
HMMR 5q34 CD168, IHABP, RHAMM -HMMR and Prostate Cancer
3
HAS3 16q22.1 -HAS3 and Prostate Cancer
3
ACTA2 10q23.3 AAT6, ACTSA, MYMY5 -ACTA2 and Prostate Cancer
3
MIR1271 5q35 MIRN1271, hsa-mir-1271 -MicroRNA miR-1271and Prostate Cancer
3
TGM4 3p22-p21.33 TGP, hTGP -TGM4 and Prostate Cancer
3
RAD23B 9q31.2 P58, HR23B, HHR23B -RAD23B and Prostate Cancer
3
CRY1 12q23-q24.1 PHLL1 -CRY1 and Prostate Cancer
3
NDRG2 14q11.2 SYLD -NDRG2 and Prostate Cancer
3
NR3C2 4q31.1 MR, MCR, MLR, NR3C2VIT -NR3C2 and Prostate Cancer
3
BIN1 2q14 AMPH2, AMPHL, SH3P9 -BIN1 and Prostate Cancer
3
PYCARD 16p11.2 ASC, TMS, TMS1, CARD5, TMS-1 -PYCARD and Prostate Cancer
3
E2F5 8q21.2 E2F-5 -E2F5 and Prostate Cancer
3
ADAR 1q21.3 DSH, AGS6, G1P1, IFI4, P136, ADAR1, DRADA, DSRAD, IFI-4, K88DSRBP -ADAR and Prostate Cancer
3
ATF2 2q32 HB16, CREB2, TREB7, CREB-2, CRE-BP1 -ATF2 and Prostate Cancer
3
LIMK1 7q11.23 LIMK, LIMK-1 -LIMK1 and Prostate Cancer
3
FOXP4 6p21.1 hFKHLA -FOXP4 and Prostate Cancer
3
STRADA 17q23.3 LYK5, PMSE, Stlk, STRAD, NY-BR-96 -STRADA and Prostate Cancer
3
KDM6B 17p13.1 JMJD3 -KDM6B and Prostate Cancer
3
PLAT 8p12 TPA, T-PA -PLAT and Prostate Cancer
3
IRAK1 Xq28 IRAK, pelle -IRAK1 and Prostate Cancer
2
CCNG2 4q21.1 -CCNG2 and Prostate Cancer
2
FOXC1 6p25 ARA, IGDA, IHG1, FKHL7, IRID1, RIEG3, FREAC3, FREAC-3 -FOXC1 and Prostate Cancer
2
ODC1 2p25 ODC -ODC1 and Prostate Cancer
2
IL7 8q12-q13 IL-7 -IL7 and Prostate Cancer
2
CXCL11 4q21.2 IP9, H174, IP-9, b-R1, I-TAC, SCYB11, SCYB9B -CXCL11 and Prostate Cancer
2
P2RX7 12q24 P2X7 -P2RX7 and Prostate Cancer
2
HYAL1 3p21.31 MPS9, NAT6, LUCA1, HYAL-1 -HYAL1 and Prostate Cancer
2
ST7 7q31.2 HELG, RAY1, SEN4, TSG7, ETS7q, FAM4A, FAM4A1 -ST7 and Prostate Cancer
2
NOX1 Xq22 MOX1, NOH1, NOH-1, GP91-2 -NOX1 and Prostate Cancer
2
MCM5 22q13.1 CDC46, P1-CDC46 -MCM5 and Prostate Cancer
2
ARNTL 11p15.3 TIC, JAP3, MOP3, BMAL1, PASD3, BMAL1c, bHLHe5 -ARNTL and Prostate Cancer
2
ACSL3 2q34-q35 ACS3, FACL3, PRO2194 -ACSL3 and Prostate Cancer
2
RAD17 5q13 CCYC, R24L, RAD24, HRAD17, RAD17SP -RAD17 and Prostate Cancer
2
TRIO 5p15.2 tgat, ARHGEF23 -TRIO and Prostate Cancer
2
PAK4 19q13.2 -PAK4 and Prostate Cancer
2
NAV1 1q32.3 POMFIL3, UNC53H1, STEERIN1 -NAV1 and Prostate Cancer
2
ROCK2 2p24 ROCK-II -ROCK2 and Prostate Cancer
2
TM4SF1 3q21-q25 L6, H-L6, M3S1, TAAL6 -TM4SF1 and Prostate Cancer
2
ITGA6 2q31.1 CD49f, VLA-6, ITGA6B -ITGA6 and Prostate Cancer
2
SOX5 12p12.1 L-SOX5, L-SOX5B, L-SOX5F -SOX5 and Prostate Cancer
2
DKC1 Xq28 DKC, CBF5, DKCX, NAP57, NOLA4, XAP101 -DKC1 and Prostate Cancer
2
HTATIP2 11p15.1 CC3, TIP30, SDR44U1 -HTATIP2 and Prostate Cancer
2
PCGF2 17q12 MEL-18, RNF110, ZNF144 -PCGF2 and Prostate Cancer
2
REST 4q12 XBR, NRSF -REST and Prostate Cancer
2
MMP8 11q22.2 HNC, CLG1, MMP-8, PMNL-CL -MMP8 and Prostate Cancer
2
WNT10B 12q13 SHFM6, WNT-12 -WNT10B and Prostate Cancer
2
MIRLET7D 9q22.32 LET7D, let-7d, MIRNLET7D, hsa-let-7d -MicroRNA let-d and Prostate Cancer
2
NKTR 3p22.1 p104 -NKTR and Prostate Cancer
2
GNMT 6p12 -GNMT and Prostate Cancer
2
NEK2 1q32.3 NLK1, RP67, NEK2A, HsPK21, PPP1R111 -NEK2 and Prostate Cancer
2
CSMD1 8p23.2 PPP1R24 -CSMD1 and Prostate Cancer
2
IFITM1 11p15.5 9-27, CD225, IFI17, LEU13, DSPA2a -IFITM1 and Prostate Cancer
2
BTRC 10q24.32 FWD1, FBW1A, FBXW1, bTrCP, FBXW1A, bTrCP1, betaTrCP, BETA-TRCP -BTRC and Prostate Cancer
2
FER 5q21 TYK3, PPP1R74, p94-Fer -FER and Prostate Cancer
2
RXRB 6p21.3 NR2B2, DAUDI6, RCoR-1, H-2RIIBP -RXRB and Prostate Cancer
2
CYP2C19 10q24 CPCJ, CYP2C, P450C2C, CYPIIC17, CYPIIC19, P450IIC19 -CYP2C19 and Prostate Cancer
2
FLNA Xq28 FLN, FMD, MNS, OPD, ABPX, CSBS, CVD1, FLN1, NHBP, OPD1, OPD2, XLVD, XMVD, FLN-A, ABP-280 -FLNA and Prostate Cancer
2
EGR2 10q21.1 AT591, CMT1D, CMT4E, KROX20 -EGR2 and Prostate Cancer
2
BIRC2 11q22.2 API1, MIHB, HIAP2, RNF48, cIAP1, Hiap-2, c-IAP1 -BIRC2 and Prostate Cancer
2
GPX2 14q24.1 GPRP, GPx-2, GI-GPx, GPRP-2, GPx-GI, GSHPx-2, GSHPX-GI -GPX2 and Prostate Cancer
2
PINX1 8p23 LPTL, LPTS -PINX1 and Prostate Cancer
2
SLC43A1 11q12.1 LAT3, PB39, POV1, R00504 -SLC43A1 and Prostate Cancer
2
MYCBP 1p33-p32.2 AMY-1 -MYCBP and Prostate Cancer
2
FOXO4 Xq13.1 AFX, AFX1, MLLT7 -FOXO4 and Prostate Cancer
2
LASP1 17q11-q21.3 MLN50, Lasp-1 -LASP1 and Prostate Cancer
2
HLA-DQB1 6p21.3 IDDM1, CELIAC1, HLA-DQB -HLA-DQB1 and Prostate Cancer
2
FGF23 12p13.3 ADHR, FGFN, HYPF, HPDR2, PHPTC -FGF23 and Prostate Cancer
2
TFPI2 7q22 PP5, REF1, TFPI-2 -TFPI2 and Prostate Cancer
2
RAP2A 13q34 KREV, RAP2, K-REV, RbBP-30 -RAP2A and Prostate Cancer
2
CCR3 3p21.3 CKR3, CD193, CMKBR3, CC-CKR-3 -CCR3 and Prostate Cancer
2
LTBR 12p13 CD18, TNFCR, TNFR3, D12S370, TNFR-RP, TNFRSF3, TNFR2-RP, LT-BETA-R, TNF-R-III -LTBR and Prostate Cancer
2
INHBA 7p15-p13 EDF, FRP -INHBA and Prostate Cancer
2
IRF3 19q13.3-q13.4 -IRF3 and Prostate Cancer
2
TRIM24 7q32-q34 PTC6, TF1A, TIF1, RNF82, TIF1A, hTIF1, TIF1ALPHA -TRIM24 and Prostate Cancer
2
CBX7 22q13.1 -CBX7 and Prostate Cancer
2
UGT2B7 4q13 UGT2B9, UDPGTH2, UDPGT2B7, UDPGT 2B9 -UGT2B7 and Prostate Cancer
2
DGCR8 22q11.2 Gy1, pasha, DGCRK6, C22orf12 -DGCR8 and Prostate Cancer
