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 08 August, 2015 using data from PubMed, MeSH and CancerIndex

Mutated Genes and Abnormal Protein Expression (554)

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, TFM, DHTR, SBMA, HYSP1, NR3C4, SMAX1, HUMARA -AR and Prostate Cancer
1221
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
PTEN 10q23.3 BZS, DEC, CWS1, GLM2, MHAM, TEP1, MMAC1, PTEN1, 10q23del -PTEN and Prostate Cancer
376
TP53 17p13.1 P53, BCC7, LFS1, TRP53 -TP53 and Prostate Cancer
343
CTNNB1 3p21 CTNNB, MRD19, armadillo -CTNNB1 and Prostate Cancer
312
BRCA1 17q21 IRIS, PSCP, BRCAI, BRCC1, FANCS, PNCA4, RNF53, BROVCA1, PPP1R53 -BRCA1 and Prostate Cancer
178
BRCA2 13q12.3 FAD, FACD, FAD1, GLM3, BRCC2, FANCD, PNCA2, FANCD1, XRCC11, BROVCA2 -BRCA2 and Prostate Cancer
156
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
120
SRD5A2 2p23 -SRD5A2 and Prostate Cancer
120
SRC 20q12-q13 ASV, SRC1, c-SRC, p60-Src -SRC and Prostate Cancer
97
KITLG 12q22 SF, MGF, SCF, FPH2, FPHH, KL-1, Kitl, SHEP7 -KITLG and Prostate Cancer
93
CDKN1B 12p13.1-p12 KIP1, MEN4, CDKN4, MEN1B, P27KIP1 -CDKN1B and Prostate Cancer
92
CD44 11p13 IN, LHR, MC56, MDU2, MDU3, MIC4, Pgp1, CDW44, CSPG8, HCELL, HUTCH-I, ECMR-III -CD44 and Prostate Cancer
87
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
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
76
EZH2 7q35-q36 WVS, ENX1, EZH1, KMT6, WVS2, ENX-1, EZH2b, KMT6A -EZH2 and Prostate Cancer
75
ETV1 7p21.3 ER81 Translocation
-ETV1 translocations in Prostate Cancer
73
GSTM1 1p13.3 MU, H-B, GST1, GTH4, GTM1, MU-1, GSTM1-1, GSTM1a-1a, GSTM1b-1b -GSTM1 and Prostate Cancer
72
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
CD82 11p11.2 R2, 4F9, C33, IA4, ST6, GR15, KAI1, SAR2, TSPAN27 -CD82 and Prostate Cancer
50
AMACR 5p13 RM, RACE, CBAS4, AMACRD -AMACR 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
47
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
44
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
FOS 14q24.3 p55, AP-1, C-FOS -FOS and Prostate Cancer
42
CASP9 1p36.21 MCH6, APAF3, APAF-3, PPP1R56, ICE-LAP6 -CASP9 and Prostate Cancer
40
VEGFA 6p12 VPF, VEGF, MVCD1 -VEGFA and Prostate Cancer
40
FOXA1 14q21.1 HNF3A, TCF3A -FOXA1 and Prostate Cancer
40
MET 7q31 HGFR, AUTS9, RCCP2, c-Met -C-MET and Prostate Cancer
40
CYP3A5 7q21.1 CP35, PCN3, CYPIIIA5, P450PCN3 -CYP3A5 and Prostate Cancer
39
RASSF1 3p21.3 123F2, RDA32, NORE2A, RASSF1A, REH3P21 -RASSF1 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
KLK2 19q13.41 hK2, hGK-1, KLK2A2 -KLK2 and Prostate Cancer
37
CAPS 19p13.3 CAPS1 -CAPS and Prostate Cancer
34
FGF2 4q26 BFGF, FGFB, FGF-2, HBGF-2 -FGF2 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
RELA 11q13 p65, NFKB3 -RELA and Prostate Cancer
32
ETV4 17q21 E1AF, PEA3, E1A-F, PEAS3 -ETV4 and Prostate Cancer
31
SHBG 17p13.1 ABP, SBP, TEBG -SHBG and Prostate Cancer
30
TNFRSF11A 18q22.1 FEO, OFE, ODFR, OSTS, PDB2, RANK, CD265, OPTB7, TRANCER, LOH18CR1 -TNFRSF11A and Prostate Cancer
30
XRCC1 19q13.2 RCC -XRCC1 and Prostate Cancer
29
ERBB2 17q12 NEU, NGL, HER2, TKR1, CD340, HER-2, MLN 19, HER-2/neu -ERBB2 and Prostate Cancer
27
CAV1 7q31.1 CGL3, PPH3, BSCL3, LCCNS, VIP21, MSTP085 -CAV1 and Prostate Cancer
26
IL6 7p21 HGF, HSF, BSF2, IL-6, IFNB2 -IL6 and Prostate Cancer
26
CHEK2 22q12.1 CDS1, CHK2, LFS2, RAD53, hCds1, HuCds1, PP1425 -CHEK2 and Prostate Cancer
26
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
ESR1 6q25.1 ER, ESR, Era, ESRA, ESTRR, NR3A1 -ESR1 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
CYP24A1 20q13 CP24, HCAI, CYP24, P450-CC24 -CYP24A1 and Prostate Cancer
23
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
GDF15 19p13.11 PDF, MIC1, PLAB, MIC-1, NAG-1, PTGFB, GDF-15 -GDF15 and Prostate Cancer
22
TNFRSF10B 8p22-p21 DR5, CD262, KILLER, TRICK2, TRICKB, ZTNFR9, TRAILR2, TRICK2A, TRICK2B, TRAIL-R2, KILLER/DR5 -TNFRSF10B 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
HPCX Xq27-q28 -HPCX and Prostate Cancer
21
SLC45A3 1q32.1 PRST, IPCA6, IPCA-2, IPCA-6, IPCA-8, PCANAP2, PCANAP6, PCANAP8 -SLC45A3 and Prostate Cancer
20
SKP2 5p13 p45, FBL1, FLB1, FBXL1 -SKP2 and Prostate Cancer
20
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
HNF1B 17q12 FJHN, HNF2, LFB3, TCF2, HPC11, LF-B3, MODY5, TCF-2, VHNF1, HNF-1B, HNF1beta, HNF-1-beta -HNF1B and Prostate Cancer
18
GPX1 3p21.3 GPXD, GSHPX1 -GPX1 and Prostate Cancer
18
TTPA 8q12.3 ATTP, AVED, TTP1, alphaTTP -TTPA and Prostate Cancer
18
TRPM8 2q37.1 TRPP8, LTRPC6 -TRPM8 and Prostate Cancer
18
UGT2B17 4q13 BMND12, UDPGT2B17 -UGT2B17 and Prostate Cancer
18
FGF8 10q24 HH6, AIGF, KAL6, FGF-8, HBGF-8 -FGF8 and Prostate Cancer
18
SLC2A1 1p34.2 PED, DYT9, GLUT, DYT17, DYT18, EIG12, GLUT1, HTLVR, GLUT-1, GLUT1DS -GLUT1 expression in Prostate Cancer
17
SPINK1 5q32 TCP, PCTT, PSTI, TATI, Spink3 -SPINK1 and Prostate Cancer
17
UGT2B15 4q13 HLUG4, UGT2B8, UDPGTH3, UDPGT 2B8, UDPGT2B15 -UGT2B15 and Prostate Cancer
17
SOD2 6q25.3 IPOB, MNSOD, MVCD6 -SOD2 and Prostate Cancer
17
TIMP2 17q25 DDC8, CSC-21K -TIMP2 and Prostate Cancer
17
SOX9 17q24.3 CMD1, SRA1, CMPD1 -SOX9 and Prostate Cancer
17
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
CCK 3p22.1 -CCK and Prostate Cancer
15
PIM1 6p21.2 PIM -PIM1 and Prostate Cancer
15
SIRT1 10q21.3 SIR2, hSIR2, SIR2L1 -SIRT1 and Prostate Cancer
15
JUND 19p13.2 AP-1 -JUND and Prostate Cancer
15
FLCN 17p11.2 BHD, FLCL -FLCN and Prostate Cancer
15
AKR1C3 10p15-p14 DD3, DDX, PGFS, HAKRB, HAKRe, HA1753, HSD17B5, hluPGFS -AKR1C3 and Prostate Cancer
14
CCL2 17q11.2-q12 HC11, MCAF, MCP1, MCP-1, SCYA2, GDCF-2, SMC-CF, HSMCR30 -CCL2 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
IGFBP2 2q35 IBP2, IGF-BP53 -IGFBP2 and Prostate Cancer
13
KLK4 19q13.41 ARM1, EMSP, PSTS, AI2A1, EMSP1, KLK-L1, PRSS17, kallikrein -KLK4 and Prostate Cancer
13
HSD17B2 16q24.1-q24.2 HSD17, SDR9C2, EDH17B2 -HSD17B2 and Prostate Cancer
13
ETV5 3q28 ERM -ETV5 and Prostate Cancer
13
COMT 22q11.21 HEL-S-98n -COMT and Prostate Cancer
13
FASN 17q25 FAS, OA-519, SDR27X1 -FASN and Prostate Cancer
13
EDNRB 13q22 ETB, ET-B, ETBR, ETRB, HSCR, WS4A, ABCDS, ET-BR, HSCR2 -EDNRB and Prostate Cancer
13
NOS3 7q36 eNOS, ECNOS -NOS3 and Prostate Cancer
13
SRD5A1 5p15 S5AR 1 -SRD5A1 and Prostate Cancer
13
MXI1 10q24-q25 MXI, MAD2, MXD2, bHLHc11 -MXI1 and Prostate Cancer
12
SPDEF 6p21.3 PDEF, bA375E1.3 -SPDEF and Prostate Cancer
12
RFX6 6q22.1 MTFS, MTCHRS, RFXDC1, dJ955L16.1 -rs339331 Polymorphism and Prostate Cancer susceptibility
-RFX6 and Prostate Cancer
6
PITX2 4q25 RS, RGS, ARP1, Brx1, IDG2, IGDS, IHG2, PTX2, RIEG, IGDS2, IRID2, Otlx2, RIEG1 -PITX2 and Prostate Cancer
12
RARB 3p24.2 HAP, RRB2, NR1B2, MCOPS12 -RARB and Prostate Cancer
12
CD24 6q21 CD24A -CD24 and Prostate Cancer
12
FGF1 5q31 AFGF, ECGF, FGFA, ECGFA, ECGFB, FGF-1, HBGF1, HBGF-1, GLIO703, ECGF-beta, FGF-alpha -FGF1 and Prostate Cancer
11
RECK 9p13.3 ST15 -RECK 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
JAZF1 7p15.2-p15.1 TIP27, ZNF802 -JAZF1 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
CTNNA1 5q31.2 CAP102 -CTNNA1 and Prostate Cancer
11
NCOA1 2p23 SRC1, KAT13A, RIP160, F-SRC-1, bHLHe42, bHLHe74 -NCOA1 and Prostate Cancer
11
HSD3B2 1p13.1 HSDB, HSD3B, SDR11E2 -HSD3B2 and Prostate Cancer
11
ELK1 Xp11.2 -ELK1 and Prostate Cancer
11
VIP 6q25 PHM27 -VIP and Prostate Cancer
10
NBN 8q21 ATV, NBS, P95, NBS1, AT-V1, AT-V2 -NBN and Prostate Cancer
10
LIMK1 7q11.23 LIMK, LIMK-1 -LIMK1 and Prostate Cancer
10
FGF7 15q21.2 KGF, HBGF-7 -FGF7 and Prostate Cancer
10
AGR2 7p21.3 AG2, GOB-4, HAG-2, XAG-2, PDIA17, HEL-S-116 -AGR2 and Prostate Cancer
10
WNT5A 3p21-p14 hWNT5A -WNT5A and Prostate Cancer
10
SMAD1 4q31 BSP1, JV41, BSP-1, JV4-1, MADH1, MADR1 -SMAD1 and Prostate Cancer
10
ANXA2 15q22.2 P36, ANX2, LIP2, LPC2, CAL1H, LPC2D, ANX2L4, PAP-IV, HEL-S-270 -ANXA2 and Prostate Cancer
10
IGFBP5 2q35 IBP5 -IGFBP5 and Prostate Cancer
10
DLC1 8p22 HP, ARHGAP7, STARD12, p122-RhoGAP -DLC1 and Prostate Cancer
10
TACSTD2 1p32 EGP1, GP50, M1S1, EGP-1, TROP2, GA7331, GA733-1 -TACSTD2 and Prostate Cancer
10
GPX3 5q33.1 GPx-P, GSHPx-3, GSHPx-P -GPX3 and Prostate Cancer
10
KLF4 9q31 EZF, GKLF -KLF4 and Prostate Cancer
10
HSD3B1 1p13.1 I, HSD3B, HSDB3, HSDB3A, SDR11E1, 3BETAHSD -HSD3B1 and Prostate Cancer
10
MIRLET7C 21q21.1 LET7C, let-7c, MIRNLET7C, hsa-let-7c -MicroRNA let-7c and Prostate Cancer
10
ERBB4 2q33.3-q34 HER4, ALS19, p180erbB4 -ERBB4 and Prostate Cancer
10
CASP1 11q23 ICE, P45, IL1BC -CASP1 and Prostate Cancer
10
IRS1 2q36 HIRS-1 -IRS1 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
HSPB1 7q11.23 CMT2F, HMN2B, HSP27, HSP28, Hsp25, SRP27, HS.76067, HEL-S-102 -HSPB1 and Prostate Cancer
10
ESR2 14q23.2 Erb, ESRB, ESTRB, NR3A2, ER-BETA, ESR-BETA -ESR2 and Prostate Cancer
10
ELK4 1q32 SAP1 -ELK4 and Prostate Cancer
10
TPD52 8q21.13 D52, N8L, PC-1, PrLZ, hD52 -TPD52 and Prostate Cancer
10
SREBF1 17p11.2 SREBP1, bHLHd1, SREBP-1c -SREBF1 and Prostate Cancer
10
BMP7 20q13 OP-1 -BMP7 and Prostate Cancer
9
EIF3E 8q22-q23 INT6, EIF3S6, EIF3-P48, eIF3-p46 -EIF3E 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
MBD2 18q21 DMTase, NY-CO-41 -MBD2 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
ALOX15 17p13.3 12-LOX, 15LOX-1, 15-LOX-1 -ALOX15 and Prostate Cancer
9
CCR5 3p21.31 CKR5, CCR-5, CD195, CKR-5, CCCKR5, CMKBR5, IDDM22, CC-CKR-5 -CCR5 and Prostate Cancer
9
HMOX1 22q13.1 HO-1, HSP32, HMOX1D, bK286B10 -HMOX1 and Prostate Cancer
9
SUZ12 17q11.2 CHET9, JJAZ1 -SUZ12 and Prostate Cancer
9
CRP 1q23.2 PTX1 -CRP and Prostate Cancer
9
BNIP3 10q26.3 NIP3 -BNIP3 and Prostate Cancer
9
CDC25C 5q31 CDC25, PPP1R60 -CDC25C and Prostate Cancer
9
NCOR1 17p11.2 N-CoR, TRAC1, N-CoR1, hN-CoR, PPP1R109 -NCOR1 and Prostate Cancer
9
NCOA3 20q12 ACTR, AIB1, RAC3, SRC3, pCIP, AIB-1, CTG26, SRC-3, CAGH16, KAT13B, TNRC14, TNRC16, TRAM-1, bHLHe42 -NCOA3 and Prostate Cancer
9
UBE2C 20q13.12 UBCH10, dJ447F3.2 -UBE2C and Prostate Cancer
8
ETS2 21q22.2 ETS2IT1 -ETS2 and Prostate Cancer
8
MED1 17q12 PBP, CRSP1, RB18A, TRIP2, PPARBP, CRSP200, DRIP205, DRIP230, PPARGBP, TRAP220 -MED1 and Prostate Cancer
8
CREB1 2q34 CREB -CREB1 and Prostate Cancer
8
MAF 16q22-q23 CCA4, c-MAF, CTRCT21 -MAF 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
NEFL 8p21 NFL, NF-L, NF68, CMT1F, CMT2E, PPP1R110 -NEFL and Prostate Cancer
8
COL18A1 21q22.3 KS, KNO, KNO1 -COL18A1 and Prostate Cancer
8
DKK3 11p15.2 RIG, REIC -DKK3 and Prostate Cancer
8
ASAH1 8p22 AC, PHP, ASAH, PHP32, ACDase, SMAPME -ASAH1 and Prostate Cancer
8
MIF 22q11.23 GIF, GLIF, MMIF -MIF and Prostate Cancer
8
CCNA2 4q27 CCN1, CCNA -CCNA2 and Prostate Cancer
8
KDM1A 1p36.12 AOF2, KDM1, LSD1, BHC110 -KDM1A and Prostate Cancer
8
PGK1 Xq13.3 PGKA, MIG10, HEL-S-68p -PGK1 and Prostate Cancer
8
TLR9 3p21.3 CD289 -TLR9 and Prostate Cancer
8
HMGB1 13q12 HMG1, HMG3, SBP-1 -HMGB1 and Prostate Cancer
8
GATA2 3q21.3 DCML, IMD21, NFE1B, MONOMAC -GATA2 and Prostate Cancer
8
KLK5 19q13.33 SCTE, KLKL2, KLK-L2 -KLK5 and Prostate Cancer
8
PWAR1 15q11.2 PAR1, PAR-1, D15S227E -PAR1 and Prostate Cancer
8
FOXP3 Xp11.23 JM2, AIID, IPEX, PIDX, XPID, DIETER -FOXP3 and Prostate Cancer
8
FYN 6q21 SLK, SYN, p59-FYN -FYN and Prostate Cancer
8
RELB 19q13.32 IREL, I-REL, REL-B -RELB and Prostate Cancer
8
PHIP 6q14 ndrp, BRWD2, WDR11, DCAF14 -PHIP and Prostate Cancer
8
CAST 5q15 BS-17, PLACK -CAST and Prostate Cancer
8
KLF5 13q22.1 CKLF, IKLF, BTEB2 -KLF5 and Prostate Cancer
8
SOX4 6p22.3 EVI16 -SOX4 and Prostate Cancer
8
PLAUR 19q13 CD87, UPAR, URKR, U-PAR -PLAUR and Prostate Cancer
8
CHIA 1p13.2 CHIT2, AMCASE, TSA1902 -CHIA and Prostate Cancer
7
CYR61 1p22.3 CCN1, GIG1, IGFBP10 -CYR61 and Prostate Cancer
7
GAS6 13q34 AXSF, AXLLG -GAS6 and Prostate Cancer
7
SOX11 2p25 MRD27 -SOX11 and Prostate Cancer
7
CTAG1B Xq28 CTAG, ESO1, CT6.1, CTAG1, LAGE-2, LAGE2B, NY-ESO-1 -CTAG1B and Prostate Cancer
7
FOXA2 20p11 HNF3B, TCF3B -FOXA2 and Prostate Cancer
7
GLIPR1 12q21.2 GLIPR, RTVP1, CRISP7 -GLIPR1 and Prostate Cancer
7
ALOX5 10q11.2 5-LO, 5LPG, LOG5, 5-LOX -ALOX5 and Prostate Cancer
7
BMP2 20p12 BDA2, BMP2A -BMP2 and Prostate Cancer
7
PON1 7q21.3 ESA, PON, MVCD5 -PON1 and Prostate Cancer
7
CDC6 17q21.3 CDC18L, HsCDC6, HsCDC18 -CDC6 and Prostate Cancer
7
ADAM9 8p11.22 MCMP, MDC9, CORD9, Mltng -ADAM9 and Prostate Cancer
7
CDH2 18q11.2 CDHN, NCAD, CD325, CDw325 -CDH2 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
MECP2 Xq28 RS, RTS, RTT, PPMX, MRX16, MRX79, MRXSL, AUTSX3, MRXS13 -MECP2 and Prostate Cancer
7
MAP2K4 17p12 JNKK, MEK4, MKK4, SEK1, SKK1, JNKK1, SERK1, MAPKK4, PRKMK4, SAPKK1, SAPKK-1 -MAP2K4 and Prostate Cancer
7
MCM7 7q21.3-q22.1 MCM2, CDC47, P85MCM, P1CDC47, PNAS146, PPP1R104, P1.1-MCM3 -MCM7 and Prostate Cancer
7
TLR6 4p14 CD286 -TLR6 and Prostate Cancer
7
HOXC6 12q13.3 CP25, HOX3, HOX3C, HHO.C8 -HOXC6 and Prostate Cancer
7
HOXA4 7p15.2 HOX1, HOX1D -HOXA4 and Prostate Cancer
7
KAT5 11q13 TIP, ESA1, PLIP, TIP60, cPLA2, HTATIP, ZC2HC5, HTATIP1 -KAT5 and Prostate Cancer
6
KLK14 19q13.3-q13.4 KLK-L6 -KLK14 and Prostate Cancer
6
BMP6 6p24-p23 VGR, VGR1 -BMP6 and Prostate Cancer
6
CEACAM1 19q13.2 BGP, BGP1, BGPI -CEACAM1 and Prostate Cancer
6
SEPP1 5q31 SeP, SELP, SEPP -SEPP1 and Prostate Cancer
6
STAT6 12q13 STAT6B, STAT6C, D12S1644, IL-4-STAT -STAT6 and Prostate Cancer
6
PDK1 2q31.1 -PDK1 and Prostate Cancer
6
RARRES1 3q25.32 LXNL, TIG1, PERG-1 -RARRES1 and Prostate Cancer
6
DAB2 5p13.1 DOC2, DOC-2 -DAB2 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
CKAP4 12q23.3 p63, CLIMP-63, ERGIC-63 -CKAP4 and Prostate Cancer
6
RICTOR 5p13.1 PIA, AVO3, hAVO3 -RICTOR and Prostate Cancer
6
BCAR1 16q23.1 CAS, CAS1, CASS1, CRKAS, P130Cas -BCAR1 and Prostate Cancer
6
TFF3 21q22.3 ITF, P1B, TFI -TFF3 and Prostate Cancer
6
BAG1 9p12 HAP, BAG-1, RAP46 Overexpression
-BAG1 overexpression in Prostate Cancer
6
TSG101 11p15 TSG10, VPS23 -TSG101 and Prostate Cancer
6
OGG1 3p26.2 HMMH, MUTM, OGH1, HOGG1 -OGG1 and Prostate Cancer
6
NFKB2 10q24 p52, p100, H2TF1, LYT10, CVID10, LYT-10, NF-kB2 -NFKB2 and Prostate Cancer
6
HOXB13 17q21.2 PSGD Germline
-Germline mutations of HOXB13 in Familiar Prostate Cancer?
-rs339331 Polymorphism and Prostate Cancer susceptibility
6
ATF3 1q32.3 -ATF3 and Prostate Cancer
6
SGK1 6q23 SGK -SGK1 and Prostate Cancer
6
CDH13 16q23.3 CDHH, P105 -CDH13 and Prostate Cancer
6
SNAI2 8q11 SLUG, WS2D, SLUGH1, SNAIL2 -SNAI2 and Prostate Cancer
6
ACPP 3q22.1 ACP3, 5'-NT, ACP-3 Prognostic
-ACPP expression in Prostate Cancer
6
HBEGF 5q23 DTR, DTS, DTSF, HEGFL -HBEGF and Prostate Cancer
6
AIDA 1q41 C1orf80 -AIDA and Prostate Cancer
6
BMPR1A 10q22.3 ALK3, SKR5, CD292, ACVRLK3, 10q23del -BMPR1A and Prostate Cancer
6
IL1B 2q14 IL-1, IL1F2, IL1-BETA -IL1B and Prostate Cancer
6
SOD1 21q22.11 ALS, SOD, ALS1, IPOA, hSod1, HEL-S-44, homodimer -SOD1 and Prostate Cancer
6
MST1 3p21 MSP, HGFL, NF15S2, D3F15S2, DNF15S2 -MST1 and Prostate Cancer
6
SOCS3 17q25.3 CIS3, SSI3, ATOD4, Cish3, SSI-3, SOCS-3 -SOCS3 and Prostate Cancer
6
ARNT 1q21 HIF1B, TANGO, bHLHe2, HIF1BETA, HIF-1beta, HIF1-beta, HIF-1-beta -ARNT and Prostate Cancer
6
CXCL5 4q13.3 SCYB5, ENA-78 -CXCL5 and Prostate Cancer
6
CXCR2 2q35 CD182, IL8R2, IL8RA, IL8RB, CMKAR2, CDw128b -CXCR2 and Prostate Cancer
6
AGO2 8q24 Q10, EIF2C2 -AGO2 and Prostate Cancer
6
CSK 15q24.1 -CSK and Prostate Cancer
6
TXNRD1 12q23-q24.1 TR, TR1, TXNR, TRXR1, GRIM-12 -TXNRD1 and Prostate Cancer
6
FHL2 2q12.2 DRAL, AAG11, FHL-2, SLIM3, SLIM-3 -FHL2 and Prostate Cancer
6
DUSP1 5q34 HVH1, MKP1, CL100, MKP-1, PTPN10 -DUSP1 and Prostate Cancer
5
ABCA1 9q31.1 TGD, ABC1, CERP, ABC-1, HDLDT1 -ABCA1 and Prostate Cancer
5
KPNA2 17q24.2 QIP2, RCH1, IPOA1, SRP1alpha -KPNA2 and Prostate Cancer
5
ZBTB7A 19p13.3 LRF, FBI1, FBI-1, ZBTB7, ZNF857A, pokemon -ZBTB7A and Prostate Cancer
5
NEDD4 15q RPF1, NEDD4-1 -NEDD4 and Prostate Cancer
5
CD151 11p15.5 GP27, MER2, RAPH, SFA1, PETA-3, TSPAN24 -CD151 and Prostate Cancer
5
TRPS1 8q24.12 GC79, LGCR -TRPS1 and Prostate Cancer
5
PDGFD 11q22.3 IEGF, SCDGFB, MSTP036, SCDGF-B -PDGFD and Prostate Cancer
5
KLK10 19q13 NES1, PRSSL1 -KLK10 and Prostate Cancer
5
SKP1 5q31 OCP2, p19A, EMC19, SKP1A, OCP-II, TCEB1L -SKP1 and Prostate Cancer
5
TLR1 4p14 TIL, CD281, rsc786, TIL. LPRS5 -TLR1 and Prostate Cancer
5
NCOR2 12q24 SMRT, TRAC, CTG26, SMRTE, TRAC1, N-CoR2, TNRC14, TRAC-1, SMAP270, SMRTE-tau -NCOR2 and Prostate Cancer
5
HIP1 7q11.23 HIP-I, ILWEQ -HIP1 and Prostate Cancer
5
THRB 3p24.2 GRTH, PRTH, THR1, ERBA2, NR1A2, THRB1, THRB2, C-ERBA-2, C-ERBA-BETA -THRB and Prostate Cancer
5
GHRH 20q11.2 GRF, INN, GHRF -GHRH and Prostate Cancer
5
XAF1 17p13.1 BIRC4BP, XIAPAF1, HSXIAPAF1 -XAF1 and Prostate Cancer
5
SPRY2 13q31.1 hSPRY2 -SPRY2 and Prostate Cancer
5
TLR2 4q32 TIL4, CD282 -TLR2 and Prostate Cancer
5
KDM4C 9p24.1 GASC1, JHDM3C, JMJD2C, TDRD14C -KDM4C and Prostate Cancer
5
SLCO1B3 12p12 LST3, HBLRR, LST-2, OATP8, OATP-8, OATP1B3, SLC21A8, LST-3TM13 -SLCO1B3 and Prostate Cancer
