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Carcinoma Risk (carcinoma + risk)
Selected AbstractsCoffee drinking and hepatocellular carcinoma risk: A meta-analysis,HEPATOLOGY, Issue 2 2007Francesca Bravi Several studies suggest an inverse relation between coffee drinking and risk of hepatocellular carcinoma (HCC). We conducted a meta-analysis of published studies on HCC that included quantitative information on coffee consumption. Ten studies were retrieved (2,260 HCC cases), including 6 case,control studies from southern Europe and Japan (1551 cases) and 4 cohort studies from Japan (709 cases). The summary relative risk (RR) for coffee drinkers versus non-drinkers was 0.54 (95% confidence interval [CI] 0.38-0.76) for case,control studies and 0.64 (95% CI 0.56-0.74) for cohort studies. The overall RR was 0.59 (95% CI 0.49-0.72), with significant heterogeneity between studies. The overall summary RR for low or moderate coffee drinkers was 0.70 (95% CI 0.57-0.85), and that for high drinkers was 0.45 (95% CI 0.38-0.53). The summary RR for an increase of 1 cup of coffee per day was 0.77 (95% CI 0.72-0.83) from case,control studies, 0.75 (95% CI 0.65-0.85) from cohort studies, and 0.77 (95% CI 0.72-0.82) overall. The consistency of an inverse relation between coffee drinking and HCC across study design and geographic areas weighs against a major role of bias or confounding. Coffee drinking has also been related to reduced risk of other liver diseases, thus suggesting a continuum of the favorable effect of coffee on liver function. However, subjects with liver conditions may selectively reduce their coffee consumption. Conclusion: The present analysis provides evidence that the inverse relation between coffee and HCC is real, though inference on causality remains open to discussion. (HEPATOLOGY 2007.) [source] Carcinogenetic impact of ADH1B and ALDH2 genes on squamous cell carcinoma risk of the esophagus with regard to the consumption of alcohol, tobacco and betel quidINTERNATIONAL JOURNAL OF CANCER, Issue 6 2008Chien-Hung Lee Abstract The consumption of alcohol, tobacco and betel quid has been found to be an important contributor to esophageal squamous cell carcinoma (ESCC) in Taiwan. The genotoxic effect of the ADH1B and ALDH2 genes modulating an individual's alcohol-metabolizing capacity on ESCC may be linked to drinking behavior, intake pattern and other exogenous factors. To investigate the interplay of these genetic and environmental factors in determining the risk of ESCC, a multicenter case-control study was conducted. Here, 406 patients with pathology-proven ESCC, as well as 656 gender, age and study hospital matched controls were recruited. Genetic polymorphisms of ADH1B and ALDH2 appeared to correlate with the abstinence of alcohol, though not with tobacco and betel quid. Within the same levels of alcohol consumption, carcinoma risks increased along with an increase in the numbers of ADH1B*1 and ALDH2*2 alleles. The inactive ALDH2*1/*2 genotype was found to multiplicatively interact with a low-to-moderate (0.1,30 g/day) and a heavy (>30 g/day) ethanol intake to increase the ESCC risk (the joint aOR = 14.5 and 102.6, respectively). Among low-to-moderate drinkers, a smoking-dependent carcinogenetic effect for the ADH1B*1/*1 and ALDH2*1/*2+*2/*2 genotypes was recognized, with significant risks found in smokers, but not in nonsmokers. Further, a supra-multiplicative combined risk of ESCC for alcohol and tobacco use was identified among carriers of the ADH1B*1/*1 genotype (p for interaction = 0.042). In conclusion, the interplay of the ADH1B and ALDH2 genotypes, in conjunction with a behaved drinking habit and a practiced drinking pattern, along with continued tobacco consumption, plays an important pathogenic role in modulating ESCC risk. © 2007 Wiley-Liss, Inc. [source] Reproducibility of cytologic atypia in repeat nipple duct lavageCANCER, Issue 6 2005April Johnson-Maddux M.D. Abstract BACKGROUND It is believed that atypical cells identified by nipple duct lavage (NDL) indicate an increased risk for breast carcinoma similar to atypical