2
KLLN 10q23 CWS4, KILLIN -KLLN and Prostate Cancer
2
BMPR1B 4q22-q24 ALK6, ALK-6, CDw293 -BMPR1B and Prostate Cancer
2
VIPR2 7q36.3 VPAC2, VPAC2R, VIP-R-2, VPCAP2R, PACAP-R3, DUP7q36.3, PACAP-R-3, C16DUPq36.3 -VIPR2 and Prostate Cancer
2
MIR107 10q23.31 MIRN107, miR-107 -MicroRNA mir-107 and Prostate Cancer
2
FEZ1 11q24.2 -FEZ1 and Prostate Cancer
2
STIM1 11p15.4 GOK, TAM, TAM1, IMD10, STRMK, D11S4896E -STIM1 and Prostate Cancer
2
PTPRK 6q22.2-q22.3 R-PTP-kappa -PTPRK and Prostate Cancer
2
PAWR 12q21 PAR4, Par-4 -PAWR and Prostate Cancer
2
TSC22D1 13q14 Ptg-2, TSC22, TGFB1I4 -TSC22D1 and Prostate Cancer
2
WNT4 1p36.23-p35.1 WNT-4, SERKAL -WNT4 and Prostate Cancer
2
GNRHR 4q21.2 HH7, GRHR, LRHR, LHRHR, GNRHR1 -GNRHR and Prostate Cancer
2
NSD1 5q35 STO, KMT3B, SOTOS, ARA267, SOTOS1 -NSD1 and Prostate Cancer
2
CTSD 11p15.5 CPSD, CLN10, HEL-S-130P -CTSD and Prostate Cancer
2
BUB1B 15q15 MVA1, SSK1, BUBR1, Bub1A, MAD3L, hBUBR1, BUB1beta -BUB1B and Prostate Cancer
2
IER3 6p21.3 DIF2, IEX1, PRG1, DIF-2, GLY96, IEX-1, IEX-1L -IER3 and Prostate Cancer
2
CANT1 17q25.3 DBQD, SCAN1, SHAPY, SCAN-1 -CANT1 and Prostate Cancer
2
IMP3 15q24 BRMS2, MRPS4, C15orf12 -IMP3 and Prostate Cancer
2
MME 3q25.2 NEP, SFE, CD10, CALLA -MME and Prostate Cancer
2
TFRC 3q29 T9, TR, TFR, p90, CD71, TFR1, TRFR -TFRC and Prostate Cancer
2
NQO2 6p25.2 QR2, DHQV, DIA6, NMOR2 -NQO2 and Prostate Cancer
2
HERPUD1 16q13 SUP, HERP, Mif1 -HERPUD1 and Prostate Cancer
2
ATF6 1q23.3 ATF6A -ATF6 and Prostate Cancer
2
PAFAH1B2 11q23.3 HEL-S-303 -PAFAH1B2 and Prostate Cancer
1
MAD1L1 7p22 MAD1, PIG9, TP53I9, TXBP181 -MAD1L1 and Prostate Cancer
1
FOXG1 14q13 BF1, BF2, QIN, FKH2, HBF2, HFK1, HFK2, HFK3, KHL2, FHKL3, FKHL1, FKHL2, FKHL3, FKHL4, HBF-1, HBF-2, HBF-3, FOXG1A, FOXG1B, FOXG1C, HBF-G2 -FOXG1 and Prostate Cancer
1
PLA2G16 11q12.3-q13.1 AdPLA, HRSL3, HRASLS3, HREV107, HREV107-1, HREV107-3, H-REV107-1 -PLA2G16 and Prostate Cancer
1
PRRX1 1q24 PMX1, PRX1, AGOTC, PHOX1, PRX-1 -PRRX1 and Prostate Cancer
1
CTDSPL 3p21.3 PSR1, SCP3, HYA22, RBSP3, C3orf8 -CTDSPL and Prostate Cancer
1
KAT6B 10q22.2 qkf, MORF, MOZ2, GTPTS, MYST4, ZC2HC6B, querkopf -KAT6B and Prostate Cancer
1
ARHGAP26 5q31 GRAF, GRAF1, OPHN1L, OPHN1L1 -ARHGAP26 and Prostate Cancer
1
SRPX Xp21.1 DRS, ETX1, SRPX1, HEL-S-83p -SRPX and Prostate Cancer
1
MIR106B 7q22.1 MIRN106B, mir-106b -MIR106B and Prostate Cancer
1
MS4A1 11q12.2 B1, S7, Bp35, CD20, CVID5, MS4A2, LEU-16 -MS4A1 and Prostate Cancer
1
LARGE 22q12.3 MDC1D, MDDGA6, MDDGB6 -LARGE and Prostate Cancer
1
PDE11A 2q31.2 PPNAD2 -PDE11A and Prostate Cancer
1
MTUS1 8p22 ATBP, ATIP, ICIS, MP44, MTSG1 -MTUS1 and Prostate Cancer
1
FBXO11 2p16.3 UBR6, VIT1, FBX11, PRMT9, UG063H01 -FBXO11 and Prostate Cancer
1
KMT2A 11q23.3 HRX, MLL, MLL1, TRX1, ALL-1, CXXC7, HTRX1, MLL1A, WDSTS -KMT2A and Prostate Cancer
1
SBDS 7q11.21 SDS, SWDS, CGI-97 -SBDS and Prostate Cancer
1
PCDH10 4q28.3 PCDH19, OL-PCDH -PCDH10 and Prostate Cancer
1
ANP32A 15q23 LANP, MAPM, PP32, HPPCn, PHAP1, PHAPI, I1PP2A, C15orf1 -ANP32A and Prostate Cancer
1
CCNC 6q21 CycC -CCNC and Prostate Cancer
1
PCDH7 4p15 BHPCDH, BH-Pcdh, PPP1R120 -PCDH7 and Prostate Cancer
1
HMGN2P46 15q21.1 D-PCa-2, C15orf21 -HMGN2P46 and Prostate Cancer
1
MIR122 18q21.31 MIR122A, MIRN122, mir-122, MIRN122A, miRNA122, miRNA122A, hsa-mir-122 -MIR122 and Prostate Cancer
1
DLG1 3q29 hdlg, DLGH1, SAP97, SAP-97, dJ1061C18.1.1 -DLG1 and Prostate Cancer
1
GSTO1 10q25.1 P28, SPG-R, GSTO 1-1, GSTTLp28, HEL-S-21 -GSTO1 and Prostate Cancer
1
RASSF10 11p15.3 -RASSF10 and Prostate Cancer
1
MIRLET7I 12q14.1 LET7I, let-7i, MIRNLET7I, hsa-let-7i -MicroRNA let-7i and Prostate Cancer
1
ARHGEF12 11q23.3 LARG, PRO2792 -ARHGEF12 and Prostate Cancer
1
RMI1 9q21.32 BLAP75, FAAP75, C9orf76 -RMI1 and Prostate Cancer
1
SST 3q28 SMST -SST and Prostate Cancer
1
FRS2 12q15 SNT, SNT1, FRS2A, SNT-1, FRS2alpha -FRS2 and Prostate Cancer
1
CDR2 16p12.3 Yo, CDR62 -CDR2 and Prostate Cancer
1
ERRFI1 1p36 MIG6, RALT, MIG-6, GENE-33 -ERRFI1 and Prostate Cancer
1
UHRF1 19p13.3 Np95, hNP95, ICBP90, RNF106, hUHRF1, huNp95 -UHRF1 and Prostate Cancer
1
SAT2 17p13.1 SSAT2 -SAT2 and Prostate Cancer
1
PIK3CD 1p36.2 APDS, PI3K, IMD14, p110D, P110DELTA -PIK3CD and Prostate Cancer
1
MYH9 22q13.1 MHA, FTNS, EPSTS, BDPLT6, DFNA17, NMMHCA, NMHC-II-A, NMMHC-IIA -MYH9 and Prostate Cancer
1
ESPL1 12q ESP1, SEPA -ESPL1 and Prostate Cancer
1
MIR1256 1 MIRN1256, hsa-mir-1256 -MicroRNA miR-1256 and Prostate Cancer
1
SLC22A18 11p15.4 HET, ITM, BWR1A, IMPT1, TSSC5, ORCTL2, BWSCR1A, SLC22A1L, p45-BWR1A -SLC22A18 and Prostate Cancer
1
SUV39H1 Xp11.23 MG44, KMT1A, SUV39H, H3-K9-HMTase 1 -SUV39H1 and Prostate Cancer
1
EPB41 1p33-p32 HE, EL1, 4.1R -EPB41 and Prostate Cancer
1
AIM2 1q22 PYHIN4 -AIM2 and Prostate Cancer
1
MIR1297 13 MIRN1297, mir-1297, hsa-mir-1297 -MicroRNA miR-1297 and Prostate Cancer
LINC00632 Xq27.1 -RP1-177G6.2 and Prostate Cancer
SRY Yp11.3 TDF, TDY, SRXX1, SRXY1 deletion
-Loss of SRY in prostate cancer
ERG 21q22.3 p55, erg-3 Intronic Deletion or Translocation
-ERG-TMPRSS2 Fusion in Prostate Cancer