5
UGT1A1 2q37 GNT1, UGT1, UDPGT, UGT1A, HUG-BR1, BILIQTL1, UDPGT 1-1 -UGT1A1 and Prostate Cancer
5
CHUK 10q24-q25 IKK1, IKKA, IKBKA, TCF16, NFKBIKA, IKK-alpha -CHUK and Prostate Cancer
5
CXCL14 5q31 KEC, KS1, BMAC, BRAK, NJAC, MIP2G, MIP-2g, SCYB14 -CXCL14 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
SSTR5 16p13.3 SS-5-R -SSTR5 and Prostate Cancer
5
PARK7 1p36.23 DJ1, DJ-1, HEL-S-67p -PARK7 and Prostate Cancer
5
PHLPP1 18q21.33 SCOP, PHLPP, PLEKHE1 -PHLPP1 and Prostate Cancer
5
LIG4 13q33-q34 LIG4S -LIG4 and Prostate Cancer
5
MUC6 11p15.5 MUC-6 -MUC6 and Prostate Cancer
5
SPRY1 4q28.1 hSPRY1 -SPRY1 and Prostate Cancer
5
PEBP1 12q24.23 PBP, HCNP, PEBP, RKIP, HCNPpp, PEBP-1, HEL-210, HEL-S-34 -PEBP1 and Prostate Cancer
5
HRK 12q24.22 DP5, HARAKIRI -HRK and Prostate Cancer
5
FLNC 7q32-q35 ABPA, ABPL, FLN2, MFM5, MPD4, ABP-280, ABP280A -FLNC 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
MYBL2 20q13.1 BMYB, B-MYB -MYBL2 and Prostate Cancer
5
GREB1 2p25.1 -GREB1 and Prostate Cancer
5
IRS2 13q34 IRS-2 -IRS2 and Prostate Cancer
5
TP53BP1 15q15-q21 p202, 53BP1 -TP53BP1 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
PPIA 7p13 CYPA, CYPH, HEL-S-69p -PPIA and Prostate Cancer
5
ADIPOQ 3q27 ACDC, ADPN, APM1, APM-1, GBP28, ACRP30, ADIPQTL1 -ADIPOQ and Prostate Cancer
5
BTG2 1q32 PC3, TIS21 -BTG2 and Prostate Cancer
5
ANXA7 10q22.2 SNX, ANX7, SYNEXIN -ANXA7 and Prostate Cancer
4
TAGLN 11q23.2 SM22, SMCC, TAGLN1, WS3-10 -TAGLN and Prostate Cancer
4
DAXX 6p21.3 DAP6, EAP1, BING2 -DAXX and Prostate Cancer
4
CHGA 14q32 CGA -CHGA and Prostate Cancer
4
IKBKE 1q32.1 IKKE, IKKI, IKK-E, IKK-i -IKBKE and Prostate Cancer
4
DDX5 17q21 p68, HLR1, G17P1, HUMP68 -DDX5 and Prostate Cancer
4
HLA-DRB1 6p21.3 SS1, DRB1, DRw10, HLA-DRB, HLA-DR1B -HLA-DRB1 and Prostate Cancer
4
IL16 15q26.3 LCF, NIL16, PRIL16, prIL-16 -IL16 and Prostate Cancer
4
ADRB2 5q31-q32 BAR, B2AR, ADRBR, ADRB2R, BETA2AR -ADRB2 and Prostate Cancer
4
MUC2 11p15.5 MLP, SMUC, MUC-2 -MUC2 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
NKX2-5 5q34 CSX, CSX1, VSD3, CHNG5, HLHS2, NKX2E, NKX2.5, NKX4-1 -NKX2-5 and Prostate Cancer
4
STK4 20q11.2-q13.2 KRS2, MST1, YSK3, TIIAC -STK4 and Prostate Cancer
4
TNFRSF25 1p36.2 DR3, TR3, DDR3, LARD, APO-3, TRAMP, WSL-1, WSL-LR, TNFRSF12 -TNFRSF25 and Prostate Cancer
4
ELF3 1q32.2 ERT, ESX, EPR-1, ESE-1 -ELF3 and Prostate Cancer
4
YWHAZ 8q23.1 HEL4, YWHAD, KCIP-1, HEL-S-3, 14-3-3-zeta -YWHAZ and Prostate Cancer
4
MED12 Xq13 OKS, FGS1, HOPA, OPA1, OHDOX, ARC240, CAGH45, MED12S, TNRC11, TRAP230 -MED12 and Prostate Cancer
4
SHMT1 17p11.2 SHMT, CSHMT -SHMT1 and Prostate Cancer
4
CEBPD 8p11.2-p11.1 CELF, CRP3, C/EBP-delta, NF-IL6-beta -CEBPD and Prostate Cancer
4
LTA 6p21.3 LT, TNFB, TNFSF1 -LTA and Prostate Cancer
4
MT2A 16q13 MT2 -MT2A and Prostate Cancer
4
INHA 2q35 -INHA and Prostate Cancer
4
AMFR 16q21 GP78, RNF45 -AMFR and Prostate Cancer
4
TNFRSF10D 8p21 DCR2, CD264, TRUNDD, TRAILR4, TRAIL-R4 -TNFRSF10D and Prostate Cancer
4
BIRC7 20q13.3 KIAP, LIVIN, MLIAP, RNF50, ML-IAP -BIRC7 and Prostate Cancer
4
HSD17B1 17q11-q21 HSD17, EDHB17, EDH17B2, SDR28C1 -HSD17B1 and Prostate Cancer
4
LCN2 9q34 24p3, MSFI, NGAL -LCN2 and Prostate Cancer
4
CCNB2 15q22.2 HsT17299 -CCNB2 and Prostate Cancer
4
GNL3 3p21.1 NS, E2IG3, NNP47, C77032 -GNL3 and Prostate Cancer
4
TES 7q31.2 TESS, TESS-2 -TES and Prostate Cancer
4
PDPK1 16p13.3 PDK1, PDPK2, PDPK2P, PRO0461 -PDPK1 and Prostate Cancer
4
GPRC6A 6q22.1 GPCR, bA86F4.3 -GPRC6A and Prostate Cancer
4
MBD4 3q21.3 MED1 -MBD4 and Prostate Cancer
4
GSTA1 6p12.1 GST2, GTH1, GSTA1-1 -GSTA1 and Prostate Cancer
4
ADAM17 2p25 CSVP, TACE, NISBD, ADAM18, CD156B, NISBD1 -ADAM17 and Prostate Cancer
4
FGF10 5p13-p12 -FGF10 and Prostate Cancer
4
PER1 17p13.1 PER, hPER, RIGUI -PER1 and Prostate Cancer
4
KRT18 12q13 K18, CYK18 -KRT18 and Prostate Cancer
4
ADAMTS1 21q21.2 C3-C5, METH1 -ADAMTS1 and Prostate Cancer
4
LZTS1 8p22 F37, FEZ1 -LZTS1 and Prostate Cancer
4
CARS 11p15.5 CARS1, CYSRS, MGC:11246 -CARS and Prostate Cancer
4
CUL1 7q36.1 -CUL1 and Prostate Cancer
4
CLMP 11q24.1 ACAM, ASAM, CSBM, CSBS -CLMP and Prostate Cancer
4
IL11 19q13.3-q13.4 AGIF, IL-11 -IL11 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
MBD1 18q21 RFT, PCM1, CXXC3 -MBD1 and Prostate Cancer
4
LINC00632 Xq27.1 -RP1-177G6.2 and Prostate Cancer
4
SOCS2 12q CIS2, SSI2, Cish2, SSI-2, SOCS-2, STATI2 -SOCS2 and Prostate Cancer
4
GAS1 9q21.3-q22 -GAS1 and Prostate Cancer
4
UPRT Xq13.3 UPP, FUR1 -UPRT and Prostate Cancer
3
IRAK2 3p25.3 IRAK-2 -IRAK2 and Prostate Cancer
3
KDM6A Xp11.2 UTX, KABUK2, bA386N14.2 -KDM6A and Prostate Cancer
3
TNFRSF10C 8p22-p21 LIT, DCR1, TRID, CD263, TRAILR3, TRAIL-R3, DCR1-TNFR -TNFRSF10C and Prostate Cancer
3
LEPR 1p31 OBR, OB-R, CD295, LEP-R, LEPRD -LEPR and Prostate Cancer
3
LAMB3 1q32 AI1A, LAM5, LAMNB1, BM600-125KDA -LAMB3 and Prostate Cancer
3
IL13RA1 Xq24 NR4, CD213A1, IL-13Ra -IL13RA1 and Prostate Cancer
3
KLK6 19q13.3 hK6, Bssp, Klk7, SP59, PRSS9, PRSS18 -KLK6 and Prostate Cancer
3
SERPINB2 18q21.3 PAI, PAI2, PAI-2, PLANH2, HsT1201 -SERPINB2 and Prostate Cancer
3
TGM4 3p22-p21.33 TGP, hTGP -TGM4 and Prostate Cancer
3
APOD 3q29 -APOD and Prostate Cancer
3
CXCL16 17p13 SRPSOX, CXCLG16, SR-PSOX -CXCL16 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
BTG1 12q22 -BTG1 and Prostate Cancer
3
CTBP1 4p16 BARS -CTBP1 and Prostate Cancer
3
ACTA2 10q23.3 AAT6, ACTSA, MYMY5 -ACTA2 and Prostate Cancer
3
MX1 21q22.3 MX, MxA, IFI78, IFI-78K -MX1 and Prostate Cancer
3
PYCARD 16p11.2 ASC, TMS, TMS1, CARD5, TMS-1 -PYCARD and Prostate Cancer
3
FOXP4 6p21.1 hFKHLA -FOXP4 and Prostate Cancer
3
PLAT 8p12 TPA, T-PA -PLAT and Prostate Cancer
3
AIFM1 Xq26.1 AIF, CMT2D, CMTX4, COWCK, NADMR, NAMSD, PDCD8, COXPD6 -AIFM1 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
ATF2 2q32 HB16, CREB2, TREB7, CREB-2, CRE-BP1 -ATF2 and Prostate Cancer
3
MUC5AC 11p15.5 TBM, leB, MUC5 -MUC5AC and Prostate Cancer
3
GNAS 20q13.3 AHO, GSA, GSP, POH, GPSA, NESP, GNAS1, PHP1A, PHP1B, PHP1C, C20orf45 -GNAS 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
STRADA 17q23.3 LYK5, PMSE, Stlk, STRAD, NY-BR-96 -STRADA and Prostate Cancer
3
ENO1 1p36.2 NNE, PPH, MPB1, ENO1L1 -ENO1 and Prostate Cancer
3
MUC4 3q29 ASGP, MUC-4, HSA276359 -MUC4 and Prostate Cancer
3
BAG3 10q25.2-q26.2 BIS, MFM6, BAG-3, CAIR-1 -BAG3 and Prostate Cancer
3
MIR1271 5q35 MIRN1271, hsa-mir-1271 -MicroRNA miR-1271and Prostate Cancer
3
HMMR 5q34 CD168, IHABP, RHAMM -HMMR and Prostate Cancer
3
CTSB 8p22 APPS, CPSB -CTSB and Prostate Cancer
3
HAS3 16q22.1 -HAS3 and Prostate Cancer
3
RXRA 9q34.3 NR2B1 -RXRA and Prostate Cancer
3
NR3C1 5q31.3 GR, GCR, GRL, GCCR, GCRST -NR3C1 and Prostate Cancer
3
PER3 1p36.23 GIG13 -PER3 and Prostate Cancer
3
STEAP2 7q21.13 STMP, IPCA1, PUMPCn, STAMP1, PCANAP1 -STEAP2 and Prostate Cancer
3
E2F5 8q21.2 E2F-5 -E2F5 and Prostate Cancer
3
PTK6 20q13.3 BRK -PTK6 and Prostate Cancer
3
SSTR1 14q13 SS1R, SS1-R, SRIF-2, SS-1-R -SSTR1 and Prostate Cancer
3
LRP1 12q13.3 APR, LRP, A2MR, CD91, APOER, LRP1A, TGFBR5, IGFBP3R -LRP1 and Prostate Cancer
3
ADAR 1q21.3 DSH, AGS6, G1P1, IFI4, P136, ADAR1, DRADA, DSRAD, IFI-4, K88DSRBP -ADAR and Prostate Cancer
3
SMAD5 5q31 DWFC, JV5-1, MADH5 -SMAD5 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
NRP1 10p12 NP1, NRP, BDCA4, CD304, VEGF165R -NRP1 and Prostate Cancer
3
PRDX1 1p34.1 PAG, PAGA, PAGB, PRX1, PRXI, MSP23, NKEFA, TDPX2, NKEF-A -PRDX1 and Prostate Cancer
3
KDM6B 17p13.1 JMJD3 -KDM6B and Prostate Cancer
3
RALBP1 18p11.3 RIP1, RLIP1, RLIP76 -RALBP1 and Prostate Cancer
3
KRT8 12q13 K8, KO, CK8, CK-8, CYK8, K2C8, CARD2 -KRT8 and Prostate Cancer
3
FABP5 8q21.13 EFABP, KFABP, E-FABP, PAFABP, PA-FABP -FABP5 and Prostate Cancer
3
ARL11 13q14.2 ARLTS1 -ARL11 and Prostate Cancer
3
CUL3 2q36.2 CUL-3, PHA2E -CUL3 and Prostate Cancer
3
RAC3 17q25.3 -RAC3 and Prostate Cancer
3
CMBL 5p15.2 JS-1 -CMBL and Prostate Cancer
3
PIAS3 1q21 ZMIZ5 -PIAS3 and Prostate Cancer
3
CAV2 7q31.1 CAV -CAV2 and Prostate Cancer
3
NBL1 1p36.13 NB, DAN, NO3, DAND1, D1S1733E -NBL1 and Prostate Cancer
3
ITGB3 17q21.32 GT, CD61, GP3A, BDPLT2, GPIIIa, BDPLT16 -ITGB3 and Prostate Cancer
3
PLAGL1 6q24-q25 ZAC, LOT1, ZAC1 -PLAGL1 and Prostate Cancer
3
DDIT4 10q22.1 Dig2, REDD1, REDD-1 -DDIT4 and Prostate Cancer
3
MTSS1 8p22 MIM, MIMA, MIMB -MTSS1 and Prostate Cancer
3
AGTR2 Xq22-q23 AT2, ATGR2, MRX88 -AGTR2 and Prostate Cancer
3
CKS2 9q22 CKSHS2 -CKS2 and Prostate Cancer
3
ADIPOR1 1q32.1 CGI45, PAQR1, ACDCR1, CGI-45, TESBP1A -ADIPOR1 and Prostate Cancer
3
LDLR 19p13.2 FH, FHC, LDLCQ2 -LDLR and Prostate Cancer
3
CARM1 19p13.2 PRMT4 -CARM1 and Prostate Cancer
3
CRY2 11p11.2 HCRY2, PHLL2 -CRY2 and Prostate Cancer
3
NDRG2 14q11.2 SYLD -NDRG2 and Prostate Cancer
3
BIN1 2q14 AMPH2, AMPHL, SH3P9 -BIN1 and Prostate Cancer
3
ST14 11q24-q25 HAI, MTSP1, SNC19, ARCI11, MT-SP1, PRSS14, TADG15, TMPRSS14 -ST14 and Prostate Cancer
3
MMP8 11q22.3 HNC, CLG1, MMP-8, PMNL-CL -MMP8 and Prostate Cancer
2
DGCR8 22q11.2 Gy1, pasha, DGCRK6, C22orf12 -DGCR8 and Prostate Cancer
2
UGT2B7 4q13 UGT2B9, UDPGTH2, UDPGT2B7, UDPGT 2B9 -UGT2B7 and Prostate Cancer
2
MIRLET7D 9q22.32 LET7D, let-7d, MIRNLET7D, hsa-let-7d -MicroRNA let-d 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
IFITM1 11p15.5 9-27, CD225, IFI17, LEU13, DSPA2a -IFITM1 and Prostate Cancer
2
STIM1 11p15.5 GOK, TAM, TAM1, IMD10, STRMK, D11S4896E -STIM1 and Prostate Cancer
2
CSMD1 8p23.2 PPP1R24 -CSMD1 and Prostate Cancer
2
BTRC 10q24.32 FWD1, FBW1A, FBXW1, bTrCP, FBXW1A, bTrCP1, betaTrCP, BETA-TRCP -BTRC and Prostate Cancer
2
ACSL3 2q34-q35 ACS3, FACL3, PRO2194 -ACSL3 and Prostate Cancer
2
RXRB 6p21.3 NR2B2, DAUDI6, RCoR-1, H-2RIIBP -RXRB 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
WNT4 1p36.23-p35.1 WNT-4, SERKAL -WNT4 and Prostate Cancer
2
IER3 6p21.3 DIF2, IEX1, PRG1, DIF-2, GLY96, IEX-1, IEX-1L -IER3 and Prostate Cancer
2
MYCBP 1p33-p32.2 AMY-1 -MYCBP and Prostate Cancer
2
IL7 8q12-q13 IL-7 -IL7 and Prostate Cancer
2
MME 3q25.2 NEP, SFE, CD10, CALLA -MME and Prostate Cancer
2
ST7 7q31.2 HELG, RAY1, SEN4, TSG7, ETS7q, FAM4A, FAM4A1 -ST7 and Prostate Cancer
2
IMP3 15q24 BRMS2, MRPS4, C15orf12 -IMP3 and Prostate Cancer
2
CXCL11 4q21.2 IP9, H174, IP-9, b-R1, I-TAC, SCYB11, SCYB9B -CXCL11 and Prostate Cancer
2
FGF23 12p13.3 ADHR, FGFN, HYPF, HPDR2, PHPTC -FGF23 and Prostate Cancer
2
IRF3 19q13.3-q13.4 -IRF3 and Prostate Cancer
2
NQO2 6p25.2 QR2, DHQV, DIA6, NMOR2 -NQO2 and Prostate Cancer
2
INHBA 7p15-p13 EDF, FRP -INHBA and Prostate Cancer
2
ATF6 1q23.3 ATF6A -ATF6 and Prostate Cancer
2
SOX5 12p12.1 L-SOX5, L-SOX5B, L-SOX5F -SOX5 and Prostate Cancer
2
CBX7 22q13.1 -CBX7 and Prostate Cancer
2
BMPR1B 4q22-q24 ALK6, ALK-6, CDw293 -BMPR1B and Prostate Cancer
2
KLLN 10q23 CWS4, KILLIN -KLLN and Prostate Cancer
2
PAK4 19q13.2 -PAK4 and Prostate Cancer
2
PCGF2 17q12 MEL-18, RNF110, ZNF144 -PCGF2 and Prostate Cancer
2
ODC1 2p25 ODC -ODC1 and Prostate Cancer
2
MIR107 10q23.31 MIRN107, miR-107 -MicroRNA mir-107 and Prostate Cancer
2
REST 4q12 XBR, NRSF -REST and Prostate Cancer
2
WNT11 11q13.5 HWNT11 -WNT11 and Prostate Cancer
2
FOXC1 6p25 ARA, IGDA, IHG1, FKHL7, IRID1, RIEG3, FREAC3, FREAC-3 -FOXC1 and Prostate Cancer
2
IL18 11q22.2-q22.3 IGIF, IL-18, IL-1g, IL1F4 -IL18 and Prostate Cancer
2
FOXO4 Xq13.1 AFX, AFX1, MLLT7 -FOXO4 and Prostate Cancer
2
P2RX7 12q24 P2X7 -P2RX7 and Prostate Cancer
2
NR3C2 4q31.1 MR, MCR, MLR, NR3C2VIT -NR3C2 and Prostate Cancer
2
TRIO 5p15.2 tgat, ARHGEF23 -TRIO and Prostate Cancer
2
NOX1 Xq22 MOX1, NOH1, NOH-1, GP91-2 -NOX1 and Prostate Cancer
2
LASP1 17q11-q21.3 MLN50, Lasp-1 -LASP1 and Prostate Cancer
2
GNRHR 4q21.2 HH7, GRHR, LRHR, LHRHR, GNRHR1 -GNRHR and Prostate Cancer
2
ARNTL 11p15 TIC, JAP3, MOP3, BMAL1, PASD3, BMAL1c, bHLHe5 -ARNTL and Prostate Cancer
2
CYP2C19 10q24 CPCJ, CYP2C, P450C2C, CYPIIC17, CYPIIC19, P450IIC19 -CYP2C19 and Prostate Cancer
2
TM4SF1 3q21-q25 L6, H-L6, M3S1, TAAL6 -TM4SF1 and Prostate Cancer
2
ROCK2 2p24 ROCK-II -ROCK2 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
UCP2 11q13 UCPH, BMIQ4, SLC25A8 -UCP2 and Prostate Cancer
2
NKTR 3p22.1 p104 -NKTR 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
WNT10B 12q13 SHFM6, WNT-12 -WNT10B and Prostate Cancer
2
CCNG2 4q21.1 -CCNG2 and Prostate Cancer
2
PPARGC1A 4p15.1 LEM6, PGC1, PGC1A, PGC-1v, PPARGC1, PGC-1(alpha) -PPARGC1A and Prostate Cancer
2
GNMT 6p12 -GNMT and Prostate Cancer
2
FER 5q21 TYK3, PPP1R74, p94-Fer -FER 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
NSD1 5q35 STO, KMT3B, SOTOS, ARA267, SOTOS1 -NSD1 and Prostate Cancer
2
FEZ1 11q24.2 -FEZ1 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
EGR2 10q21.1 AT591, CMT1D, CMT4E, KROX20 -EGR2 and Prostate Cancer
2
BUB1B 15q15 MVA1, SSK1, BUBR1, Bub1A, MAD3L, hBUBR1, BUB1beta -BUB1B and Prostate Cancer
2
HYAL1 3p21.31 MPS9, NAT6, LUCA1, HYAL-1 -HYAL1 and Prostate Cancer
2
NEK2 1q32.3 NLK1, RP67, NEK2A, HsPK21, PPP1R111 -NEK2 and Prostate Cancer
2
RAD17 5q13 CCYC, R24L, RAD24, HRAD17, RAD17SP -RAD17 and Prostate Cancer
2
PTPRK 6q22.2-q22.3 R-PTP-kappa -PTPRK and Prostate Cancer
2
CANT1 17q25.3 DBQD, SCAN1, SHAPY, SCAN-1 -CANT1 and Prostate Cancer
2
HLA-DQB1 6p21.3 IDDM1, CELIAC1, HLA-DQB -HLA-DQB1 and Prostate Cancer
2
MCM5 22q13.1 CDC46, P1-CDC46 -MCM5 and Prostate Cancer
2
PAWR 12q21 PAR4, Par-4 -PAWR and Prostate Cancer
2
NAV1 1q32.3 POMFIL3, UNC53H1, STEERIN1 -NAV1 and Prostate Cancer
2
TSC22D1 13q14 Ptg-2, TSC22, TGFB1I4 -TSC22D1 and Prostate Cancer
2
ITGA6 2q31.1 CD49f, VLA-6, ITGA6B -ITGA6 and Prostate Cancer
2
CTSD 11p15.5 CPSD, CLN10, HEL-S-130P -CTSD and Prostate Cancer
2
HTATIP2 11p15.1 CC3, TIP30, SDR44U1 -HTATIP2 and Prostate Cancer
2
HERPUD1 16q13 SUP, HERP, Mif1 -HERPUD1 and Prostate Cancer
2
CCR3 3p21.3 CKR3, CD193, CMKBR3, CC-CKR-3 -CCR3 and Prostate Cancer
2
TRIM24 7q32-q34 PTC6, TF1A, TIF1, RNF82, TIF1A, hTIF1, TIF1ALPHA -TRIM24 and Prostate Cancer
2
PAFAH1B2 11q23 HEL-S-303 -PAFAH1B2 and Prostate Cancer
1
SLC22A18 11p15.5 HET, ITM, BWR1A, IMPT1, TSSC5, ORCTL2, BWSCR1A, SLC22A1L, p45-BWR1A -SLC22A18 and Prostate Cancer
1
EPB41 1p33-p32 HE, EL1, 4.1R -EPB41 and Prostate Cancer
1
AIM2 1q22 PYHIN4 -AIM2 and Prostate Cancer
1
KAT6B 10q22.2 qkf, MORF, MOZ2, GTPTS, MYST4, ZC2HC6B, querkopf -KAT6B 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
UHRF1 19p13.3 Np95, hNP95, ICBP90, RNF106, hUHRF1, huNp95 -UHRF1 and Prostate Cancer
1
CTDSPL 3p21.3 PSR1, SCP3, HYA22, RBSP3, C3orf8 -CTDSPL and Prostate Cancer
1
MIR122 18q21.31 MIR122A, MIRN122, MIRN122A, miRNA122, miRNA122A, hsa-mir-122 -MIR122 and Prostate Cancer
1
SAT2 17p13.1 SSAT2 -SAT2 and Prostate Cancer
1
MIRLET7I 12q14.1 LET7I, MIRNLET7I, hsa-let-7i -MicroRNA let-7i and Prostate Cancer
1
GSTO1 10q25.1 P28, SPG-R, GSTO 1-1, GSTTLp28, HEL-S-21 -GSTO1 and Prostate Cancer
1
SRPX Xp21.1 DRS, ETX1, SRPX1, HEL-S-83p -SRPX and Prostate Cancer
1
PRRX1 1q24 PMX1, PRX1, AGOTC, PHOX1, PRX-1 -PRRX1 and Prostate Cancer
1
MAD1L1 7p22 MAD1, PIG9, TP53I9, TXBP181 -MAD1L1 and Prostate Cancer
1
LARGE 22q12.3 MDC1D, MDDGA6, MDDGB6 -LARGE and Prostate Cancer
1
KMT2A 11q23 HRX, MLL, MLL1, TRX1, ALL-1, CXXC7, HTRX1, MLL1A, WDSTS, MLL/GAS7, TET1-MLL -KMT2A and Prostate Cancer
1
FRS2 12q15 SNT, SNT1, FRS2A, SNT-1, FRS2alpha -FRS2 and Prostate Cancer
1
SUV39H1 Xp11.23 MG44, KMT1A, SUV39H, H3-K9-HMTase 1 -SUV39H1 and Prostate Cancer
1
MTUS1 8p22 ATBP, ATIP, ICIS, MP44, MTSG1 -MTUS1 and Prostate Cancer
1
HMGN2P46 15q21.1 D-PCa-2, C15orf21 -HMGN2P46 and Prostate Cancer
1
CDR2 16p12.3 Yo, CDR62 -CDR2 and Prostate Cancer
1
PDE11A 2q31.2 PPNAD2 -PDE11A and Prostate Cancer
1
ANP32A 15q23 LANP, MAPM, PP32, HPPCn, PHAP1, PHAPI, I1PP2A, C15orf1 -ANP32A and Prostate Cancer
1
ESPL1 12q ESP1, SEPA -ESPL1 and Prostate Cancer
1
PCDH7 4p15 BHPCDH, BH-Pcdh, PPP1R120 -PCDH7 and Prostate Cancer
1
ARHGEF12 11q23.3 LARG, PRO2792 -ARHGEF12 and Prostate Cancer
1
PIK3CD 1p36.2 APDS, PI3K, IMD14, p110D, P110DELTA -PIK3CD and Prostate Cancer
1
PCDH10 4q28.3 PCDH19, OL-PCDH -PCDH10 and Prostate Cancer
1
DLG1 3q29 hdlg, DLGH1, SAP97, SAP-97, dJ1061C18.1.1 -DLG1 and Prostate Cancer
1
MIR1256 1 MIRN1256, hsa-mir-1256 -MicroRNA miR-1256 and Prostate Cancer
1
RASSF10 11p15.2 -RASSF10 and Prostate Cancer
1
MIR1297 13 MIRN1297, hsa-mir-1297 -MicroRNA miR-1297 and Prostate Cancer
1
RMI1 9q21.32 BLAP75, FAAP75, C9orf76 -RMI1 and Prostate Cancer
1
SBDS 7q11.21 SDS, SWDS, CGI-97 -SBDS and Prostate Cancer
1
CCNC 6q21 CycC -CCNC and Prostate Cancer
1
MYH9 22q13.1 MHA, FTNS, EPSTS, BDPLT6, DFNA17, NMMHCA, NMHC-II-A, NMMHC-IIA -MYH9 and Prostate Cancer
1
ERRFI1 1p36 MIG6, RALT, MIG-6, GENE-33 -ERRFI1 and Prostate Cancer
1
SST 3q28 SMST -SST and Prostate Cancer
1
MIR106B 7q22.1 MIRN106B -MIR106B and Prostate Cancer
1
ROCK1 18q11.1 ROCK-I, P160ROCK -ROCK1 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

