Association of FGFR4 genetic polymorphisms with prostate cancer risk and prognosis

被引：23

作者：

FitzGerald, L. M. ^{[2
]}

Karlins, E. ^{[1
]}

Karyadi, D. M. ^{[1
]}

Kwon, E. M. ^{[1
]}

Koopmeiners, J. S. ^{[2
]}

Stanford, J. L. ^{[2
,3
]}

Ostrander, E. A. ^{[1
]}

机构：

[1] NHGRI, Canc Genet Branch, NIH, Bethesda, MD 20892 USA

[2] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA

[3] Univ Washington, Sch Publ Hlth & Community Med, Dept Epidemiol, Seattle, WA 98195 USA

来源：

PROSTATE CANCER AND PROSTATIC DISEASES | 2009年 / 12卷 / 02期

关键词：

population-based association analysis; FGFR4; radical prostatectomy; GLY388ARG POLYMORPHISM; OVER-EXPRESSION; BREAST-CANCER; INTRAEPITHELIAL NEOPLASIA; ARG(388) ALLELE; GROWTH; RECEPTOR; ADENOCARCINOMA; THERAPY; PROGRESSION;

D O I：

10.1038/pcan.2008.46

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The fibroblast growth factor receptor 4 (FGFR4) is thought to be involved in many critical cellular processes and has been associated with prostate cancer risk. Four single nucleotide polymorphisms (SNPs) within or near FGFR4 were analyzed in a population-based study of 1458 prostate cancer patients and 1352 age-matched controls. We found no evidence to suggest that any of the FGFR4 SNP genotypes were associated with prostate cancer risk or with disease aggressiveness, Gleason score or stage. A weak association was seen between rs351855 and prostate cancer-specific mortality. Subset analysis of cases that had undergone radical prostatectomy revealed an association between rs351855 and prostate cancer risk. Although our results confirm an association between FGFR4 and prostate cancer risk in radical prostatectomy cases, they suggest that the role of FGFR4 in disease risk and outcomes at a population-based level appears to be minor. Prostate Cancer and Prostatic Diseases (2009) 12, 192-197; doi:10.1038/pcan.2008.46; published online 2 September 2008

引用

页码：192 / 197

页数：6

共 30 条

[1] Inducible FGFR-1 activation leads to irreversible prostate adenocarcinoma and an epithelial-to-mesenchymal transition [J].

Acevedo, Victor D. ;

Gangula, Rama D. ;

Freeman, Kevin W. ;

Li, Rile ;

Zhang, Youngyou ;

Wang, Fen ;

Ayala, Gustavo E. ;

Peterson, Leif E. ;

Ittmann, Michael ;

Spencer, David M. .

CANCER CELL, 2007, 12 (06) :559-571

[2] Statin use and risk of prostate cancer: Results from a population-based epidemiologic study [J].

Agalliu, Ilir ;

Salinas, Claudia A. ;

Hansten, Philip D. ;

Ostrander, Elaine A. ;

Stanford, Janet L. .

AMERICAN JOURNAL OF EPIDEMIOLOGY, 2008, 168 (03) :250-260

[3]

Bange J, 2002, CANCER RES, V62, P840

[4]

Breslow N E, 1980, IARC Sci Publ, P5

[5]

COX DR, 1972, J R STAT SOC B, V187, P220

[6] Targeting FGF19 inhibits tumor growth in colon cancer xenograft and FGF19 transgenic hepatocellular carcinoma models [J].

Desnoyers, Lr ;

Pai, R. ;

Ferrando, Re ;

Hotzel, K. ;

Le, T. ;

Ross, J. ;

Carano, R. ;

D'Souza, A. ;

Qing, J. ;

Mohtashemi, I. ;

Ashkenazi, A. ;

French, Dm .

ONCOGENE, 2008, 27 (01) :85-97

[7] FGF8 over-expression in prostate cancer is associated with decreased patient survival and persists in androgen independent disease [J].

Dorkin, TJ ;

Robinson, MC ;

Marsh, C ;

Bjartell, A ;

Neal, DE ;

Leung, HY .

ONCOGENE, 1999, 18 (17) :2755-2761

[8]

Freeman KW, 2003, CANCER RES, V63, P6237

[9]

Freeman KW, 2003, CANCER RES, V63, P8256

[10] Evaluation of the fibroblast growth factor system as a potential target for therapy in human prostate cancer [J].

Gowardhan, B ;

Douglas, DA ;

Mathers, ME ;

McKie, AB ;

McCracken, SRC ;

Robson, CN ;

Leung, HY .

BRITISH JOURNAL OF CANCER, 2005, 92 (02) :320-327

← 1 2 3 →