Note: list is not exhaustive. Number of papers are based on searches of PubMed (click on topic title for arbitrary criteria used).

Latest Publications

Svenson U, Roos G, Wikström P
Long leukocyte telomere length in prostate cancer patients at diagnosis is associated with poor metastasis-free and cancer-specific survival.
Tumour Biol. 2017; 39(2):1010428317692236 [PubMed] Related Publications
Previous studies have suggested that leukocyte telomere length is associated with risk of developing prostate cancer. Investigations of leukocyte telomere length as a prognostic factor in prostate cancer are, however, lacking. In this study, leukocyte telomere length was investigated both as a risk marker, comparing control subjects and patient risk groups (based on serum levels of prostate-specific antigen, tumor differentiation, and tumor stage), and as a prognostic marker for metastasis-free and cancer-specific survival. Relative telomere length was measured by a well-established quantitative polymerase chain reaction method in 415 consecutively sampled individuals. Statistical evaluation included 162 control subjects without cancer development during follow-up and 110 untreated patients with newly diagnosed localized prostate cancer at the time of blood draw. Leukocyte telomere length did not differ significantly between control subjects and patients, or between patient risk groups. Interestingly, however, and in line with our previous results in breast and kidney cancer patients, relative telomere length at diagnosis was an independent prognostic factor. Patients with long leukocyte telomeres (⩾median) had a significantly worse prostate cancer-specific and metastasis-free survival compared to patients with short telomere length. In contrast, for patients who died of other causes than prostate cancer, long relative telomere length was not coupled to shorter survival time. To our knowledge, these results are novel and give further strength to our hypothesis that leukocyte telomere length might be used as a prognostic marker in malignancy.

Fraga A, Ribeiro R, Coelho A, et al.
Genetic polymorphisms in key hypoxia-regulated downstream molecules and phenotypic correlation in prostate cancer.
BMC Urol. 2017; 17(1):12 [PubMed] Free Access to Full Article Related Publications
BACKGROUND: In this study we sought if, in their quest to handle hypoxia, prostate tumors express target hypoxia-associated molecules and their correlation with putative functional genetic polymorphisms.
METHODS: Representative areas of prostate carcinoma (n = 51) and of nodular prostate hyperplasia (n = 20) were analysed for hypoxia-inducible factor 1 alpha (HIF-1α), carbonic anhydrase IX (CAIX), lysyl oxidase (LOX) and vascular endothelial growth factor (VEGFR2) immunohistochemistry expression using a tissue microarray. DNA was isolated from peripheral blood and used to genotype functional polymorphisms at the corresponding genes (HIF1A +1772 C > T, rs11549465; CA9 + 201 A > G; rs2071676; LOX +473 G > A, rs1800449; KDR - 604 T > C, rs2071559).
RESULTS: Immunohistochemistry analyses disclosed predominance of positive CAIX and VEGFR2 expression in epithelial cells of prostate carcinomas compared to nodular prostate hyperplasia (P = 0.043 and P = 0.035, respectively). In addition, the VEGFR2 expression score in prostate epithelial cells was higher in organ-confined and extra prostatic carcinoma compared to nodular prostate hyperplasia (P = 0.031 and P = 0.004, respectively). Notably, for LOX protein the immunoreactivity score was significantly higher in organ-confined carcinomas compared to nodular prostate hyperplasia (P = 0.015). The genotype-phenotype analyses showed higher LOX staining intensity for carriers of the homozygous LOX +473 G-allele (P = 0.011). Still, carriers of the KDR-604 T-allele were more prone to have higher VEGFR2 expression in prostate epithelial cells (P < 0.006).
CONCLUSIONS: Protein expression of hypoxia markers (VEGFR2, CAIX and LOX) on prostate epithelial cells was different between malignant and benign prostate disease. Two genetic polymorphisms (LOX +473 G > A and KDR-604 T > C) were correlated with protein level, accounting for a potential gene-environment effect in the activation of hypoxia-driven pathways in prostate carcinoma. Further research in larger series is warranted to validate present findings.

Feng F, Wu J, Gao Z, et al.
Screening the key microRNAs and transcription factors in prostate cancer based on microRNA functional synergistic relationships.
Medicine (Baltimore). 2017; 96(1):e5679 [PubMed] Free Access to Full Article Related Publications
Prostate cancer (PC) is a common neoplasm, and metastatic PC remains incurable. The study aims to screen key microRNAs (miRNAs) and transcription factors (TFs) involved in PC.The miRNA expression profile dataset (GSE45604) was downloaded from Gene Expression Omnibus database, including 50 PC and 10 normal specimens. Differentially expressed miRNAs (DEmiRNAs) were identified through limma package in R, and DEmiRNA-DEmiRNA co-regulation network was constructed based on the number of co-regulated target genes. Functional enrichment analysis of co-regulated target genes was performed using clusterProfiler package in R, and miRNA interactions sharing at least 1 functional term were used to construct a DEmiRNA-DEmiRNA functional synergistic network (MFSN). Based on Transcriptional Regulatory Element Database, cancer-related TFs which were co-regulated by DEmiRNAs were utilized to construct a DEmiRNA-TF regulation network.A total of 66 DEmiRNAs were identified, including 7 up-regulated miRNAs with 18,642 target genes and 59 down-regulated miRNAs with 130,694 target genes. Then, the DEmiRNA-DEmiRNA co-regulation network was constructed, including 66 DEmiRNAs and 2024 co-regulation relationships. In MFSN, hsa-miR-1184, hsa-miR-1207-5p, and hsa-miR-24 had significant functional synergistic relationships. The DEmiRNA-TF network contained 6 up-regulated DEmiRNAs and 4 of them were highlighted, as hsa-miR-1184, hsa-miR-1207-5p, hsa-miR-182, and hsa-miR-183. In subnetwork of the 4 miRNAs, peroxisome proliferative activated receptor, alpha (PPARA) and cyclic AMP-responsive element modulator (CREM) were the critical regulated TFs.Four up-regulated miRNAs (hsa-miR-1207-5p, hsa-miR-1184, hsa-miR-182, and hsa-miR-183) and 2 TFs (PPARA and CREM) were identified as key regulators in PC progression. The above 4 miRNAs might participate in PC progression by targeting PPARA and CREM.

Xu W, Chang J, Liu G, et al.
Knockdown of FOXR2 suppresses the tumorigenesis, growth and metastasis of prostate cancer.
Biomed Pharmacother. 2017; 87:471-475 [PubMed] Related Publications
Fork-head box R2 (FOXR2), a member of FOX protein family, was reported to play important roles in the development and progression of cancers. However, the expression and function of FOXR2 in prostate cancer remain unclear. In this study, we investigated the role of FOXR2 in prostate cancer and cancer progression including the molecular mechanism that drives FOXR2-mediated oncogenesis. Our results showed that FOXR2 was overexpressed in prostate cancer cell lines. The in vitro experiments demonstrated that knockdown of FOXR2 significantly repressed the proliferation, migration and invasiveness of prostate cancer cells. Furthermore, the in vivo experiments indicated that knockdown of FOXR2 significantly attenuated prostate cancer growth. Finally, knockdown of FOXR2 significantly down-regulated the protein expression levels of β-catenin, cyclinD1 and c-Myc in DU-145 cells. Taken together, our results demonstrated for the first time that FOXR2 plays a critical role in cell proliferation and invasion, at least in part, through inhibiting the Wnt/β-catenin signaling pathway during prostate cancer progression. Thus, FOXR2 may be an attractive therapeutic target for the treatment of prostate cancer.