Zhang BY, Li YF, Lai Y, et al.
[Effect of compound Chinese traditional medicine PC-SPES II in inhibiting proliferation of human prostate cancer cell LNCaP and on expressions of AR and PSA].
Zhongguo Zhong Yao Za Zhi. 2015; 40(5):950-6 [PubMed] Related Publications
To investigate the effect of compound Chinese traditional medicine PC-SPES II I in inhibiting proliferation of human prostate cancer cell LNCaP based on the androgen receptor (AR) signaling pathway. The effect of PC-SPES II on LNCaP cell proliferation was detected by MTT assay. According to the findings, at the mass concentration of 180-1 440 mg x L(-1), PC-SPES II significantly inhibited the proliferation of LNCaP cells; the IC50 of PC-SPES II at 24 h and 48 h were 311.48, 199.01 mg x L(-1), respectively. The flow Cytometry detection showed 240 mg x L(-1) PC-SPES II arrested cells in G2/M phase, and an obvious apoptotic peak appeared before G0/G1 peak and rose over time. Meanwhile, Hoechst 33258 staining revealed apoptotic cellular morphology. Annexin V-FITC/PI staining manifested an increase in apoptotic cell ratio at the PC-SPES II concentration of 480 mg x L(-1) in a dose dependent manner. The prostate specific antigen (PSA) secretion of LNCaP cells was tested by PSA ELISA kit. Besides, compared with 25 mg x L(-1) Bic, 480 mg x L(-1) PC-SPES II significantly reduced the cell secretion of PSA. The AR and PSA mRNA and protein expressions were detected by qRT-PCR and Western blot. According to the results, after the induction of LNCaP cells with synthetic androgen 25 μg x L(-1) R1881, 240-480 mg x L(-1) PC-SPES II notably down-regulated the AR and PSA mRNA and protein expressions and inhibited the translocation of AR from cytoplasm to nucleus. In summary, PC-SPES II significantly can inhibit the in vitro proliferation of LNCaP cells and arrest cell cycle arrest in G2/M phase. Its mechanism may be associated with the down-regulation of the AR and PSA expressions and the inhibition of AR nuclear translocation.