ductal hyperplasia diagnosed by tissue biopsy, but many basic performance characteristics of NDL currently are undefined. METHODS NDL was performed in 108 patients unselected for breast carcinoma risk and then was repeated after 2,14 months (median, 8 months) if the initial lavage was classified as atypical. Breast magnetic resonance images (MRIs) were obtained from a subset of patients who had atypical lavage results. RESULTS Marked atypia was diagnosed in 22% of 36 breasts with an incident carcinoma compared with 7% of 172 unaffected breasts (P = 0.01). After excluding breasts with an incident carcinoma, there were 32 patients (30%) with either mild or marked atypia. The lavage was repeated in 23 of these women, and the second lavage was classified as atypical in 48%. Neither marked atypia on the initial lavage nor a 5-year Gail risk , 1.7% predicted atypia on repeat lavage, but there was a trend for improved reproducibility when the atypia initially was diagnosed in a fluid-producing duct. MRIs were abnormal in 13% of 24 breasts with an atypical lavage, and ductal carcinoma in situ was diagnosed subsequently in 1 breast. CONCLUSIONS Atypia frequently is diagnosed by NDL, but the reproducibility of repeat lavage is low. Lavage atypia may be physiologic or artifactual rather than pathologic in many instances. Marked atypia occasionally may represent mammographically occult ductal carcinoma in situ. Cancer 2005. © 2005 American Cancer Society. [source] Reproductive factors and risk of breast carcinoma in a study of white and African-American women,,CANCER, Issue 2 2004Giske Ursin M.D., Ph.D. Abstract BACKGROUND Few studies have investigated the association between reproductive factors and the risk of breast carcinoma among African-American women. The authors assessed whether the number of full-term pregnancies, age at first full-term pregnancy, and total duration of breastfeeding were associated with similar relative risk estimates in white and African-American women in a large multicenter, population-based case,control study of breast carcinoma. METHODS Case patients were 4567 women (2950 white women and 1617 African-American women) ages 35,64 years with newly diagnosed invasive breast carcinoma between 1994 and 1998. Control patients were 4668 women (3012 white women and 1656 African-American women) who were identified by random-digit dialing and were frequency matched to case patients according to study center, race, and age. Adjusted odds ratios and 95% confidence intervals were estimated using unconditional logistic regression. RESULTS For white women, the reduction in risk of breast carcinoma per full-term pregnancy was 13% among younger women (ages 35,49 years) and 10% among older women (ages 50,64 years). The corresponding risk reductions for African-American women were 10% and 6%, respectively. Risk decreased significantly with increasing number of full-term pregnancies for both races and both age categories. Duration of lactation was inversely associated with breast carcinoma risk among younger parous white (trend P = 0.0001) and African-American (trend P = 0.01) women. African-American women tended to have more children compared with white women, but parity rates were lower in younger women than in older women in both racial groups. However, breastfeeding was substantially more common in young white women than in young African-American women. CONCLUSIONS Overall, parity and lactation had similar effects on breast carcinoma risk in white and African-American women. If younger African-American women now are giving birth to fewer children than in the past, without a substantial increase in breastfeeding, breast carcinoma rates may continue to increase at a more rapid rate among these women compared with white women. Cancer 2004. Published 2004 by the American Cancer Society. [source] Acceptance of tamoxifen chemoprevention by physicians and women at riskCANCER, Issue 9 2004Julia Tchou M.D., Ph.D. Abstract BACKGROUND In the National Surgical Adjuvant Breast and Bowel Project (NSABP) P-1 trial, tamoxifen was shown to reduce breast