Lee J, Ryu J, Lee C
Strong cis-acting expression quantitative trait loci for the genes encoding SNHG5 and PEX6.
Medicine (Baltimore). 2016; 95(52):e5793 [PubMed] Free Access to Full Article Related Publications
Expression of quantitative trait loci (eQTLs) for the genes located in human chromosome 6 were examined. Data on RNA expression in lymphoblastoid cells of 373 unrelated Europeans were used to identify eQTLs.Genome-wide analysis resulted in 24,447 nucleotide variants associated with gene expression (P < 2.16 × 10). We found 36variants with P < 10, which were all associated with expression levels of the genes encoding small nucleolar RNA host gene 5 (SNHG5) and peroxisomal biogenesis factor 6 (PEX6). Enhancer eQTLs downstream of theSNHG5 gene might be candidate genetic factors for susceptibility to cancer. This is because nucleotide substitutions (eg, G→T at rs6922) of the enhancer eQTLs may cause low expression of SNHG5 gene, and low expression of snoRNA U50, a product generated from introns of the SNHG5gene, can induce cancer. One presently identified eQTL for the PEX6 gene was rs10948059, which had been associated with prostate cancer from previous association studies. The results imply that variants associated with prostate cancer can be identified through expressional change in the PEX6 gene, but not in the overlapped glycine N-methyltransferase gene which had been considered as a candidate gene.Further studies are required to understand their underlying mechanisms for the strong eQTLs for the SNHG5 and PEX6 genes.

Paschke L, Jopek K, Szyszka M, et al.
ZFP91: A Noncanonical NF-κB Signaling Pathway Regulator with Oncogenic Properties Is Overexpressed in Prostate Cancer.
Biomed Res Int. 2016; 2016:6963582 [PubMed] Free Access to Full Article Related Publications
Novel molecular targets are being searched to aid in prostate cancer diagnosis and therapy. Recently, ZFP91 zinc finger protein has been found to be upregulated in prostate cancer cell lines. It is a potentially important oncogenic protein; however only limited data regarding its biological function and expression patterns are available. To date, ZFP91 has been shown to be a key factor in activation of noncanonical NF-κB signaling pathway as well as to be involved in HIF-1α signaling in cancer cells. The present study aimed to characterize ZFP91 expression in prostate cancer specimens. Furthermore, since our earlier reports showed discrepancies between ZFP91 mRNA and protein levels, we studied this interrelationship in LNCaP and PC-3 prostate cancer cell lines using siRNA mediated knockdown. QPCR analysis revealed marked upregulation of ZFP91 mRNA in the majority of prostate cancer specimens. Transfection of prostate cancer cells with ZFP91 siRNA resulted in a 10-fold decrease in mRNA levels. On a protein level, however, no inhibitory effect was observed over the time of the cell culture. We conclude that ZFP91 is overexpressed in prostate cancer and that potential accumulation of the ZFP91 protein in studied cells may be of importance in prostate cancer biology.

Koo KM, Wee EJ, Trau M
High-speed biosensing strategy for non-invasive profiling of multiple cancer fusion genes in urine.
Biosens Bioelectron. 2017; 89(Pt 2):715-720 [PubMed] Related Publications
Aberrant chromosal rearrangements, such as the multiple variants of TMPRSS2:ERG fusion gene mutations in prostate cancer (PCa), are promising diagnostic and prognostic biomarkers due to their specific expression in cancerous tissue only. Additionally, TMPRSS2:ERG variants are detectable in urine to provide non-invasive PCa diagnostic sampling as an attractive surrogate for needle biopsies. Therefore, rapid and simplistic assays for identifying multiple urinary TMPRSS2:ERG variants are potentially useful to aid in early cancer detection, immediate patient risk stratification, and prompt personalized treatment. However, current strategies for simultaneous detection of multiple gene fusions are limited by tedious and prolonged experimental protocols, thus limiting their use as rapid clinical screening tools. Herein, we report a simple and rapid gene fusion strategy which expliots the specificity of DNA ligase and the speed of isothermal amplification to simultaneously detect multiple fusion gene RNAs within a short sample-to-answer timeframe of 60min. The method has a low detection limit of 2 amol (1000 copies), and was successfully applied for non-invasive fusion gene profiling in patient urine samples with subsequent validation by a PCR-based gold standard approach.

Oliveira JS, Ferreira RS, Santos LM, et al.
Self-declared ethnicity and genomic ancestry in prostate cancer patients from Brazil.
Genet Mol Res. 2016; 15(4) [PubMed] Related Publications
Some studies of polymorphisms in prostate cancer (PCa) analyze individuals in a uniform manner, regardless of genetic ancestry. However, PCa aggressiveness differs between subjects of African descent and those of European extraction. Thus, genetic ancestry analysis may be used to detect population stratification in case-control association studies. We genotyped 11 ancestry informative markers to estimate the contributions of African, European, and Amerindian ancestries in a case-control sample of 213 individuals from Bahia State, Northeast Brazil, including 104 PCa patients. We compared this data with self-reported ancestry and the stratification of cases by PCa aggressiveness according to Gleason score. A larger African genetic contribution (44%) was detected among cases, and a greater European contribution (61%) among controls. Self-declaration data revealed that 74% of PCa patients considered themselves non-white (black and brown), and 41.3% of controls viewed themselves as white. Our data showed a higher degree of European ancestry among fast-growing cancer cases than those of intermediate and slow development. This differs from many previous studies, in which the prevalence of African ancestry has been reported for all grades. Differences were observed between degrees of PCa aggressiveness in terms of genetic ancestry. In particular, the greater European contribution among patients with high-grade PCa indicates that a population's genetic structure can influence case-control studies. This investigation contributes to our understanding of the genetic basis of tumor aggressiveness among groups of different genetic ancestries, especially admixed populations, and has significant implications for the assessment of inter-population heterogeneity in drug treatment effects.

Shahbazi S, Khorasani M, Mahdian R
Gene expression profile of FVII and AR in primary prostate cancer.
Cancer Biomark. 2016; 17(3):353-358 [PubMed] Related Publications
OBJECTIVES: The ectopic expression of coagulation Factor VII has been shown in various cancers. Recently, F7 gene has been identified as a direct target of the androgen receptor in breast cancer. In this study, we examined the mRNA expression of F7 and AR in clinical sample series of prostate cancer and BPH.
MATERIAL AND METHODS: All the prostate cancer patients were new cases with no medical history of surgery or chemotherapy. The tissue samples were assigned as either prostate cancer tumor (n= 45) harboring at least 80% tumor cell content, or BPH (n= 36). Relative AR and F7 mRNA expression in each tissue sample was normalized to the mean of the Ct values determined for GAPDH and PSA genes.
RESULTS: Mean plasma level of prostate specific antigen (PSA) was 17.82 ± 3.71 ng/ml and 7.71 ± 1.28 ng/ml (Mean ± SEM) in PCa and BPH group, respectively. AR mean expression was up-regulated 22.468 fold in clinical tumor sample cohort (S.E., 0.175-2,916, 95% CI: 0.001-126,764, P= 0.001). The mean expression of F7 gene in tumor tissues relative to PBH samples was 6.981 (S.E., 0.099-413.001, 95% CI: 0.002-34,183, P= 0.012). ANOVA analysis of the gene expression results showed significant correlation between F7 and AR mRNA expression in tumor samples (p< 0.001).
CONCLUSIONS: Our study findings suggest a link between FVII and AR in prostate cancer pathogenesis. F7 gene expression could be up-regulated via various AR mediators affecting the promoter region of the F7 gene. Should this be confirmed by further studies, it may be suggested as a potential contributing factor in prostate cancer.

Chelluri R, Caza T, Woodford MR, et al.
Valproic Acid Alters Angiogenic and Trophic Gene Expression in Human Prostate Cancer Models.
Anticancer Res. 2016; 36(10):5079-5086 [PubMed] Related Publications
BACKGROUND/AIM: Only a minority of men succumb to prostate cancer (PCa). Therapy to prevent progression would change treatment paradigms. We investigated the effect of valproic acid (VPA) on PCa cell proliferation and the effects on both angiogenesis and PCa-specific signaling.
MATERIALS AND METHODS: LNCaP cells were treated with VPA for 72 h and proliferation was measured. Cellular RNA extracts were used to measure gene expression with RT-profiler(2) arrays. Genes with alterations were validated using real-time polymerase chain reaction and western blot.
RESULTS: VPA led to a dose-dependent decrease in proliferation. Expression array data revealed an impact on modulators of angiogenesis. Additionally, several cell-cycle control transcripts were affected. There was a strong correlation between gene and protein expression levels for validated targets.
CONCLUSION: VPA decreases cellular proliferation of PCa cells in vitro and also affects gene expression suggestive of anti-angiogenic effect with a concomitant decrease in proliferation-related genes.