Tsvetkova A, Todorova A, Todorov T, et al.
Molecular and clinico-histological data in aggressive prostate cancer patients from Bulgaria.
J BUON. 2015 Mar-Apr; 20(2):498-504 [PubMed] Related Publications
PURPOSE: Metastatic prostate cancer (PCa) is one of the leading causes of death in men worldwide. We report Bulgarian patients with strongly aggressive, castration-resistant PCa.
METHODS: PCA3 overexpression, GSTP1 promoter hyper-methylation, TMPRSS2-ERG gene fusions, IVS1-27G>A in the KLF6 gene and mutations in androgen receptor (AR) gene, for diagnostic purposes were assessed. PCR, real-time PCR (RT-PCR), sequencing, and bisulfite conversion of DNA were applied. We correlated the molecular data to the histological and clinical findings.
RESULTS: The obtained molecular profile in 11 PCa Bulgarian patients coincided with the clinico-histological data of strongly aggressive PCa. Association was detected between the tumor stage (assessed by TNM as T3 and T4) and the detected molecular profile of aggressive cancer behavior with one exception, assessed as T2. None of our patients had positive family history of prostate cancer and no somatic mutations were detected in the AR gene. All patients showed normal genotype with respect to the KLF6 IVS1- 27G>A polymorphism. The rest of the markers were positive in fresh prostatic tissues and biopsies from all patients, whereas only one blood sample showed triple positive result.
CONCLUSIONS: The appearance of PCa-specific markers in blood was considered as a predictor for a PCa (micro) dissemination into the circulation. The GSTP1 promoter hypermethylation is the earliest epigenetic alteration, which indicates cancerous changes and the first and long-lasting marker that is detectable in blood circulation. The molecular profile needs to be strictly monitored during treatment, which is of great help in determining the patient's individual response to therapy.