carcinoma risk by 49% in high-risk women. The purpose of the current study was to identify factors associated with being offered, and accepting, tamoxifen chemoprevention. METHODS The records of 219 women who sought risk evaluation after the publication of the NSABP P-1 trial between September 1998 and October 2002 were reviewed. Risk was calculated using the model of either Gail et al. or Claus et al. The impact of individual risk factors on the offering and acceptance of tamoxifen was compared using the Fisher exact test and logistic regression analysis. RESULTS Tamoxifen was offered to 137 women (63%) in the current study. The magnitude of Gail risk, age, menopausal status, hysterectomy, and history of lobular carcinoma in situ (LCIS) or atypical hyperplasia (AH) were all found to be significant predictors of a patient being offered tamoxifen. On multivariate analysis, only a history of AH or LCIS and hysterectomy were found to be significant, with odds ratios of 20.3 and 3.4, respectively. Fifty-seven of the women who were offered tamoxifen (42%) took the drug. Only a history of LCIS or AH and older age were found to be predictive of tamoxifen acceptance. CONCLUSIONS In the current study, risk due to AH or LCIS was found to be the main predictor of being offered and accepting tamoxifen chemoprevention. Cancer 2004. © 2004 American Cancer Society. [source] Genetic polymorphisms of estrogen receptor alpha, CYP19, catechol- O -methyltransferase are associated with familial prostate carcinoma risk in a Japanese populationCANCER, Issue 7 2003Kazuhiro Suzuki M.D. Abstract BACKGROUND Estrogen is one of the crucial hormones participating in the proliferation and carcinogenesis of the prostate glands. Genetic polymorphisms in the estrogen metabolism pathway might be involved in the risk of prostate carcinoma development. The authors evaluated the association between genetic polymorphisms in estrogen-related enzymes and receptors and the risk of developing familial prostate carcinoma. METHODS In the current study, 101 cases with prostate carcinoma whose first-degree relatives had prostate carcinoma and 114 healthy age and residence-matched male controls were enrolled. The genotypes of estrogen receptor (ER) alpha, aromatase (CYP19), and catechol- O -methyltransferase (COMT) genes were analyzed. RESULTS For single polymorphisms, a significant association of the T/T genotype of the PvuII site in the ER alpha gene (odds ratio [OR], 3.44; 95% confidence interval [CI], 1.97,5.99; P = 0.0028), and the C/T and T/T genotypes of the CYP19 gene (OR, 1.77; 95% CI, 1.02,3.09; P = 0.037) with prostate carcinoma risk, was observed. The G/A genotype of the COMT gene showed a weak tendency toward increased risk (OR, 1.48; 95% CI, 0.85,2.57; P = 0.18). Stratification of cases according to clinical stage and pathologic grade showed that the C/T and T/T genotypes of the CYP19 gene were associated significantly with high-grade carcinoma (OR, 2.59; 95% CI, 1.47,4.46; P = 0.048). The number of high-risk genotypes (the T/T in ER alpha, the C/T and T/T in CYP19, and the G/A in COMT) significantly increased the risk of developing prostate carcinoma (2 genotypes: OR, 3.00; 95% CI, 1.72,5.23; P = 0.008; 3 genotypes: OR, 6.30; 95% CI, 3.61,10.99; P = 0.002). CONCLUSIONS Genetic polymorphisms of genes in the estrogen metabolism pathway were associated significantly with familial prostate carcinoma risk. Single nucleotide polymorphisms of low-penetrance genes are targets for understanding the genetic susceptibility of familial prostate carcinoma. Cancer 2003;98:1411,6. © 2003 American Cancer Society. DOI 10.1002/cncr.11639 [source] Effects of smoking and radiotherapy on lung carcinoma in breast carcinoma survivorsCANCER, Issue 7 2003Melissa B. Ford Ph.D. Abstract BACKGROUND The combined effects of thoracic radiotherapy (XRT) and cigarette smoking are not known with certainty, but they have important implications for lung carcinogenesis after cancer therapy in some patients. The authors analyzed smoking, radiation, and both exposures on lung carcinoma development in women who were