Qi P, Cao M, Song L, et al.
The biological activity of cationic liposomes in drug delivery and toxicity test in animal models.
Environ Toxicol Pharmacol. 2016; 47:159-164 [PubMed] Related Publications
In the study we made use of DOTAP (1,2-dioleoyl-3-trimethylammonium), DOPE (1,2-dioleoyl-snglycero-3-phosphoethanolamine) and PEG-PE (polyethylene glycol- polyethylene) to make cationic PEG-liposomes by ultrasonic dispersion method. The plasmid pGPU6 combined with cationic PEG-liposomes or Liopofectamin 2000 was used to transfect PC3 cells to judge the transfection efficiency. HE staining showed that the pGUP6-shAurora B plasmid/liposomes complex could significantly inhibit tumor growth in mice tumor model. The results indicated that there was no remarkable difference between the homemade liposomes and Lipofectamin 2000 after transfection, with transfection efficiency over 80%. And the homemade liposomes also had high transfection efficiency in vivo. No significant side effects were observed on weight, coat condition, behavior or appetite and the life span of mice treated with pGPU6-shAurora B were extended. Beyond that, there were no differences in mortality or in pathological changes to the heart, liver, spleen, lungs and kidneys among all the mice.

Guo K, Zheng S, Xu Y, et al.
Loss of miR-26a-5p promotes proliferation, migration, and invasion in prostate cancer through negatively regulating SERBP1.
Tumour Biol. 2016; 37(9):12843-12854 [PubMed] Related Publications
The biological role of miR-26a involved in the carcinogenesis of prostate cancer (PC) has been controversial. Besides, the underlying mechanism by which miR-26a plays a role in PC has been unclear. To investigate the role of miR-26a-5p in the PC, miR-26a-5p was detected and statistically analyzed in clinical PC tissues and a panel of PC cell lines. Using bioinformatics analysis, we found that serpine1 messenger RNA (mRNA) binding protein 1 (SERBP1) was a potential downstream target of miR-26a-5p. Using luciferase reporter and western blot, we identified that miR-26a-5p negatively regulated SERBP1 on the PC cell line level. It was confirmed that miR-26a-5p was markedly downregulated in PC tissues compared with normal controls whose reduced expression was significantly associated with metastasis and poor overall prognosis and found that miR-26a-5p was able to prevent proliferation and motility of PC cells in vitro. Additionally, SERBP1 was identified as a downstream target of miR-26a-5p. Moreover, it was observed that SERBP1 was markedly upregulated in prostate cancer tissues and was significantly associated with tissue metastasis and Gleason score. Taken together, our results for the first time demonstrate that the loss of miR-26a-5p promotes proliferation, migration, and invasion through targeting SERBP1 in PC, supporting the tumor-suppressing role of miR-26a-5p in PC.

Jiang H, Mao X, Huang X, et al.
TMPRSS2:ERG fusion gene occurs less frequently in Chinese patients with prostate cancer.
Tumour Biol. 2016; 37(9):12397-12402 [PubMed] Related Publications
Prostate cancer is the commonest male malignancy in the Western world, but its morbidity is much lower in China. The principal aim of this study was to evaluate the frequency of TMPRSS2:ERG fusion in Chinese prostate cancer patients using immunohistochemistry and reverse transcription polymerase chain (RT-PCR). In addition, we compared the ERG protein expression with TMPRSS2:ERG fusion gene. The relationship between ERG expression and clinicopathologic features was also examined. Samples from patients who underwent radical prostatectomies in Changhai Hospital (Shanghai, China) were collected and stored in ethically approved tissue banks. One hundred seventy-four prostate cancer tissue samples and 10 normal tissues were marked on standard hematoxylin-eosin (HE) sections, punched out of the paraffin blocks and inserted into a recipient block using tissue arrayer instruments. Immunohistochemistry and RT-PCR were employed to detect TMPRSS2:ERG fusion gene. ERG was highly expressed in the nuclei of endothelial cells of vessels and weak cytoplasmic staining was occasionally observed. ERG positive staining was present in 14.9 % (26/174) of the tumor samples in microarray. All benign prostate samples were found to be negative. RT-PCR results revealed that 11.1 % (15/135) were TMPRSS2:ERG fusion positive. Altogether, there was a good agreement of ERG immunostaining with the presence of TMPRSS2:ERG. However, no correlation was observed between ERG expression and age, Gleason score, stage, surgical margin, and seminal vesicle involvement in Chinese patients. In the present study, we identified a high correlation between ERG expression and ERG TMPRSS2:ERG, with 100 % sensitivity and 88.9 % specificity. The expression level of ERG was unrelated to the age, Gleason score, stage, surgical margin, and seminal vesicle involvement. Therefore, the association between ERG expression and prostate cancer based on Chinese population should be further investigated in the future.

Zhang Y, Huang Y, Jin Z, et al.
A convenient and effective strategy for the enrichment of tumor-initiating cell properties in prostate cancer cells.
Tumour Biol. 2016; 37(9):11973-11981 [PubMed] Related Publications
Stem-like prostate cancer (PrCa) cells, also called PrCa stem cells (PrCSCs) or PrCa tumor-initiating cells (PrTICs), are considered to be involved in the mediation of tumor metastasis and may be responsible for the poor prognosis of PrCa patients. Currently, the methods for PrTIC sorting are mainly based on cell surface marker or side population (SP). However, the rarity of these sorted cells limits the investigation of the molecular mechanisms and therapeutic strategies targeting PrTICs. For PrTIC enrichment, we induced cancer stem cell (CSC) properties in PrCa cells by transducing three defined factors (OCT3/4, SOX2, and KLF4), followed by culture with conventional serum-containing medium. The CSC properties in the transduced cells were evaluated by proliferation, cell cycle, SP assay, drug sensitivity technology, in vivo tumorigenicity, and molecular marker analysis of PrCSCs compared with parental cells and spheroids. After culture with serum-containing medium for 8 days, the PrCa cells transduced with the three factors showed significantly enhanced CSC properties in terms of marker gene expression, sphere formation, chemoresistance to docetaxel, and tumorigenicity. The percentage of CD133(+)/CD44(+) cells was ninefold higher in the transduced cell population than in the adherent PC3 cell population (2.25 ± 0.62 vs. 0.25 ± 0.12 %, respectively), and the SP increased to 1.22 ± 0.18 % in the transduced cell population, but was undetectable in the adherent population. This method can be used to obtain abundant PrTIC material and enables a complete understanding of PrTIC biology and development of novel therapeutic agents targeting PrTICs.

Zhang Y, Zhang P, Wan X, et al.
Downregulation of long non-coding RNA HCG11 predicts a poor prognosis in prostate cancer.
Biomed Pharmacother. 2016; 83:936-941 [PubMed] Related Publications
Long non-coding RNAs (lncRNA) have been reported as key regulators in the progression and metastasis of prostate cancer (PCa). In this study, we found that the expression levels of HCG11 in PCa tissues were significantly lower than those in non-tumor tissues in publically available databases and in human PCa samples. Our results showed the expression levels of HCG11 in patients with PCa were associated with the age, Lymph Node Status (LN status), preoperative PSA level, Gleason score, and biochemical recurrence (BCR). Kaplan-Meier analysis indicated that downregulation of HCG11 expression in tissues was associated with poor survival of PCa patients. GO and KEGG pathway analysis were applied to explore the potential roles of HCG11. Moreover, a HCG11 mediated ceRNA network was built using co-expression relationships of the differentially expressed mRNAs and miRNAs. We believed that this study will provide a potential new therapeutic and prognostic target for prostate cancer.

Gao T, Mei Y, Sun H, et al.
The association of Phosphatase and tensin homolog (PTEN) deletion and prostate cancer risk: A meta-analysis.
Biomed Pharmacother. 2016; 83:114-121 [PubMed] Related Publications
OBJECTIVE: Phosphatase and tensin homolog (PTEN) deleted on chromosome 10, a tumor suppressor that negatively regulates the phosphoinositide-3-kinase(PI3K) which has been implicated in a number of human malignancies including prostate cancer. However the prognostic value of PTEN deletion in prostate cancer patient's diagnosis and the mechanism of PTEN deletion in prostate cancer development still remain unclear.
METHOD: A meta-analysis of 26 published studies including 8097 prostate cancer patients was performed.
RESULTS: Compared to PTEN normal patients, PTEN deletion patients showed a higher aggressive Gleason score(OR: 1.284, 95%CI=1.145-1.439) and pathological stage(OR: 1.628, 95%CI=1.270-2.087) which generally had a higher risk in prostate replace(HR: 1.738, 95%CI=1.264-2.390). Significant association between PTEN deletion and ERG rearrangements in prostate cancer development was also proved that compared to PTEN normal patients, patients with PTEN deletion showed a higher risk in ERG rearrangements(OR: 1.345, 95%CI=1.102-1.788).
CONCLUSION: This study indicated that patients with PTEN deletion were associated with higher pathological stage or Gleason score and a higher risk in prostate cancer replace potentially represent a novel clinically relevant event to identify individuals at increased risk for the occurrence, progression and prognosis of prostate cancer. Prostate cancer patients with PTEN deletion usually had a higher risk in ERG rearrangements than other patients may be a potential new area for identifying poor prognosis patients and selecting patients for targeted therapies which required confirmation through adequately designed prospective studies.