Robinson D, Van Allen EM, Wu YM, et al.
Integrative clinical genomics of advanced prostate cancer.
Cell. 2015; 161(5):1215-28 [PubMed] Article available free on PMC after 21/05/2016 Related Publications
Toward development of a precision medicine framework for metastatic, castration-resistant prostate cancer (mCRPC), we established a multi-institutional clinical sequencing infrastructure to conduct prospective whole-exome and transcriptome sequencing of bone or soft tissue tumor biopsies from a cohort of 150 mCRPC affected individuals. Aberrations of AR, ETS genes, TP53, and PTEN were frequent (40%-60% of cases), with TP53 and AR alterations enriched in mCRPC compared to primary prostate cancer. We identified new genomic alterations in PIK3CA/B, R-spondin, BRAF/RAF1, APC, β-catenin, and ZBTB16/PLZF. Moreover, aberrations of BRCA2, BRCA1, and ATM were observed at substantially higher frequencies (19.3% overall) compared to those in primary prostate cancers. 89% of affected individuals harbored a clinically actionable aberration, including 62.7% with aberrations in AR, 65% in other cancer-related genes, and 8% with actionable pathogenic germline alterations. This cohort study provides clinically actionable information that could impact treatment decisions for these affected individuals.

Zhou W, Tao Z, Wang Z, et al.
[Association of polymorphism in the promoter region of PCA3 gene with risk of prosate cancer].
Zhonghua Zhong Liu Za Zhi. 2015; 37(2):107-12 [PubMed] Related Publications
OBJECTIVE: To investigate the polymorphism in the promoter region of PCA3 gene and its relationship with risk of prostate cancer (PCa).
METHODS: The promoter region of PCA3 gene of the DNA of peripheral blood mononuclear cells was detected by sequence analysis in the 186 PCa and 141 BPH patients and 135 healthy control individuals. If the samples were detected with polymorphism of insection/deletion, clone sequence analysis was used with pBS-T carrier to verify it.
RESULTS: There were 5 polymorphisms. TAAA repeat times: 4, 5, 6, 7, 8, and 8 genotypes (TAAA 4/5, TAAA 4/6, TAAA 5/5, TAAA 5/6, TAAA 5/7, TAAA 5/8, TAAA 6/6, and TAAA 6/7) were detected in the promoter region of PCA3 gene. The eight genotypes were divided into three groups: ≤10TAAA, 11TAAA, ≥12TAAA. Unconditional logistic regression analysis models were used to analyze the relationship between different genotypes and cancer risks adjusted by sex and age. The type 11TAAA and ≥12TAAA was associated with higher relative risk for prostate cancer than the group ≤10TAAA [OR=1.74, 95% CI=1.06-2.87 (for type 11TAAA); OR=5.63, 95% CI=1.85-17.19 (for type ≥12TAAA)]. In the 186 PCa patients, there was 62.4% allele of PCA3 gene with AG/CA mutation found in the promoter 18-19 bp region of PCA3 gene and it had a close relation with the development of prostate cancer.
CONCLUSIONS: Short tandem repeats are found in the promoter region of the PCA3 gene in PCa patients, and the increase of TAAA repeat sequences highly enhance the relative risk of prostate cancer development. The occurrence of such STR might be related to the mutations in their upstream loci.

