Prevalence, Treatment Modalities and Prognosis of Familial Prostate Cancer in a Screened Population

Roemeling, Stijn; Roobol, Monique J.; Vries, Stijn H. de; Gosselaar, Claartje; Kwast, Theodorus H. van der; Schröder, Fritz H.

doi:10.1016/s0022-5347(05)00698-1

Cited by 31 publications

(18 citation statements)

References 18 publications

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“…A risk ratio of 1.8 for first-degree relatives found in our sample was higher than the RR of 1.53 found by Roemeling et al (2006) but lower than reported in the meta-analysis by Noe et al (2008; RR range between 2.2 and 2.5; refs. 49, 50). This could be explained by the smaller number of participants in our study as compared with the meta-analysis and/or because we did not stratify the analysis by ethnicity.…”

Section: Discussionmentioning

confidence: 99%

Single and Multivariate Associations of MSR1, ELAC2, and RNASEL with Prostate Cancer in an Ethnic Diverse Cohort of Men

Beuten

Gelfond

Franke

et al. 2010

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Three genes, namely, ELAC2 (HPC2 locus) on chromosome 17p11, 2′-5′-oligoisoadenlyate-synthetase-dependent ribonuclease L (RNASEL, HPC1 locus), and macrophage scavenger receptor 1 (MSR1) within a region of linkage on chromosome 8p, have been identified as hereditary tumor suppressor genes in prostate cancer. We genotyped 41 tagged single nucleotide polymorphisms (SNPs) covering the three genes in a case-control cohort, which included 1,436 Caucasians, 648 Hispanics, and 270 African Americans. SNPs within MSR1, ELAC2, and RNASEL were significantly associated with risk of prostate cancer albeit with differences among the three ethnic groups (P = 0.043–1.0 × 10−5). In Caucasians, variants within MSR1 and ELAC2 are most likely to confer prostate cancer risk, and rs11545302 (ELAC2) showed a main effect independent of other significant SNPs (P = 2.03 × 10−5). A major haplotype G-A-C-G-C-G combining five SNPs within MSR1 was further shown to increase prostate cancer risk significantly in this study group. Variants in RNASEL had the strongest effects on prostate cancer risk estimates in Hispanics and also showed an interaction effect of family history. In African Americans, single SNPs within MSR1 were significantly associated with prostate cancer risk. A major risk haplotype C-G-G-C-G of five SNPs within ELAC2 was found in this group. Combining high-risk genotypes of MSR1 and ELAC2 in Caucasians and of RNASEL and MSR1 in Hispanics showed synergistic effects and suggest that an interaction between both genes in each ethnicity is likely to confer prostate cancer risk. Our findings corroborate the involvement of ELAC2, MSR1, and RNASEL in the etiology of prostate cancer even in individuals without a family history.

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Section: Discussionmentioning

confidence: 99%

Single and Multivariate Associations of MSR1, ELAC2, and RNASEL with Prostate Cancer in an Ethnic Diverse Cohort of Men

Beuten

Gelfond

Franke

et al. 2010

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…The etiology of PC is largely unknown, although several risk factors such as ethnicity, family history, and age are associated with the disease (2,3). In addition, several dietary constituents have been linked to PC risk and prevention (4,5).…”

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confidence: 99%

CXCL12 G801A Polymorphism Is a Risk Factor for Sporadic Prostate Cancer Susceptibility