Rudnicka C, Mochizuki S, Okada Y, et al.
Overexpression and knock-down studies highlight that a disintegrin and metalloproteinase 28 controls proliferation and migration in human prostate cancer.
Medicine (Baltimore). 2016; 95(40):e5085 [PubMed] Free Access to Full Article Related Publications
Prostate cancer is one of the most prevalent cancers in men. It is critical to identify and characterize oncogenes that drive the pathogenesis of human prostate cancer. The current study builds upon previous research showing that a disintegrin and metallproteinase (ADAM)28 is involved in the pathogenesis of numerous cancers. Our novel study used overexpression, pharmacological, and molecular approaches to investigate the biological function of ADAM28 in human prostate cancer cells, with a focus on cell proliferation and migration. The results of this study provide important insights into the role of metalloproteinases in human prostate cancer.The expression of ADAM28 protein levels was assessed within human prostate tumors and normal adjacent tissue by immunohistochemistry. Immunocytochemistry and western blotting were used to assess ADAM28 protein expression in human prostate cancer cell lines. Functional assays were conducted to assess proliferation and migration in human prostate cancer cells in which ADAM28 protein expression or activity had been altered by overexpression, pharmacological inhibition, or by siRNA gene knockdown.The membrane bound ADAM28 was increased in human tumor biopsies and prostate cancer cell lines. Pharmacological inhibition of ADAM28 activity and/or knockdown of ADAM28 significantly reduced proliferation and migration of human prostate cancer cells, while overexpression of ADAM28 significantly increased proliferation and migration.ADAM28 is overexpressed in primary human prostate tumor biopsies, and it promotes human prostate cancer cell proliferation and migration. This study supports the notion that inhibition of ADAM28 may be a potential novel therapeutic strategy for human prostate cancer.

Kim H, Skowronski J, Den RB
Prognostic outlier genes for enhanced prostate cancer treatment.
Future Oncol. 2017; 13(3):249-261 [PubMed] Related Publications
AIM: To review the current landscape of outlier genes in the field of prostate cancer.
METHODS: A comprehensive review was performed.
RESULTS: Prostate cancer continues to be a significant worldwide health issue. In the era of personalized medicine, more emphasis is being placed on the ability to determine the timing, intensity and type of treatment, according to each patient's unique disease. Several commercial tests are available to determine the risk of aggressive prostate cancer based on genomic biomarkers and gene expression. Outlier genes represent a form of cancer classification that focuses on bimodal expression of a gene in a specific subset of patients. Outlier genes identified in prostate cancer include TMPRSS2-ERG, SPINK1, ScHLAP1, NVL, SMC4 and SQLE.
CONCLUSION: Classifying patient prostate cancers by outlier genes may allow for individualized cancer therapies and improved cancer therapy outcomes.

Choi HE, Shin JS, Leem DG, et al.
6-(3,4-Dihydro-1H-isoquinoline-2-yl)-N-(6-methoxypyridine-2-yl) nicotinamide-26 (DIMN-26) decreases cell proliferation by induction of apoptosis and downregulation of androgen receptor signaling in human prostate cancer cells.
Chem Biol Interact. 2016; 260:196-207 [PubMed] Related Publications
Previously, we reported that 6-(3,4-dihydro-1H-isoquinolin-2-yl)-N-(6-methylpyridin-2-yl) nicotinamide (DIMN) analogues inhibited the growth of prostate cancer cells as an anti-androgenic compound. In the present study, we evaluated cytotoxic effects of these DIMN derivatives and found that DIMN-26 most potently inhibited the proliferation of the LNCap-LN3 androgen-dependent and DU145 androgen-independent prostate cancer cells through induction of G2/M phase cell cycle arrest and subsequent apoptosis. The G2/M phase arrest was found due to increases in the activation of cdc2 (also known as cyclin-dependent kinase 1, CDK1)/cyclin B1 complex. DIMN-26 also induced apoptosis in LNCap-LN3 and DU145 prostate cancer cells through activation of caspase-3, -8, and -9, and cleavage of poly(ADP-ribose) polymerase-1 (PARP-1). In addition, DIMN-26 caused the dephosphorylation and mitochondrial accumulation of Bad protein and induced the loss of mitochondria membrane potential, consequently releasing cytochrome c into the cytosol of the cell. Furthermore, overexpression of AKT protein significantly reduced DIMN-26-induced PARP-1 cleavage and p-Bad decrease and cdc2 activation. In addition, DIMN-26 inhibited the 5α-dihydrotestosterone (DHT)-induced cell growth and proliferation and nuclear translocation and transcriptional activities of androgen receptor (AR) in LNCap-LN3 prostate cancer cells. Consistent with these findings, DIMN-26 significantly inhibited the DHT-induced expression of AR-response genes (ARGs), such as prostate-specific antigen (PSA), AR, β2-microglobulin (B2M), selenoprotein P (SEPP1), and ste20-related proline-alanine-rich kinase (SPAK) in LNCap-LN3 prostate cancer cells. Taken together, these results suggest that DIMN-26 plays a therapeutic role not only in induction of G2/M arrest and apoptosis but also in suppression of androgen receptor signaling in androgen-dependent and androgen-independent prostate cancer cells.

Huang WJ, Wu LJ, Min ZC, et al.
Interleukin-6 -572G/C polymorphism and prostate cancer susceptibility.
Genet Mol Res. 2016; 15(3) [PubMed] Related Publications
Strong evidence suggests that cancer-associated inflammation promotes tumor growth and progression, and interleukin-6 (IL6) is an important modulator of inflammation. However, the roles of IL6 and mutations of its corresponding gene in prostate cancer have not been clearly documented. We retrieved data from the Oncomine database concerning IL6 expression in prostate cancer and its role in prostate-specific antigen (PSA) recurrence. We also performed a case-control study of the IL6 -572G/C polymorphism (rs1800796) in 236 sporadic prostate cancer patients and 256 healthy controls from a southern Han Chinese population. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated to assess the association between rs1800796 and prostate cancer susceptibility. A dual-luciferase reporter assay was used to test the transcriptional activity of the IL6 promoter G and C alleles. IL6 was overexpressed in prostate cancer tissues compared to normal tissues, especially in those with higher Gleason scores. Moreover, elevated IL6 expression was associated with high PSA recurrence rate in Oncomine data. Our case-control study demonstrated that compared with the -572C allele, the -572G allele conferred a borderline increased risk of prostate cancer (OR = 1.31, 95%CI = 0.99-1.74, P = 0.061). This was more pronounced in the subgroup of individuals having never smoked (OR = 1.85, 95%CI = 1.07-3.22). Moreover, the G allele showed increased activity relative to the C allele in the dual-luciferase reporter assay. Our results suggest that the -572G/C polymorphism may be associated with IL6 expression, which in turn plays a role in prostate cancer development.

Ceylan GG, Ceylan C, Gülmemmedov B, et al.
Polymorphisms of eNOS, catalase, and myeloperoxidase genes in prostate cancer in Turkish men: preliminary results.
Genet Mol Res. 2016; 15(3) [PubMed] Related Publications
Prostate cancer (PCa) is the most common type of neoplasm in European males. Genetic and epigenetic factors contribute to PCa development and progression. In this study, we aimed to assess the relationship between PCa and polymorphisms in the genes encoding endothelial nitric oxide synthase (eNOS), catalase (CAT), and myeloperoxidase (MPO). In total, 193 patients were included in the study. Patients were divided into three groups: PCa (78), benign prostate hyperplasia (40), and control males (75). The parameters assessed included body mass index (BMI), smoking habits, presence of prostatism, prostate-specific antigen (PSA) levels, Gleason scores of prostate specimens, as well as polymorphisms in eNOS-G894T, CAT- 262T, and MPO G-463T genes. BMI and smoking status of controls and patient groups showed no significant difference. CAT-262T gene polymorphism was found to be homozygous in 35.4% of PCa patients, which was 4.02-fold that in the controls (P = 0.006). There was no statistically significant difference in eNOS-G894T and MPO G-463T gene polymorphisms between any of the groups. In conclusion, we found catalase levels to be associated with PCa diagnosis and PSA value. We did not find any significant differences between groups for other polymorphisms, but we believe that further studies with a large sample size may be needed before drawing definite conclusions.