treated previously for breast carcinoma. METHODS Case patients (n = 280) were female residents of the United States, ages 30,89 years, with breast carcinoma prior to primary lung carcinoma diagnosed between 1960 and 1997. Control patients (n = 300) were selected randomly from 37,000 patients with breast carcinoma who were treated at The University of Texas M. D. Anderson Cancer Center and frequency matched with women in the case group based on age at diagnosis (5-year strata), ethnicity, year of breast carcinoma diagnosis (5-year strata), and survival from breast carcinoma diagnosis to lung carcinoma diagnosis. Using stratified analysis and unconditional logistic regression, the authors evaluated the main and combined effects of smoking and XRT on lung carcinoma risk. RESULTS At the time of breast carcinoma diagnosis, 84% of case patients had ever smoked cigarettes, compared with 37% of control patients, whereas 45% of case patients and control patients received XRT for breast carcinoma. Smoking increased the odds of lung carcinoma in women without XRT (odds ratio [OR], 6.0; 95% confidence interval [95% CI], 3.6,10.1), but XRT did not increase lung carcinoma risk in nonsmoking women (OR, 0.5; 95% CI, 0.3,1.1). Overall, the OR for both XRT and smoking, compared with no XRT or smoking, was 9.0 (95% CI, 5.1,15.9). Logistic regression modeling yielded an adjusted OR of 5.6 for the smoking main effect (95% CI, 2.9,10.5), 0.6 for the XRT main effect (95% CI, 0.3,1.4), and 8.6 (P = 0.08) for the combined effect. CONCLUSIONS Smoking was a significant independent risk factor for lung carcinoma after breast carcinoma, but XRT alone was not. Smoking and XRT combined enhanced the effect of either alone, with marked increased risks of lung carcinoma after XRT for breast carcinoma. Cancer 2003;98:1457,64. © 2003 American Cancer Society. DOI 10.1002/cncr.11669 [source] Energy restriction early in life and colon carcinoma riskCANCER, Issue 1 2003Results of the Netherlands Cohort Study after 7.3 years of follow-up Abstract BACKGROUND This study evaluated the effects of severe undernutrition during adolescence and subsequent colon carcinoma risk. METHODS The authors evaluated The Netherlands Cohort Study on Diet and Cancer (NLCS) among 62,573 women and 58,279 men aged 55,69 years at baseline. Information on diet and risk factors was collected by questionnaire in 1986. Additional information was collected concerning residence during the hunger winter (1944,1945), the World War II years (1940,1944), and father's employment status during the economic depression of 1932,1940, which were used as indicators of exposure. After 7.3 years of follow-up, 807 colon carcinoma cases (388 females and 419 males) were available for analysis. RESULTS Multivariate analysis showed that both men and women who had lived in a western city in 1944,1945 had a decreased colon carcinoma risk (men: relative risk [RR] = 0.85, 95% confidence interval [CI] = 0.62,1.16; women: RR = 0.80, 95%CI = 0.59,1.09). No association between colon carcinoma risk and urban versus rural residence was found during the war years (1940,1944). Having an unemployed father during the economic depression (1932,1940) was also associated with a small decrease in colon carcinoma risk for men (RR = 0.90, 95% CI =0.62,1.31) and women (RR = 0.75, 95%CI 0.49-1.14). In subgroup analyses, a decreased colon carcinoma risk for men and women who were in their adolescent growth spurt and living in a western city during the hunger winter of 1944,1945 was noted (men: RR = 0.72, 95% CI = 0.31,1.65; women: RR = 0.88, 95% CI = 0.40,1.96). No associations were statistically significant because of the limited study size. CONCLUSIONS In the current study, a weak inverse relation was found between energy restriction early in life and subsequent colon carcinoma risk for men and women. However, these findings need replication in a larger study. Cancer 2003;97:46,55. © 2003 American Cancer Society. DOI 10.1002/cncr.11052 [source] BPDE-induced lymphocytic 3p21.3 aberrations may predict head and neck carcinoma riskCANCER, Issue 3 2002Yong Zhu