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    BACKGROUND:Screening by fecal occult blood test and lower endoscopy has lowered colorectal cancer (CRC) mortality, but compliance gaps persist. Of concern are possible disparities in uptake of CRC screening between white and African American men. The goal of this study was to assess for disparities in uptake of CRC screening among men participating in a high-risk prostate cancer clinic. If present, such disparities could support hypotheses for further research examining racial differences in awareness and patient preferences in undergoing CRC screening.METHODS:Baseline data on a racially diverse cohort of men aged 50 to 69 years at increased risk of prostate cancer collected via the Prostate Cancer Risk Assessment Program at Fox Chase Cancer Center were analyzed. Predictors of uptake of CRC screening were assessed using multivariate logistic regression.RESULTS:Compared with whites, African American men had statistically significantly lower uptake of fecal occult blood testing (African American 49.0% vs white 60.7%, P = .035), lower endoscopy (African American 44.1% vs white 58.5%, P = .011), and any CRC screening (African American 66.2% vs white 76.3%, P = .053). Predictors of uptake of lower endoscopy among African American men included older age (odds ratio [OR], 3.61; 95% confidence interval [CI], 1.87-6.97), family history of CRC (OR, 3.47; 95% CI, 1.30-9.25), and insurance status (OR, 1.90; 95% CI, 1.04-3.46).CONCLUSIONS:Despite awareness of cancer risk and motivation to seek prostate cancer screening through a specialized prostate cancer risk assessment program, evidence supporting compliance gaps with CRC screening among men was found. Tailored messages to younger African American men with and without a family history of CRC are needed. Cancer 2011;. © 2011 American Cancer Society.dx.doi.org


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    BACKGROUND:Single nucleotide polymorphisms (SNPs) in nucleotide excision repair (NER) pathway genes may modulate DNA repair capacity and increase susceptibility to breast cancer (BC). A case-control study was conducted by evaluating genes involved in DNA repair to identify polymorphisms associated with BC.METHODS:The 384 SNPs of 38 candidate genes were genotyped using the Illumina GoldenGate method. Genotypes were determined in a case-control study that consisted of 346 BC patients and 361 controls. Odds ratios and 95% confidence intervals were computed using logistic regression models. Multiple logistic regression models adjusted for age, family history of BC, and body mass index were used.RESULTS:Gene–gene interaction analysis among the DNA repair pathway genes showed significant effects on BC risk. ERCC2 rs50872 (TC genotype) in combination with XPA rs2808668 (TC genotype) and rs1800975 (AG genotype) was strongly associated with an increased risk of BC (P = .0004 and .0002, PBonferroni = .023 and .014, respectively). Moreover, the T-G (including rs2808668 and rs1800975) haplotype in XPA combined with the ERCC2 T allele in rs50872 carriers was also associated with additive risk effect of BC (odds ratios: 2.58, 2.62, and 3.49, respectively).CONCLUSION:Genetic variation in DNA repair genes involved in NER mechanisms increased the risk of BC development. These results suggested that a stronger combined effect of SNPs via gene–gene interaction may help to predict BC risk. Cancer 2011;. © 2011 American Cancer Society.dx.doi.org


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    BACKGROUND:Statins are widely used cholesterol-lowering agents that may have potential antitumor effect. Epidemiological studies on statin use and renal cell carcinoma (RCC) risk have been inconsistent.METHODS:The authors investigated the association between statin use and RCC risk in the Nurses' Health Study and Health Professionals Follow-Up Study. In total, 80,782 women and 37,869 men were followed for 14 years and 16 years, respectively. Regular statin use was assessed at baseline and was updated biennially during follow-up. RCC diagnosis was confirmed by medical record review.RESULTS:Two hundred seventy-seven incident RCC cases (164 women and 113 men) were identified. Compared with no current use, the multivariate relative risks of current statin use were 0.68 (95% confidence interval, 0.46-1.00) in women and 1.17 (95% confidence interval, 0.75-1.82) in men. The results for ever versus never users of statins were similar. No dose-response relation with duration of statin use and RCC risk was observed. On subgroup analyses, statin use was associated with a reduced RCC risk among women who had no history of hypertension.CONCLUSIONS:The current study indicated that statin use may be associated with a lower risk of RCC in women, although these results need to be investigated further. Cancer 2011;. © 2011 American Cancer Society.dx.doi.org


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    BACKGROUND:Genetic counseling and testing is recommended for women at high but not average risk of ovarian cancer. National estimates of physician adherence to genetic counseling and testing recommendations are lacking.METHODS:Using a vignette-based study, we surveyed 3200 United States family physicians, general internists, and obstetrician/gynecologists and received 1878 (62%) responses. The questionnaire included an annual examination vignette asking about genetic counseling and testing. The vignette varied patient age, race, insurance status, and ovarian cancer risk. Estimates of physician adherence to genetic counseling and testing recommendations were weighted to the United States primary care physician population. Multivariable logistic regression identified independent patient and physician predictors of adherence.RESULTS:For average-risk women, 71% of physicians self-reported adhering to recommendations against genetic counseling or testing. In multivariable modeling, predictors of adherence against referral/testing included black versus white race (relative risk [RR], 1.16; 95% confidence interval [CI], 1.03-1.31), Medicaid versus private insurance (RR, 1.15; 95% CI, 1.02-1.29), and rural versus urban location. Among high-risk women, 41% of physicians self-reported adhering to recommendations to refer for genetic counseling or testing. Predictors of adherence for referral/testing were younger patient age [35 vs 51 years [RR, 1.78; 95% CI, 1.41-2.24]), physician sex (female vs male [RR, 1.30; 95% CI, 1.07-1.64]), and obstetrician/gynecologist versus family medicine specialty (RR, 1.64; 95% CI, 1.31-2.05). For both average-risk and high-risk women, physician-estimated ovarian cancer risk was the most powerful predictor of recommendation adherence.CONCLUSION:Physicians reported that they would refer many average-risk women and would not refer many high-risk women for genetic counseling/testing. Intervention efforts, including promotion of accurate risk assessment, are needed. Cancer 2011;. © 2011 American Cancer Society.dx.doi.org


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    BACKGROUND:Earlier studies have suggested that type 2 diabetes mellitus (T2DM) alters the risk of developing a variety of cancers, but little has been known about the impact of T2DM on cancer prognosis. On the basis of nationwide population-based Swedish registries, the authors of this report compared the cause-specific survival among cancer patients with and without T2DM.METHODS:Patients with T2DM were identified from the nationwide Swedish Hospital Discharge Register, and cancers were recorded from the Swedish Cancer Registry. Hazard ratios (HRs) were calculated using Cox regression models to compare variations in cause-specific survival between cancer patients with and without T2DM.RESULTS:Of the 1016,105 cancer patients, 16,123 had been hospitalized with T2DM before their diagnosis of cancer. The mortality rate was significantly higher among cancer patients with T2DM than among those without T2DM (cause-specific HR, 1.38; 95% confidence interval, 1.35-1.41). There were no differences in TNM stage distribution among cancer patients with or without T2DM for the main cancers, with an exception of tumor and metastatic classifications for breast cancer and prostate cancer, respectively.CONCLUSIONS:The current results indicated that patients with T2DM who are diagnosed with a subsequent cancer are at an increased risk for cause-specific mortality compared with patients who have cancer without T2DM. Cancer 2011;. © 2011 American Cancer Society.dx.doi.org


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