Díaz P, Cardenas H, Orihuela PA
Red Maca (Lepidium meyenii) did not affect cell viability despite increased androgen receptor and prostate-specific antigen gene expression in the human prostate cancer cell line LNCaP.
Andrologia. 2016; 48(8):922-6 [PubMed] Related Publications
We examined whether aqueous extract of Lepidium meyenii (red Maca) could inhibit growth, potentiate apoptotic activity of two anticancer drugs Taxol and 2-methoxyestradiol (2ME) or change mRNA expression for the androgen target genes, androgen receptor (Ar) and prostate-specific antigen (Psa) in the human prostate cancer cell line LNCaP. Red Maca aqueous extract at 0, 10, 20, 40 or 80 μg/ml was added to LNCaP cells, and viability was evaluated by the MTS assay at 24 or 48 hr after treatment. Furthermore, LNCaP cells were treated with 80 μg/ml of red Maca plus Taxol or 2ME 5 μM and viability was assessed 48 hr later. Finally, LNCaP cells were treated with red Maca 0, 20, 40 or 80 μg/ml, and 12 hr later, mRNA level for Ar or Psa was assessed by real-time PCR. Treatment with red Maca did not affect viability of LNCaP cells. Apoptotic activity induced by Taxol and 2ME in LNCaP cells was not altered with red Maca treatment. Relative expression of the mRNA for Ar and Psa increased with red Maca 20 and 40 μg/ml, but not at 80 μg/ml. We conclude that red Maca aqueous extract does not have toxic effects, but stimulates androgen signalling in LNCaP cells.

Kong X, Qian X, Duan L, et al.
microRNA-372 Suppresses Migration and Invasion by Targeting p65 in Human Prostate Cancer Cells.
DNA Cell Biol. 2016; 35(12):828-835 [PubMed] Article available free on PMC after 01/12/2017 Related Publications
Prostate cancer (PCa) is one of the most prevalent malignant tumors. microRNAs (miRNAs) play an important role in cancer initiation, progression, and metastasis, and their roles in PCa are becoming more apparent. In this study, we found that microRNA-372 (miR-372) is downregulated in human PCa and inhibits the proliferation activity, migration, and invasion of DU145 cells. Subsequently, p65 is confirmed as a target of miR-372, and knockdown of p65 expression similarly resulted in decreased proliferation activity, migration, and invasion. CDK8, MMP-9, and prostate-specific antigen were involved in both these processes. Taken together, our results show evidence that miR-372 may function as a tumor suppressor gene by regulating p65 in PCa and may provide a strategy for blocking PCa metastasis.

Kulda V, Topolcan O, Kucera R, et al.
Prognostic Significance of TMPRSS2-ERG Fusion Gene in Prostate Cancer.
Anticancer Res. 2016; 36(9):4787-93 [PubMed] Related Publications
BACKGROUND/AIM: Current research of prostate cancer (PCa) offers a promising way of identifying patients with adverse prognosis who do benefit from radical treatment that can affect quality of life as resections are associated with numerous side-effects. The aim of our study was to evaluate the relationship of TMPRSS2-ERG fusion gene status, tumor tissue prostate-specific antigen (PSA), prostate cancer antigen 3 (PCA3), miR-23b, miR-26a and miR-221 expression levels in combination with preoperative serum PSA level to the risk of PCa recurrence after radical prostatectomy.
PATIENTS AND METHODS: The study group consisted of 108 patients who underwent radical prostatectomy. PSA was measured in peripheral blood collected preoperativelly. The expression of TMPRSS2-ERG transcript and the expression of miR-23b, miR-26a and miR-221 in formalin-fixed, paraffin-embedded (FFPE) tumor tissues was analyzed by reverse transcription (RT) real-time polymerase chain reaction (PCR).
RESULTS: Significantly shorter time to recurrence was observed in patients with high expression of TMPRSS2-ERG (p=0.0020). High levels of preoperative PSA (>10.0 ng/ml) proved to be marker of shorter time to recurrence (p=0.0153). The most promising marker of the risk of recurrence after radical prostatectomy was a combination of high level of preoperative serum PSA and high expression of TMPRSS2-ERG fusion transcript in tumor tissue (p=0.0001).
CONCLUSION: A combination of high preoperative serum PSA and high expression of TMPRSS2-ERG could be promising in distinguishing those tumors that are aggressive and life-threatening.

Mahajan N
Signatures of prostate-derived Ets factor (PDEF) in cancer.
Tumour Biol. 2016; 37(11):14335-14340 [PubMed] Related Publications
The Ets proteins are a family of transcription factors characterized by an evolutionarily conserved DNA-binding domain and have diverse biological functions including tumor suppressor as well as tumor promoter functions. They are regulated via a complex and diverse number of mechanisms and control key cellular processes. Prostate-derived Ets transcription factor (PDEF), a unique member of the ETS family, is present in tissues with high epithelial content are hormone-regulated, such as prostate, breast, salivary glands, ovaries, colon, airways, and stomach tissues. PDEF (prostate-derived Ets factor) is also referred to as SPDEF (SAM pointed domain containing Ets transcription factor), PSE (mouse homolog), or hPSE (human PSE) in the literature and is the sole member of the PDEF ETS sub-family. The role of PDEF in cancer development is still not fully elucidated though. The present article focuses on the key findings about the PDEF's biological functions, interacting proteins, and its target genes. There is a strong urge to focus on the clinical studies in larger cohort, which elucidate the regulation of PDEF and its target genes, to determine the potential of PDEF as biomarker. Based on the studies discussed in the present article, one can anticipate that PDEF offers a great potential for developing therapeutics against cancer.

Hashemi M, Moradi N, Rezaei M, et al.
ERBB4 gene polymorphisms and the risk of prostate cancer in a sample of Iranian Population.
Cell Mol Biol (Noisy-le-grand). 2016; 62(10):43-8 [PubMed] Related Publications
Genetic polymorphisms in ERBB4 are thought to be associated with cancer susceptibility. In the present study, we aimed to assess the impact of ERBB4 rs12052398 T>C, rs13393577 A>G, rs13424871 A>T, rs16847082 A>G and rs6147150 (12-bp I/D) polymorphisms on risk of prostate cancer (PCa) in a sample of Iranian population. In a case-control study, we enrolled 169 patients with pathologically confirmed PCa and 182 subjects with benign prostatic hyperplasia (BPH). No significant association was found among ERBB4 polymorphisms and risk of PCa. Subjects carrying TT/AA/AA/AG/ID, TC/AA/AA/AA/II, TT/AA/AT/AA/II and TT/AA/AT/AG/ID genotypes are associated with a decreased risk of PCa. Our findings suggest that haplotypes CAAAI and TAAAD (rs12052398, rs13393577, rs13424871, rs16847082 and rs6147150I) of the ERBB4 polymorphisms are associated with a significantly lower risk of PCa. Further studies with a larger sample sizes and diverse ethnicities are necessary to verify our findings.

Martignano F, Gurioli G, Salvi S, et al.
GSTP1 Methylation and Protein Expression in Prostate Cancer: Diagnostic Implications.
Dis Markers. 2016; 2016:4358292 [PubMed] Article available free on PMC after 01/12/2017 Related Publications
GSTP1 belongs to the GSTs family, a group of enzymes involved in detoxification of exogenous substances and it also plays an important role in cell cycle regulation. Its dysregulation correlates with a large variety of tumors, in particular with prostate cancer. We investigated GSTP1 methylation status with methylation specific PCR (MS-PCR) in prostate cancer (PCa) and in benign tissue of 56 prostatectomies. We also performed immunohistochemistry (IHC) so as to correlate gene methylation with gene silencing. GSTP1 appears methylated in PCa and not in healthy tissue; IHC confirmed that methylation leads to protein underexpression (p < 0.001). GSTP1 is highly expressed in basal cell layer and luminal cells in benign glands while in prostatic intraepithelial neoplasia (PIN) it stains only basal cell layer, whereas PCa glands are completely negative. We demonstrated that methylation leads to underexpression of GSTP1. The progressive loss of GSTP1 expression from healthy glands to PIN and to PCa glands underlines its involvement in early carcinogenesis.

García-Tobilla P, Solórzano SR, Salido-Guadarrama I, et al.
SFRP1 repression in prostate cancer is triggered by two different epigenetic mechanisms.
Gene. 2016; 593(2):292-301 [PubMed] Related Publications
Worldwide, prostate cancer (PCa) is the second cause of death from malignant tumors among men. Establishment of aberrant epigenetic modifications, such as histone post-translational modifications (PTMs) and DNA methylation (DNAme) produce alterations of gene expression that are common in PCa. Genes of the SFRP family are tumor suppressor genes that are frequently silenced by DNA hypermethylation in many cancer types. The SFRP family is composed of 5 members (SFRP1-5) that modulate the WNT pathway, which is aberrantly activated in PCa. The expression of SFRP genes in PCa and their regulation by DNAme has been controversial. Our objective was to determine the gene expression pattern of the SFRP family in prostatic cell lines and fresh frozen tissues from normal prostates (NP), benign prostatic hyperplasia (BPH) and prostate cancer (PCa), by qRT-PCR, and their DNAme status by MSP and bisulfite sequencing. In prostatic cancer cell lines, the 5 SFRPs showed significantly decreased expression levels compared to a control normal prostatic cell line (p<0.0001). In agreement, SFRP1 and SFRP5 genes showed decreased expression levels in CaP fresh frozen tissues compared to NP (p<0.01), while a similar trend was observed for SFRP2. Conversely, increased levels of SFRP4 expression were found in PCa compared to BPH (p<0.01). Moreover, SFRP2, SFRP3, and SFRP5 showed DNA hypermethylation in PCa cell lines. Interestingly, we observed DNA hypermethylation at the promoter of SFRP1 in the PC3 cell line, but not in LNCaP. However, in the LNCaP cell line we found an aberrant gain of the repressive histone posttranslational modification Histone H3 lysine 27 trimethylation (H3K27me3). In conclusion, decreased expression by DNA hypermethylation of SFRP5 is a common feature of PCa, while decreased expression of SFRP1 can be due to DNA hypermethylation, but sometimes an aberrant gain of the histone mark H3K27me3 is observed instead.