Ph.D. Abstract BACKGROUND Tobacco exposure is an established risk factor for head and neck squamous cell carcinoma (HNSCC). Benzo[,]pyrene diol expoxide (BPDE), a main metabolic product of the tobacco smoke constituent benzo[,]pyrene, induces chromosomal aberrations at specific loci. Chromosomal aberrations in peripheral blood lymphocytes (PBLs) induced by BPDE may reflect individuals' genetic susceptibility to tobacco carcinogens. METHODS This study was designed to detect BPDE-induced aberrations in PBLs at locus 3p21.3 in cultured lymphocytic cells. Our hypothesis is that the presence of BPDE-induced 3p21.3 aberrations is a biomarker of an individual's genetic susceptibility and that individuals with these aberrations are at an increased risk for HNSCC. PBL cultures from 52 cases and 54 controls were treated with 2 ,M BPDE for 24 hours before the 3p21.3 aberrations were assessed by flourescence in situ hybridization. One thousand lymphocyte interphases were scored for each sample. RESULTS We found that BPDE-induced chromosome 3p21.3 aberrations occurred more frequently in cases (mean: 31.4 per 1000 cells) than in controls (mean: 22.1 per 1000 cells; P < 0.001). However, when 6q27 was selected as a control locus, no such difference was observed (P = 0.545). When the 75th percentile value of induced aberrations in the controls was used as a cutoff point to classify 3p21.3 BPDE-induced sensitivity, 30 of the 52 cases (57.69%) and only 14 of the 54 controls (25.93%) were sensitive to BPDE exposure. This approach resulted in an odds ratio of 4.8 (95% confidence interval: 1.87,12.28) for HNSCC risk associated with BPDE-induced 3p21.3 aberrations. There was also a dose-response relationship between the number of BPDE-induced aberrations at 3p21.3 and risk for HNSCC. CONCLUSIONS The results from this study demonstrated that 3p21.3 may be a specific molecular target of tobacco carcinogens and that BPDE sensitivity at this locus may reflect an individual's genetic susceptibility to HNSCC. Cancer 2002;95:563,8. © 2002 American Cancer Society. DOI 10.1002/cncr.10689 [source] Carcinogenetic impact of ADH1B and ALDH2 genes on squamous cell carcinoma risk of the esophagus with regard to the consumption of alcohol, tobacco and betel quidINTERNATIONAL JOURNAL OF CANCER, Issue 6 2008Chien-Hung Lee Abstract The consumption of alcohol, tobacco and betel quid has been found to be an important contributor to esophageal squamous cell carcinoma (ESCC) in Taiwan. The genotoxic effect of the ADH1B and ALDH2 genes modulating an individual's alcohol-metabolizing capacity on ESCC may be linked to drinking behavior, intake pattern and other exogenous factors. To investigate the interplay of these genetic and environmental factors in determining the risk of ESCC, a multicenter case-control study was conducted. Here, 406 patients with pathology-proven ESCC, as well as 656 gender, age and study hospital matched controls were recruited. Genetic polymorphisms of ADH1B and ALDH2 appeared to correlate with the abstinence of alcohol, though not with tobacco and betel quid. Within the same levels of alcohol consumption, carcinoma risks increased along with an increase in the numbers of ADH1B*1 and ALDH2*2 alleles. The inactive ALDH2*1/*2 genotype was found to multiplicatively interact with a low-to-moderate (0.1,30 g/day) and a heavy (>30 g/day) ethanol intake to increase the ESCC risk (the joint aOR = 14.5 and 102.6, respectively). Among low-to-moderate drinkers, a smoking-dependent carcinogenetic effect for the ADH1B*1/*1 and ALDH2*1/*2+*2/*2 genotypes was recognized, with significant risks found in smokers, but not in nonsmokers. Further, a supra-multiplicative combined risk of ESCC for alcohol and tobacco use was identified among carriers of the ADH1B*1/*1 genotype (p for interaction = 0.042). In conclusion, the interplay of the ADH1B and ALDH2 genotypes, in conjunction with a behaved drinking habit and a practiced drinking pattern, along with continued tobacco consumption, plays an important pathogenic role in modulating ESCC risk. © 2007 Wiley-Liss, Inc. [source] | ||||||||||