Sedelaar JP, Schalken JA
The need for a personalized approach for prostate cancer management.
BMC Med. 2015; 13:109 [PubMed] Article available free on PMC after 21/05/2016 Related Publications
The stratification of patients for treatment of prostate cancer is based on very general parameters like prostate-specific antigen, Gleason score, and TNM classification. We use these rough parameters for selection of active surveillance, active treatment, and even for the treatment selection in metastasized or castration-resistant prostate cancers. Up to now, we have not used individualized genetic classifiers for detailed sub-stratification, thus treating all patients as equal, and being only moderately successful. With the expected increase in systemic treatments, there is an apparent need for such classifiers. We will address these needs in this short commentary.

Lu K, Liu C, Tao T, et al.
MicroRNA-19a regulates proliferation and apoptosis of castration-resistant prostate cancer cells by targeting BTG1.
FEBS Lett. 2015; 589(13):1485-90 [PubMed] Related Publications
MicroRNAs (miRNAs) play a significant role in tumor development. Recent studies indicate that miRNAs are implicated in prostate cancer (PCa). In this study, we found that miR-19a expression was significantly increased in castration-resistant prostate cancer (CRPC) tissues compared with androgen-dependent prostate cancer (ADPC) tissues. We found that inhibiting the overexpression of miR-19a in CRPC cells suppressed proliferation and increased apoptosis. Additionally, we found that miR-19a repressed BTG1 expression by binding to its 3'-untranslated region. The overexpression of BTG1 in CRPC cells significantly suppressed proliferation and increased apoptosis. We conclude that miR-19a regulates proliferation and apoptosis of CRPC cells by directly targeting the tumor suppressor gene BTG1.

Egbers L, Luedeke M, Rinckleb A, et al.
Obesity and Prostate Cancer Risk According to Tumor TMPRSS2:ERG Gene Fusion Status.
Am J Epidemiol. 2015; 181(9):706-13 [PubMed] Article available free on PMC after 01/05/2016 Related Publications
The T2E gene fusion, formed by fusion of the transmembrane protease, serine 2, gene (TMPRSS2) with the erythroblast transformation-specific (ETS)-related gene (ERG), is found in approximately 50% of prostate cancers and may characterize distinct molecular subtypes of prostate cancer with different etiologies. We investigated the relationship between body mass index (BMI; weight (kg)/height (m)(2)) and prostate cancer risk by T2E status. Study participants were residents of King County, Washington, recruited for 2 population-based case-control studies conducted in 1993-1996 and 2002-2005. Tumor T2E status was determined for 563 prostate cancer patients who underwent radical prostatectomy. Information on weight, height, and covariables was obtained through in-person interviews. We performed polytomous logistic regression to calculate odds ratios and 95% confidence intervals for T2E-positive and -negative prostate cancer. Comparing the highest BMI quartile with the lowest, inverse associations were observed between recent (≥29.7 vs. <24.5: odds ratio = 0.66, 95% confidence interval: 0.45, 0.97) and maximum (≥31.8 vs. <25.9: odds ratio = 0.69, 95% confidence interval: 0.47, 1.02) BMI and the risk of T2E-positive prostate cancer. No significant associations were seen for men with T2E-negative tumors. This study provides evidence that obesity is specifically associated with reduced risk of developing androgen-responsive T2E fusion-positive tumors. The altered steroid hormone profile in obese men may contribute to this inverse association.

Guo S, Jiang X, Chen X, et al.
The protective effect of methylenetetrahydrofolate reductase C677T polymorphism against prostate cancer risk: Evidence from 23 case-control studies.
Gene. 2015; 565(1):90-5 [PubMed] Related Publications
Genetic polymorphisms of methylenetetrahydrofolate reductase (MTHFR) were considered to have some influence on both folate metabolism and cancer risk. Previous studies on the relation between MTHFR C677T polymorphism and prostate cancer (PCa) risk remained controversial. To derive a more precise estimation of the relationship, we carried out an update comprehensive meta-analysis to assess the associations of the MTHFR C677T polymorphism with the susceptibility of PCa. Twenty-three trials with a total of 24,024 participants on the MTHFR C677T polymorphism that met inclusion criteria were analyzed in the current study. Overall, no statistical relationship was found with any MTHFR C677T genetic model associated with susceptibility to PCa (TT versus CC, OR=0.83, 95% CI 0.68-1.02, P=0.07; CT versus CC, OR=0.95, 95% CI 0.85-1.07, P=0.43; Dominant, OR=0.93, 95% CI 0.83-1.03, P=0.17; Recessive, OR=0.84, 95% CI 0.70-1.02, P=0.09.). Nevertheless, subgroup analysis found a reduced PCa risk associated with polymorphism in Asian population (TT versus CC, CT versus CC, dominant and recessive model). Moreover, the protective effect of polymorphism against PCa risk was also shown upon hospital-based studies (TT versus CC, and recessive model). When benign prostate hyperplasia was chosen as controls, both TT versus CC and recessive model showed significant difference. In addition, the protective effect of homozygote TT against high aggressive PCa was proved to have significant difference. Taken together, the existing evidence indicates the homozygote TT of MTHFR C677T should be viewed as a protective factor against PCa risk for clinical practice with the consideration of different gene background, study design as well as specific controls.

Ateeq B, Kunju LP, Carskadon SL, et al.
Molecular profiling of ETS and non-ETS aberrations in prostate cancer patients from northern India.
Prostate. 2015; 75(10):1051-62 [PubMed] Related Publications
BACKGROUND: Molecular stratification of prostate cancer (PCa) based on genetic aberrations including ETS or RAF gene-rearrangements, PTEN deletion, and SPINK1 over-expression show clear prognostic and diagnostic utility. Gene rearrangements involving ETS transcription factors are frequent pathogenetic somatic events observed in PCa. Incidence of ETS rearrangements in Caucasian PCa patients has been reported, however, occurrence in Indian population is largely unknown. The aim of this study was to determine the prevalence of the ETS and RAF kinase gene rearrangements, SPINK1 over-expression, and PTEN deletion in this cohort.
METHODS: In this multi-center study, formalin-fixed paraffin embedded (FFPE) PCa specimens (n = 121) were procured from four major medical institutions in India. The tissues were sectioned and molecular profiling was done using immunohistochemistry (IHC), RNA in situ hybridization (RNA-ISH) and/or fluorescence in situ hybridization (FISH).
RESULTS: ERG over-expression was detected in 48.9% (46/94) PCa specimens by IHC, which was confirmed in a subset of cases by FISH. Among other ETS family members, while ETV1 transcript was detected in one case by RNA-ISH, no alteration in ETV4 was observed. SPINK1 over-expression was observed in 12.5% (12/96) and PTEN deletion in 21.52% (17/79) of the total PCa cases. Interestingly, PTEN deletion was found in 30% of the ERG-positive cases (P = 0.017) but in only one case with SPINK1 over-expression (P = 0.67). BRAF and RAF1 gene rearrangements were detected in ∼1% and ∼4.5% of the PCa cases, respectively.
CONCLUSIONS: This is the first report on comprehensive molecular profiling of the major spectrum of the causal aberrations in Indian men with PCa. Our findings suggest that ETS gene rearrangement and SPINK1 over-expression patterns in North Indian population largely resembled those observed in Caucasian population but differed from Japanese and Chinese PCa patients. The molecular profiling data presented in this study could help in clinical decision-making for the pursuit of surgery, diagnosis, and in selection of therapeutic intervention.

Hsieh CL, Botta G, Gao S, et al.
PLZF, a tumor suppressor genetically lost in metastatic castration-resistant prostate cancer, is a mediator of resistance to androgen deprivation therapy.
Cancer Res. 2015; 75(10):1944-8 [PubMed] Article available free on PMC after 15/05/2016 Related Publications
Whole-exome sequencing of metastatic castration-resistant prostate cancer (mCRPC) reveals that 5% to 7% of tumors harbor promyelocytic leukemia zinc finger (PLZF) protein homozygous deletions. PLZF is a canonical androgen-regulated putative tumor suppressor gene whose expression is inhibited by androgen deprivation therapy (ADT). Here, we demonstrate that knockdown of PLZF expression promotes a CRPC and enzalutamide-resistant phenotype in prostate cancer cells. Reintroduction of PLZF expression is sufficient to reverse androgen-independent growth mediated by PLZF depletion. PLZF loss enhances CRPC tumor growth in a xenograft model. Bioinformatic analysis of the PLZF cistrome shows that PLZF negatively regulates multiple pathways, including the MAPK pathway. Accordingly, our data support an oncogenic program activated by ADT. This acquired mechanism together with the finding of genetic loss in CRPC implicates PLZF inactivation as a mechanism promoting ADT resistance and the CRPC phenotype.

Liu YN, Yin J, Barrett B, et al.
Loss of Androgen-Regulated MicroRNA 1 Activates SRC and Promotes Prostate Cancer Bone Metastasis.
Mol Cell Biol. 2015; 35(11):1940-51 [PubMed] Article available free on PMC after 01/12/2015 Related Publications
Bone metastasis is the hallmark of progressive and castration-resistant prostate cancers. MicroRNA 1 (miR-1) levels are decreased in clinical samples of primary prostate cancer and further reduced in metastases. SRC has been implicated as a critical factor in bone metastasis, and here we show that SRC is a direct target of miR-1. In prostate cancer patient samples, miR-1 levels are inversely correlated with SRC expression and a SRC-dependent gene signature. Ectopic miR-1 expression inhibited extracellular signal-regulated kinase (ERK) signaling and bone metastasis in a xenograft model. In contrast, SRC overexpression was sufficient to reconstitute bone metastasis and ERK signaling in cells expressing high levels of miR-1. Androgen receptor (AR) activity, defined by an AR output signature, is low in a portion of castration-resistant prostate cancer. We show that AR binds to the miR-1-2 regulatory region and regulates miR-1 transcription. Patients with low miR-1 levels displayed correlated low canonical AR gene signatures. Our data support the existence of an AR-miR-1-SRC regulatory network. We propose that loss of miR-1 is one mechanistic link between low canonical AR output and SRC-promoted metastatic phenotypes.

Burdelski C, Ruge OM, Melling N, et al.
HDAC1 overexpression independently predicts biochemical recurrence and is associated with rapid tumor cell proliferation and genomic instability in prostate cancer.
Exp Mol Pathol. 2015; 98(3):419-26 [PubMed] Related Publications
Histone deacetylases (HDACs) play an important role in tumor development and progression by modifying histone and non-histone proteins. In the current study we analyzed prevalence and prognostic impact of HDAC1 in prostate cancer. HDAC1 expression was analyzed by immunohistochemistry on a tissue microarray containing more than 12,400 prostate cancer specimens. Results were compared to tumor phenotype, biochemical recurrence, and molecular subtypes defined by ERG status as well as genomic deletions of 3p, 5q, 6q and PTEN. HDAC1 immunostaining was detectable in 75.4% of 9744 interpretable cancers and considered strong in 15.4%, moderate in 39.4% and weak in 20.7% of cases. High HDAC1 expression was associated with high Gleason grade (p<0.0001), advanced pathological tumor stage (p<0.0001), positive nodal status (p=0.0010), elevated preoperative PSA-level (p=0.0127), early PSA recurrence (p<0.0001) and increased cell proliferation (p<0.0001). Moreover, high-level HDAC1 staining was associated with TMPRSS2:ERG rearrangement and ERG expression in prostate cancers (p<0.0001) and was linked to deletions of PTEN (p<0.0001), 6q (p<0.0001) and 5q (p=0.0028) in ERG-negative cancers. The prognostic impact of HDAC1 was independent of established clinicopathological parameters and was mostly driven by ERG-negative cancers as revealed by subgroup analyses. HDAC1 has strong prognostic impact in prostate cancer and might contribute to the development of a fraction of genetically instable and particularly aggressive prostate cancers. HDAC1 measurement might therefore be of clinical value for risk stratification of prostate cancer and should be further evaluated in this regard.