Hirata

Hinoda

Kikuno

et al. 2007

Clinical Cancer Research

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Purpose: The chemokine CXCL12 and its receptor CXCR4 have been found to be associated with cancer metastasis. A single nucleotide polymorphism of CXCL12 G801A has been described and is regarded as a target for cis-acting factor that has the ability to up-regulate CXCL12 expression. Currently, there are no reports investigating the role of CXCL12 G801A polymorphism in prostate cancer (PC). Experimental Design: We genotyped CXCL12 G801A and p53Arg72Pro in 167 PC patients and 167 age-matched healthy subjects. Genotyping was done with PCR-RFLP and confirmed by direct DNA sequencing. To investigate the effect of the CXCL12 G801A polymorphism on CXCL12 and CXCR4 expression, immunohistochemistry was done in genotyped PC tissues. Results: A significant increase in the GA + AA genotype of the CXCL12 G801A polymorphism was observed in PC patients compared with healthy controls. The frequency of CXCL12 AA genotype was significantly higher in a group of patients with lymph node metastasis (23%) compared with those without metastasis (7 %). The frequency of CXCL12 expression in AA + GA genotype carriers was significantly higher than that in GG genotype carriers. Among the carriers with CXCL12 GA + AA genotypes, CXCR4 expression was also significantly higher compared with those with the GG genotype. Moreover, among the groups with both CXCL12-and CXCR4-positive staining, the frequency of the CXCL12 GA + AA genotype was high. Although we did not find a significant relationship between the frequency of the Arg/Pro + Pro/Pro genotype of p53 Arg72Pro and susceptibility in PC, there was a combined effect of CXCL12 GA + AA genotype and the p53 72Arg/Pro + Pro/Pro genotype on the frequency of PC. These results indicate that the p53 codon 72 polymorphism may interact with CXCL12 G801A. Conclusions: This is the first report showing that CXCL12 G801A polymorphism may be a risk factor for PC. Moreover, this study suggests that this polymorphism can be an important marker for detecting microinvasion and PC metastasis.

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“…The causes of familial and sporadic cancers may differ and many studies have examined the possible differences in survival, however, overall with inconclusive results. For the commonest cancers, such as prostate and breast cancers, recent evidence has suggested no survival difference between the sporadic and familial diseases [3][4][5][6][7][8][9][10][11][12][13][14][15][16]. A similar survival experience was noted for familial and sporadic cancers for most of the cancer sites examined.…”

Section: Discussionmentioning

confidence: 64%

“…Many other studies have been done to examine the survival difference between familial and sporadic cancers, such as breast and prostate cancers [3][4][5][6][7][8][9][10][11][12][13][14][15][16]. However, the results were inconsistent at present, and study design limitations, such as such as small sample size, biased selection of study subjects and poor selection of controls, could be related to the inconsistent data.…”

Section: Introductionmentioning

confidence: 99%

Survival in common cancers defined by risk and survival of family members

Försti

Sundquist

et al. 2010

Oncol Rev

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Studies on survival between familial and sporadic cancers have been inconclusive and only recent data on a limited number of cancers are available on the concordance of survival between family members. In this review, we address these questions by evaluating the published and unpublished data from the nation-wide Swedish Family-Cancer Database and a total of 13 cancer sites were assessed. Using sporadic cancer as reference, HRs were close to 1.0 for most of the familial cancers in both the offspring and parental generations, which suggested that survival in patients with familial and sporadic cancers was equal, with an exception for ovarian cancer with a worse prognosis. Compared to offspring whose parents had a poor survival, those with a good parental survival had a decreased risk of death for most cancers and HR was significantly decreased for cancers in the breast, prostate, bladder, and kidney. For colorectal and nervous system cancers, favorable survival between the generations showed a borderline significance. These data are consistent in showing that both good and poor survival in certain cancers aggregate in families. Genetic factors are likely to contribute to the results. These observations call for intensified efforts to consider heritability in survival as one mechanism regulating prognosis in cancer patients.

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Prevalence, Treatment Modalities and Prognosis of Familial Prostate Cancer in a Screened Population

Abstract: Although screened men 55 to 75 years old with a father or a brother having prostate cancer themselves are at a substantially greater risk for the disease, the clinical presentation, treatment modalities and prognosis by biochemical progression are not different compared to sporadic cases.

Cited by 31 publications

References 18 publications

Single and Multivariate Associations of MSR1, ELAC2, and RNASEL with Prostate Cancer in an Ethnic Diverse Cohort of Men

Single and Multivariate Associations of MSR1, ELAC2, and RNASEL with Prostate Cancer in an Ethnic Diverse Cohort of Men

CXCL12 G801A Polymorphism Is a Risk Factor for Sporadic Prostate Cancer Susceptibility

Survival in common cancers defined by risk and survival of family members

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