Caspar A, Mostertz J, Leymann M, et al.
In Vitro Cultivation of Primary Prostate Cancer Cells Alters the Molecular Biomarker Pattern.
In Vivo. 2016 09-10; 30(5):573-9 [PubMed] Related Publications
BACKGROUND/AIM: The high variability of primary cells propagated in vitro led us to study the expression patterns of 11 most commonly accepted and widely used biomarkers specific for prostate cancer (PC) cells in primary cell models.
MATERIALS AND METHODS: Primary PC cells from five PC patients were partially subjected to RNA preparation immediately and remaining cells were propagated up to 84 days followed by RNA preparation. Subsequently, biomarker mRNA quantification was performed by quantitative reverse transcription-polymerase chain reaction (RT-PCR) and biomarker transcript concentrations before and after cultivation of primary PC cells were compared.
RESULTS: Evaluation of androgen receptor, prostate-specific antigen, acid phosphatase, prostate-specific membrane antigen, fatty acid synthase, cytokeratin types 5/8/19, E-cadherin, epithelial cell adhesion molecule and fibroblast-specific protein 1 demonstrated temporal changes, as well as individual differences in expression, during primary PC cell propagation.
CONCLUSION: Experimental design, as well as data evaluation, may need to take under consideration the high variability of biomarker expression in primary PC cells.

Erdmann K, Kaulke K, Rieger C, et al.
MiR-26a and miR-138 block the G1/S transition by targeting the cell cycle regulating network in prostate cancer cells.
J Cancer Res Clin Oncol. 2016; 142(11):2249-61 [PubMed] Related Publications
PURPOSE: The tumor-suppressive microRNAs miR-26a and miR-138 are significantly down-regulated in prostate cancer (PCa) and have been identified as direct regulators of enhancer of zeste homolog 2 (EZH2), which is a known oncogene in PCa. In the present study, the influence of miR-26a and miR-138 on EZH2 and cellular function including the impact on the cell cycle regulating network was evaluated in PCa cells.
METHODS: PC-3 and DU-145 PCa cells were transfected with 100 nM of miRNA mimics, siRNA against EZH2 (siR-EZH2) or control constructs for 4 h. Analyses of gene expression and cellular function were conducted 48 h after transfection.
RESULTS: Both miRNAs influenced the EZH2 expression and activity only marginally, whereas siR-EZH2 led to a notable decrease of the EZH2 expression and activity. Both miRNAs inhibited short- and/or long-term proliferation of PCa cells but showed no effect on viability and apoptosis. In PC-3 cells, miR-26a and miR-138 caused a significant surplus of cells in the G0/G1 phase of 6 and 12 %, respectively, thus blocking the G1/S-phase transition. Treatment with siR-EZH2 was without substantial influence on cellular function and cell cycle. Therefore, alternative target genes involved in cell cycle regulation were identified in silico. MiR-26a significantly diminished the expression of its targets CCNE1, CCNE2 and CDK6, whereas CCND1, CCND3 and CDK6 were suppressed by their regulator miR-138.
CONCLUSIONS: The present findings suggest an anti-proliferative role for miR-26a and miR-138 in PCa by blocking the G1/S-phase transition independent of EZH2 but via a concerted inhibition of crucial cell cycle regulators.

Recurrent Structural Abnormalities

Selected list of common recurrent structural abnormalities

Abnormality Type Gene(s)
del(8p22) in Prostate CancerDeletion
ERG-TMPRSS2 Fusion in Prostate CancerIntronic Deletion or TranslocationERG (21q22.3)TMPRSS2 (21q22.3)
ETV1 translocations in Prostate CancerTranslocationETV1 (7p21.3)TMPRSS2 (21q22.3)

This is a highly selective list aiming to capture structural abnormalies which are frequesnt and/or significant in relation to diagnosis, prognosis, and/or characterising specific cancers. For a much more extensive list see the Mitelman Database of Chromosome Aberrations and Gene Fusions in Cancer.

del(8p22) in Prostate Cancer

Arbieva ZH, Banerjee K, Kim SY, et al.
High-resolution physical map and transcript identification of a prostate cancer deletion interval on 8p22.
Genome Res. 2000; 10(2):244-57 [PubMed] Free Access to Full Article Related Publications
A genomic interval of approximately 1-1.5 Mb centered at the MSR marker on 8p22 has emerged as a possible site for a tumor suppressor gene, based on high rates of allele loss and the presence of a homozygous deletion found in metastatic prostate cancer. The objective of this study was to prepare a bacterial contig of this interval, integrate the contig with radiation hybrid (RH) databases, and use these resources to identify transcription units that might represent the candidate tumor suppressor genes. Here we present a complete bacterial contig across the interval, which was assembled using 22 published and 17 newly originated STSs. The physical map provides twofold or greater coverage over much of the interval, including 17 BACs, 15 P1s, 2 cosmids, and 1 PAC clone. The position of the selected markers across the interval in relation to the other markers on the larger chromosomal scale was confirmed by RH mapping using the Stanford G3 RH panel. Transcribed units within the deletion region were identified by exon amplification, searching of the Human Transcript Map, placement of unmapped expressed sequence tags (ESTs) from the Radiation Hybrid Database (RHdb), and from other published sources, resulting in the isolation of six unique expressed sequences. The transcript map of the deletion interval now includes two known genes (MSR and N33) and six novel ESTs.

Bova GS, MacGrogan D, Levy A, et al.
Physical mapping of chromosome 8p22 markers and their homozygous deletion in a metastatic prostate cancer.
Genomics. 1996; 35(1):46-54 [PubMed] Related Publications
Numerous studies have implicated the short arm of chromosome 8 as the site of one or more tumor suppressor genes inactivated in carcinogenesis of the prostate, colon, lung, and liver. Previously, we identified a homozygous deletion on chromosome 8p22 in a metastatic prostate cancer. To map this homozygous deletion physically, long-range restriction mapping was performed using yeast artificial chromosomes (YACs) spanning approximately 2 Mb of chromosome band 8p22. Subcloned genomic DNA and cDNA probes isolated by hybrid capture from these YACs were mapped in relation to one another, reinforcing map integrity. Mapped single-copy probes from the region were then applied to DNA isolated from a metastatic prostate cancer containing a chromosome 8p22 homozygous deletion and indicated that its deletion spans 730-970 kb. Candidate genes PRLTS (PDGF-receptor beta-like tumor suppressor) and CTSB (cathepsin B) are located outside the region of homozygous deletion. Généthon marker D8S549 is located approximately at the center of this region of homozygous deletion. Two new microsatellite polymorphisms, D8S1991 and D8S1992, also located within the region of homozygous deletion on chromosome 8p22, are described. Physical mapping places cosmid CI8-2644 telomeric to MSR (macrophage scavenger receptor), the reverse of a previously published map, altering the interpretation of published deletion studies. This work should prove helpful in the identification of candidate tumor suppressor genes in this region.

Familial Prostate Cancer

Hereditary prostate cancer accounts for about 9% of cases. A prostate cancer susceptibility locus (HPC1) on chromosome 1q24-25 was idenified by Smith (1996). However, McIndoe (1997) found no evidence of HPC1 mutation in 49 high-risk families. Also in a study of "small" families [3-5 affected members], Dunsmuir (1998) found less than 8% of cases had allelic loss in HPC1. Other studies suggest that mutations in HPC1 are uncommon and are restricted to people with early onset disease.

Other candidate genes have been proposed. HPCX at chromosome Xq27-28 was identified by a large international linkage study of 360 families (Xu, 1998). Another locus - HPC2 (PCAP) on chromosome 1q42.2-q43 was proposed by Berthon (1998), though a subsequent linkage study (Gibbs, 1999) indicated this gene could only account for a small proportion of cases.

Other specific gene(s) associated with familial prostate cancer have yet to be identified.

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Cite this page: Cotterill SJ. Prostate Cancer- Molecular Biology, Cancer Genetics Web: http://www.cancer-genetics.org/X0904.htm Accessed:

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