Sun H, Deng Q, Pan Y, et al.
Association between estrogen receptor 1 (ESR1) genetic variations and cancer risk: a meta-analysis.
J BUON. 2015 Jan-Feb; 20(1):296-308 [PubMed] Related Publications
PURPOSE: Emerging published reports on the association between estrogen receptor 1 (ESR1) genetic variation and cancer susceptibility are inconsistent. This review and meta- analysis was performed to achieve a more precise evaluation of this relationship.
METHODS: A literature search of PubMed database was conducted from the inception of this study through April 1st 2014. Crude odds ratios (ORs) with 95% confidence intervals (95% CIs) were calculated to assess the association.
RESULTS: 87 studies were enrolled in this meta-analysis. The results indicated that PvuII (T>C) polymorphism was associated with an increased risk of hepatocellular carcinoma (HCC) and prostate cancer, in contrast with the decreased risk of gallbladder cancer. No significant association was found in Asian and Caucasian populations. Furthermore, XbaI (A>G) genetic variation was only associated with an increased risk of prostate cancer, but was not related with race. In addition, T594T (G>A) polymorphisms were significantly associated with an increased risk of cancer, especially in Asian populations.
CONCLUSIONS: This meta-analysis indicated that PvuII (T>C) genetic variation may be risk factor for HCC, prostate cancer and gallbladder cancer. Meanwhile, XbaI (A>G) polymorphism may be potential prognostic factor for prostate cancer. Furthermore, T594T (G>A) was closely related with cancer susceptibility, especially in Asian populations.

Dezhong L, Xiaoyi Z, Xianlian L, et al.
miR-150 is a factor of survival in prostate cancer patients.
J BUON. 2015 Jan-Feb; 20(1):173-9 [PubMed] Related Publications
PURPOSE: Prostate cancer (PC) is the most common malignant disease in males and the second leading cause of cancer related deaths in men in developed countries. The purpose of this study was to investigate whether microRNA (miR)-150 is a factor influencing survival in prostate cancer patients.
METHODS: miR-150 mRNA and protein expression levels in prostatic cancer cell lines and healthy tissues were determined by quantitative (q) RT-PCR and Western blotting. Additionally, the protein expression of miR-150 was detected by immunohistochemistry.
RESULTS: High miR-150 expression was positively correlated with tumor recurrence or metastasis (p=0.010). In addition, PC patients with high miR-150 expression had significantly poorer overall survival/OR (hazard ratio/HR, 1.87; 95% confidence interval/CI, 1.19-2.94; p=0.006) and poorer disease-free survival/DFS (HR, 1.90; 95% CI, 1.21- 2.98; p=0.005) than those with low miR-150 expression. The cumulative 5-year OS was only 35.19% (95% CI, 26.18- 44.20) in the high miR-150 expression group, whereas it was 55.93% (95% CI, 43.26-68.60) in the low miR-150 expression group (p<0.05). Multivariate Cox regression analysis demonstrated that the expression of miR-150, tumor size, and number of tumor lesions were independent prognostic predictors for OS in PC patients.
CONCLUSION: miR-150 was overexpressed in PC at both the mRNA and protein levels, and high expression of miR-150 could serve as a novel and reliable prognostic biomarker for PC patients.

Jingwi EY, Abbas M, Ricks-Santi L, et al.
Vitamin D receptor genetic polymorphisms are associated with PSA level, Gleason score and prostate cancer risk in African-American men.
Anticancer Res. 2015; 35(3):1549-58 [PubMed] Related Publications
BACKGROUND/AIM: Several studies have revealed an association between single nucleotide polymorphisms (SNPs) in the VDR gene and prostate cancer (PCa) risk in European and Asian populations. To investigate whether VDR SNPs are associated with PCa risk in African-American (AA) men, nine VDR SNPs were analyzed in a case-control study.
MATERIALS AND METHODS: Multiple and binary logistic regression models were applied to analyze the clinical and genotypic data.
RESULTS: rs731236 and rs7975232 were significantly associated with PCa risk (p<0.05). In the analysis of clinical phenotypes, rs731236, rs1544410 and rs3782905 were strongly associated with high PSA level (p<0.05), whereas rs1544410 and rs2239185 showed a statistically significant association with high Gleason score (p<0.05). Haplotype analysis revealed several VDR haplotypes associated with PCa risk. Additionally, a trend existed, where as the number of risk alleles increased in the haplotype, the greater was the association with risk (p-trend=0.01).
CONCLUSION: These results suggest that the VDR SNPs may be associated with PCa risk and other clinical phenotypes of PCa in AA men.

Xue G, Ren Z, Chen Y, et al.
A feedback regulation between miR-145 and DNA methyltransferase 3b in prostate cancer cell and their responses to irradiation.
Cancer Lett. 2015; 361(1):121-7 [PubMed] Related Publications
It is believed that epigenetic modification plays roles in cancer initiation and progression. Both microRNA and DNA methyltransferase are epigenetic regulation factors. It was found that miR-145 upregulates while DNMT3b downregulates in PC3 cells. Presence of any negative correlationship and their response to irradiation were investigated in the current study. We found that miR-145 downregulated DNMT3b expression by directly targeting the 3'-UTR of DNMT3b mRNA and knockdown of DNMT3b increased expression of miR-145 via CpG island promoter hypomethylation, suggesting that there is a crucial crosstalk between miR-145 and DNMT3b via a double-negative feedback loop. Responses of the miR-145 and DNMT3b to irradiation are a negative correlation. We also found that either overexpression of miR-145 or knockdown of DNMT3b sensitized prostate cancer cells to X-ray radiation. Our findings enrich the complex relationships between miRNA and DNMTs in carcinogenesis and irradiation stress. It also sheds light on the potential combination of ionizing radiation and epigenetic regulation in prostate cancer therapy.

Cooper CS, Eeles R, Wedge DC, et al.
Analysis of the genetic phylogeny of multifocal prostate cancer identifies multiple independent clonal expansions in neoplastic and morphologically normal prostate tissue.
Nat Genet. 2015; 47(4):367-72 [PubMed] Article available free on PMC after 01/10/2015 Related Publications
Genome-wide DNA sequencing was used to decrypt the phylogeny of multiple samples from distinct areas of cancer and morphologically normal tissue taken from the prostates of three men. Mutations were present at high levels in morphologically normal tissue distant from the cancer, reflecting clonal expansions, and the underlying mutational processes at work in morphologically normal tissue were also at work in cancer. Our observations demonstrate the existence of ongoing abnormal mutational processes, consistent with field effects, underlying carcinogenesis. This mechanism gives rise to extensive branching evolution and cancer clone mixing, as exemplified by the coexistence of multiple cancer lineages harboring distinct ERG fusions within a single cancer nodule. Subsets of mutations were shared either by morphologically normal and malignant tissues or between different ERG lineages, indicating earlier or separate clonal cell expansions. Our observations inform on the origin of multifocal disease and have implications for prostate cancer therapy in individual cases.

Graff RE, Pettersson A, Lis RT, et al.
The TMPRSS2:ERG fusion and response to androgen deprivation therapy for prostate cancer.
Prostate. 2015; 75(9):897-906 [PubMed] Article available free on PMC after 01/06/2016 Related Publications
BACKGROUND: In the United States, half of men with prostate cancer harbor the androgen-regulated gene fusion TMPRSS2:ERG. We hypothesized that men with TMPRSS2:ERG positive tumors are more responsive to androgen deprivation therapy (ADT).
METHODS: We studied a cohort of 239 men with prostate cancer from the Physicians' Health Study and Health Professionals Follow-up Study who received ADT during their disease course. Fusion status was assessed on available tumor tissue by immunohistochemistry for ERG protein expression. We used Cox models to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for assessment of prostate cancer-specific mortality after ADT initiation.
RESULTS: Roughly half of the men had stage T3 or higher tumors at diagnosis and 39% had Gleason 8-10 tumors. During an average follow up of 10.2 years, 42 men died from prostate cancer. There was a non-significant inverse association between positive fusion status and time to death from prostate cancer after ADT (multivariable HR: 0.76; 95% CI: 0.40-1.45). Harboring the TMPRSS2:ERG fusion was associated with a statistically significant lower risk of prostate cancer mortality among men who were treated with orchiectomy (multivariable HR: 0.13; 95% CI: 0.03-0.62), based on 15 events.
CONCLUSIONS: Our results, combined with those from earlier studies, provide suggestive evidence that men with TMPRSS2:ERG positive tumors may have longer prostate cancer survival after ADT. Larger cohorts are needed for more robust results and to assess whether men with tumors harboring the fusion benefit from treatment with ADT in the (neo) adjuvant or metastatic setting specifically.

Helfand BT, Roehl KA, Cooper PR, et al.
Associations of prostate cancer risk variants with disease aggressiveness: results of the NCI-SPORE Genetics Working Group analysis of 18,343 cases.
Hum Genet. 2015; 134(4):439-50 [PubMed] Related Publications
Genetic studies have identified single nucleotide polymorphisms (SNPs) associated with the risk of prostate cancer (PC). It remains unclear whether such genetic variants are associated with disease aggressiveness. The NCI-SPORE Genetics Working Group retrospectively collected clinicopathologic information and genotype data for 36 SNPs which at the time had been validated to be associated with PC risk from 25,674 cases with PC. Cases were grouped according to race, Gleason score (Gleason ≤ 6, 7, ≥ 8) and aggressiveness (non-aggressive, intermediate, and aggressive disease). Statistical analyses were used to compare the frequency of the SNPs between different disease cohorts. After adjusting for multiple testing, only PC-risk SNP rs2735839 (G) was significantly and inversely associated with aggressive (OR = 0.77; 95 % CI 0.69-0.87) and high-grade disease (OR = 0.77; 95 % CI 0.68-0.86) in European men. Similar associations with aggressive (OR = 0.72; 95 % CI 0.58-0.89) and high-grade disease (OR = 0.69; 95 % CI 0.54-0.87) were documented in African-American subjects. The G allele of rs2735839 was associated with disease aggressiveness even at low PSA levels (<4.0 ng/mL) in both European and African-American men. Our results provide further support that a PC-risk SNP rs2735839 near the KLK3 gene on chromosome 19q13 may be associated with aggressive and high-grade PC. Future prospectively designed, case-case GWAS are needed to identify additional SNPs associated with PC aggressiveness.

Selkirk CG, Wang CH, Lapin B, Helfand BT
Family history of prostate cancer in men being followed by active surveillance does not increase risk of being diagnosed with high-grade disease.
Urology. 2015; 85(4):742-7 [PubMed] Related Publications
OBJECTIVE: To assess whether men with a family history of prostate cancer are more likely to fail active surveillance because of recategorization of their tumors on subsequent surveillance biopsies.
METHODS: Men enrolled in an institutional review board-approved active surveillance program were studied, and data on first- and/or second-degree family history of prostate cancer was collected. Analyses were performed to compare the frequency of family history with recategorization (higher grade or volume disease) on surveillance biopsies.
RESULTS: Men with and without family history were recategorized with higher grade disease at a similar frequency (30.9% vs 32.8%). There was no evidence that men with a family history with higher grade disease had more aggressive pathology at the time of radical prostatectomy than men without a family history. Although those with a family history tended to have a shorter time period to recategorization with more positive cores, the difference was not significant.
CONCLUSION: Our results suggest that men with a family history of prostate cancer are not at an increased risk for recategorization on active surveillance. Men with a family history of prostate cancer should not be deterred from considering active surveillance as a treatment option.

Li X, Li C, Zhu LH
[Correlation of autophagy-associated gene Atg5 with tumorigenesis of prostate cancer].
Zhonghua Nan Ke Xue. 2015; 21(1):31-4 [PubMed] Related Publications
OBJECTIVE: To investigate the correlation of the autophagy-associated gene Atg5 with the pathogenesis of prostate cancer.
METHODS: Using real-time fluorescent quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and immunohistochemistry, we detected the expression of Atg5 in 50 cases of prostate intraepithelial neoplasm (PIN), 69 cases of prostate cancer (PCa), and 30 cases of benign prostatic hyperplasia (BPH).
RESULTS: The expression level of Atg5 mRNA was significantly higher in PIN (5.270 ± 0.230) and PCa (5.131 ± 0.252) than in the BPH tissue (1.723 ± 0.017) (P <0.01), and so was the positive rate of the Atg5 expression in the patients of the PIN group (94%) and PCa group (88.4%) than in those of the BPH group (6.7%) (P<0.01), but with no statistically significant differences between the PIN and PCa groups (P >0.05). No significant correlation was observed between the expression of Atg5 and the Gleason score of PCa (P >0.05).
CONCLUSION: The upregulated expression of Atg5 might play a role in the tumorigenesis of prostate cancer.

Yen AM, Auvinen A, Schleutker J, et al.
Prostate cancer screening using risk stratification based on a multi-state model of genetic variants.
Prostate. 2015; 75(8):825-35 [PubMed] Related Publications
BACKGROUND: Risk-stratified screening for prostate cancer (PCa) with prostate-specific antigen (PSA) testing incorporating genetic variants has received some attention but has been scarcely investigated. We developed a model to stratify the Finnish population by different risk profiles related to genetic variants to optimize the screening policy.
METHODS: Data from the Finnish randomized controlled trial on screening for PCa with PSA testing were used to estimate a six-state Markov model of disease progression. Blood samples from Finnish men were used to assess the risk of PCa related to three genetic variants (rs4242382, rs138213197, and rs200331695). A risk score-based approach combined with a series of computer simulation models was applied to optimize individual screening policies.
RESULTS: The 10-year risk of having progressive prostate cancer detected ranged from 43% in the top 5% risk group to approximately 11% in the bottom half of the population. Using the median group, with screening every four years beginning at 55 years-old, as the reference group, the recommended age beginning screening was approximately 47 years-old for the top 5% risk group and 55 years-old for those in the lower 60% risk group. The recommended interscreening interval has been shortened for individuals in the high risk group. The increased availability of genomic information allows the proposed multistate model to be more discriminating with respect to risk stratification and the suggested screening policy, particularly for the lowest risk groups-. --
CONCLUSIONS: A multi-state genetic variant-based model was developed for further application to population risk stratification to optimize the interscreening interval and the age at which to begin screening for PSA. A small sub-group of the population is likely to benefit from more intensive screening with early start and short interval, while half of the population is unlikely to benefit from such protocol (compared with four-year interval after age 55 years).

Vidal SJ, Rodriguez-Bravo V, Quinn SA, et al.
A targetable GATA2-IGF2 axis confers aggressiveness in lethal prostate cancer.
Cancer Cell. 2015; 27(2):223-39 [PubMed] Article available free on PMC after 09/08/2015 Related Publications
Elucidating the determinants of aggressiveness in lethal prostate cancer may stimulate therapeutic strategies that improve clinical outcomes. We used experimental models and clinical databases to identify GATA2 as a regulator of chemotherapy resistance and tumorigenicity in this context. Mechanistically, direct upregulation of the growth hormone IGF2 emerged as a mediator of the aggressive properties regulated by GATA2. IGF2 in turn activated IGF1R and INSR as well as a downstream polykinase program. The characterization of this axis prompted a combination strategy whereby dual IGF1R/INSR inhibition restored the efficacy of chemotherapy and improved survival in preclinical models. These studies reveal a GATA2-IGF2 aggressiveness axis in lethal prostate cancer and identify a therapeutic opportunity in this challenging disease.

Plymate SR, Bhatt RS, Balk SP
Taxane resistance in prostate cancer mediated by AR-independent GATA2 regulation of IGF2.
Cancer Cell. 2015; 27(2):158-9 [PubMed] Related Publications
GATA2 has been well-characterized as a critical pioneer transcription factor for androgen receptor (AR) in prostate cancer. In this issue of Cancer Cell, Vidal and colleagues identify increased GATA2 and its AR-independent transactivation of IGF2 as a mechanism that can mediate taxane resistance through activation of IGF1/insulin receptor signaling.

Den RB, Yousefi K, Trabulsi EJ, et al.
Genomic classifier identifies men with adverse pathology after radical prostatectomy who benefit from adjuvant radiation therapy.
J Clin Oncol. 2015; 33(8):944-51 [PubMed] Related Publications
PURPOSE: The optimal timing of postoperative radiotherapy (RT) after radical prostatectomy (RP) is unclear. We hypothesized that a genomic classifier (GC) would provide prognostic and predictive insight into the development of clinical metastases in men receiving post-RP RT and inform decision making.
PATIENTS AND METHODS: GC scores were calculated from 188 patients with pT3 or margin-positive prostate cancer, who received post-RP RT at Thomas Jefferson University and Mayo Clinic between 1990 and 2009. The primary end point was clinical metastasis. Prognostic accuracy of the models was tested using the concordance index for censored data and decision curve analysis. Cox regression analysis tested the relationship between GC and metastasis.
RESULTS: The cumulative incidence of metastasis at 5 years after RT was 0%, 9%, and 29% for low, average, and high GC scores, respectively (P = .002). In multivariable analysis, GC and pre-RP prostate-specific antigen were independent predictors of metastasis (both P < .01). Within the low GC score (< 0.4), there were no differences in the cumulative incidence of metastasis comparing patients who received adjuvant or salvage RT (P = .79). However, for patients with higher GC scores (≥ 0.4), cumulative incidence of metastasis at 5 years was 6% for patients treated with adjuvant RT compared with 23% for patients treated with salvage RT (P < .01).
CONCLUSION: In patients treated with post-RP RT, GC is prognostic for the development of clinical metastasis beyond routine clinical and pathologic features. Although preliminary, patients with low GC scores are best treated with salvage RT, whereas those with high GC scores benefit from adjuvant therapy. These findings provide the first rational selection of timing for post-RP RT.

Haluskova J, Lachvac L, Nagy V
The investigation of GSTP1, APC and RASSF1 gene promoter hypermethylation in urine DNA of prostate-diseased patients.
Bratisl Lek Listy. 2015; 116(2):79-82 [PubMed] Related Publications
OBJECTIVES: Prostate cancer (PCa) represents one of the most complicated human tumors and, like many others malignancies, arises from progressive genetic and epigenetic alterations. Among all recognized epigenetic alterations, aberrant DNA methylation (hypo- and hypermethylation) is the most important and the best characterized change in PCa.
BACKGROUND: We analyzed GSTP1, APC and RASSF1 gene promoter hypermethylation in urine DNA of ten previously non-treated prostate-diseased patients.
METHODS: For the purpose, the quantitative real-time methylation specific PCR (MSP) with primers designed for amplification of methylated bisulfite-converted human DNA, followed by melting procedure, was currently optimized.
RESULTS: GSTP1 gene promoter hypermethylation was detected in 2 and 1 out of 5 patients with biopsy-confirmed PCa using the primers covering the 3´ and 5´ CpG regions of the promoter, respectively. The APC gene promoter hypermethylation was found in neither of PCa or non-PCa patients and the RASSFI gene promoter hypermethylation was found in some non-PCa and not in all PCa patients.
CONCLUSIONS: Our results suggest that GSTP1 gene promoter hypermethylation can be detected in urine DNA of PCa patients with real-time MSP followed by melting. This enables evaluation of its potential as a useful biomarker in the diagnosis and prognosis of PCa (Tab. 1, Fig. 1, Ref. 9).

Chin SP, Marthick JR, West AC, et al.
Regulation of the ITGA2 gene by epigenetic mechanisms in prostate cancer.
Prostate. 2015; 75(7):723-34 [PubMed] Related Publications
BACKGROUND: Integrin alpha2 beta1 (α2 β1 ) plays an integral role in tumour cell invasion, metastasis and angiogenesis, and altered expression of the receptor has been linked to tumour prognosis in several solid tumours. However, the relationship is complex, with both increased and decreased expression associated with different stages of tumour metastases in several tumour types. The ITGA2 gene, which codes for the α2 subunit, was examined to investigate whether a large CpG island associated with its promoter region is involved in the differential expression of ITGA2 observed in prostate cancer.
METHODS: Bisulphite sequencing of the ITGA2 promoter was used to assess methylation in formalin-fixed paraffin-embedded (FFPE) prostate tumour specimens and prostate cancer cell lines, PC3, 22Rv1 and LNCaP. Changes in ITGA2 mRNA expression were measured using quantitative PCR. ITGA2 functionality was interrogated using cell migration scratch assays and siRNA knockdown experiments.
RESULTS: Bisulphite sequencing revealed strikingly decreased methylation at key CpG sites within the promoter of tumour samples, when compared with normal prostate tissue. Altered methylation of this CpG island is also associated with differences in expression in the non-invasive LNCaP, and the highly metastatic PC3 and 22Rv1 prostate cancer cell lines. Further bisulphite sequencing confirmed that selected CpGs were highly methylated in LNCaP cells, whilst only low levels of methylation were observed in PC3 and 22Rv1 cells, correlating with ITGA2 transcript levels. Examination of the increased expression of ITGA2 was shown to influence migratory potential via scratch assay in PC3, 22Rv1 and LNCaP cells, and was confirmed by siRNA knockdown experiments.
CONCLUSIONS: Taken together, our data supports the assertion that epigenetic modification of the ITGA2 promoter is a mechanism by which ITGA2 expression is regulated.

Qin F, Song Z, Babiceanu M, et al.
Discovery of CTCF-sensitive Cis-spliced fusion RNAs between adjacent genes in human prostate cells.
PLoS Genet. 2015; 11(2):e1005001 [PubMed] Article available free on PMC after 09/08/2015 Related Publications
Genes or their encoded products are not expected to mingle with each other unless in some disease situations. In cancer, a frequent mechanism that can produce gene fusions is chromosomal rearrangement. However, recent discoveries of RNA trans-splicing and cis-splicing between adjacent genes (cis-SAGe) support for other mechanisms in generating fusion RNAs. In our transcriptome analyses of 28 prostate normal and cancer samples, 30% fusion RNAs on average are the transcripts that contain exons belonging to same-strand neighboring genes. These fusion RNAs may be the products of cis-SAGe, which was previously thought to be rare. To validate this finding and to better understand the phenomenon, we used LNCaP, a prostate cell line as a model, and identified 16 additional cis-SAGe events by silencing transcription factor CTCF and paired-end RNA sequencing. About half of the fusions are expressed at a significant level compared to their parental genes. Silencing one of the in-frame fusions resulted in reduced cell motility. Most out-of-frame fusions are likely to function as non-coding RNAs. The majority of the 16 fusions are also detected in other prostate cell lines, as well as in the 14 clinical prostate normal and cancer pairs. By studying the features associated with these fusions, we developed a set of rules: 1) the parental genes are same-strand-neighboring genes; 2) the distance between the genes is within 30kb; 3) the 5' genes are actively transcribing; and 4) the chimeras tend to have the second-to-last exon in the 5' genes joined to the second exon in the 3' genes. We then randomly selected 20 neighboring genes in the genome, and detected four fusion events using these rules in prostate cancer and non-cancerous cells. These results suggest that splicing between neighboring gene transcripts is a rather frequent phenomenon, and it is not a feature unique to cancer cells.

Wang C, Tao W, Ni S, et al.
Tumor-suppressive microRNA-145 induces growth arrest by targeting SENP1 in human prostate cancer cells.
Cancer Sci. 2015; 106(4):375-82 [PubMed] Related Publications
Prostate cancer (PCa) prevails as the most commonly diagnosed malignancy in men and the third leading cause of cancer-related deaths in developed countries. One of the distinct characteristics of prostate cancer is overexpression of the small ubiquitin-like modifier (SUMO)-specific protease 1 (SENP1), and the upregulation of SENP1 contributes to the malignant progression and cell proliferation of PCa. Previous studies have shown that the expression of microRNA-145 (miRNA-145) was extensively deregulated in PCa cell lines and primary clinical prostate cancer samples. Independent target prediction methods have indicated that the 3'-untranslated region of SENP1 mRNA is a potential target of miR-145. Here we found that low expression of miR-145 was correlated with high expression of SENP1 in PCa cell line PC-3. The transient introduction of miR-145 caused cell cycle arrest in PC-3 cells, and the opposite effect was observed when miR-145 inhibitor was transfected. Further studies revealed that the SENP1 3'-untranslated region was a regulative target of miR-145 in vitro. MicroRNA-145 also suppressed tumor formation in vivo in nude mice. Taken together, miR-145 plays an important role in tumorigenesis of PCa through interfering SENP1.

Tiscornia MM, González HS, Lorenzati MA, Zapata PD
Association between methylation of SHP-1 isoform I and SSTR2A promoter regions with breast and prostate carcinoma development.
Cancer Invest. 2015; 33(3):61-9 [PubMed] Related Publications
Methylation pattern is presented here for first time as a potential molecular marker of changes on SSTR2A and SHP-1(I) gene promoter related to breast and prostate carcinoma. Our results have shown low concordances with SSTR2A and methylated state in prostate cancer and moderate relationship with unmethylated CpG-27 in breast cancer. We found significant concordances for both cancers and SHP-1(I) unmethylation, and increased HER2 expression and SSTR2A methylation in breast cancer. Moreover, we found a correlation between methylation patterns of two genes in normal breast tissue. These data might assist to select subgroups of patients for the administration of alternative therapies.

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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