1,721,094 research outputs found
FAMILY HISTORY OF CANCER AND FAMILY HISTORY SCORES FOR ASSESSING THE LEVEL OF DISEASE RISK IN FAMILIES
Full text linkIn the last decades genetic factors are playing an increasingly important role in medical research, given the evidence for the existence of a heritable susceptibility for various diseases, including common cancers, based on reports of families with multiple affected relatives. Epidemiologists have utilized family history, usually of first-degree relatives, as a surrogate for genetic risk, aware that family history reflects the consequences of genetic susceptibilities, shared environment, and common behaviors.
During my PhD I have dealt with two different aspects of family history, i.e., the role of family history of cancer in epidemiological cancer research (Chapter 1) and the use of complex family history score for assessing the level of disease risk in families (Chapter 2).
In particular, I have systematically examined the extent to which a family history of cancer might be a risk factor for cancer within the same cancer site and across multiple cancer sites, analyzing a large and comprehensive dataset based on a network of integrated case-control studies, conducted in Italy and Switzerland since the early 90's. The database included 1468 cases of cancer of the oral cavity and pharynx, 198 of the rhinopharynx, 505 of the esophagus, 230 of the stomach, 2390 of the colorectum, 185 of the liver, 326 of the pancreas, 852 of the larynx, 3034 of the breast, 367 of the endometrium, 1031 of the ovary, 1294 of the prostate, 767 of the renal cell, and a total of 16022 corresponding controls. Unconditional multiple logistic regression models, adjusted for the major possible confounding factors, and a procedure for controlling for multiplicity using a false discovery rate were used. The risk of developing cancer at a particular site was increased, although not always significantly, in subjects with a first-degree relative affected by cancer at the same site, with odds ratios ranging from 1.4 for pancreatic cancer, to 7.4 for ovarian cancer. Several across sites associations emerged, some of which possibly due to shared environmental exposures or lifestyle practices among family members (e.g., alcohol, smoking, unhealthy diet, infections) or to the inheritance of one or more predisposing gene mutations (high penetrance gene mutations, such as BRCA1/2 in breast and ovarian cancer, and/or low penetrance polymorphisms, as those involved in carcinogens metabolism, such as GST genes in oral cancer) or to a combination of both. The analysis I performed confirmed that several associations were stronger for a younger age at diagnosis in relatives. A detailed discussion of the findings is reported in paragraph 4 of Chapter 1.
In addition to the investigation of the role of family history of cancer in cancer etiology, I have performed a statistical evaluation of the performance of different family history scores to recommend the measure that performs best. Family history scores summarize familial information and are used for estimating the familiar risk, i.e. the level of risk for a particular disease among members of that family. The simplest and most common family history scores are the dichotomous measure indicator, positive in families that have at least one relative with the disease, the number of affected family members, and the proportion of affected relatives, which takes into account the size of the family. The other family history scores proposed in the literature are statistics that describe the deviation of the observed situation from the expected risk for each family. More detailed information on family members (affected and unaffected) as well as incidence rates of the diseases of interest in strata of selected covariates are needed to compute these more complex family history scores. To evaluate family history scores’ performance I used two different complementary approaches: a data-derived approach, using data from the Italian HI-WATE study, with the aim of examining the power of various family history scores in predicting a particular diseases (i.e., colorectal cancer), and a simulation approach to evaluate their accuracy of predicting the true familial risk. From 200 simulations for 48 different settings, Reed’s score and FHS2 seem to perform slightly better than the other scores. However, the simple proportion of affected relatives is not so far in terms of predictivity of the true familial risk. The use of this simple score seems therefore justified, at least until stronger evidence is brought for the advantages of using a more complex score
Risk factors for breast cancer in China : similarities and differences with western populations
No full textHepatocellular carcinoma epidemiology
No full textPrimary liver cancer (namely hepatocellular carcinoma, HCC) is worldwide the fifth most common cancer in men and the seventh one in women, and it represents the third most frequent cause of cancer death. HCC rates are particularly high in eastern/south-eastern Asia and in Africa, intermediate in Southern Europe, and low in most high-income countries. Persistent infections by HBV or HCV are the main recognized risk factors for HCC. Aflatoxin exposure is also an important risk factor for HCC development in Africa and eastern Asia. In high-income countries heavy alcohol drinking, tobacco smoking, overweight, diabetes, familial/genetic factors, and selected dietary aspects, have a relevant role. Updated geographic patterns and time trends in mortality from HCC in Europe, USA, Japan, and Australia are provided in the present review, together with an overview of relevant etiologic factors for HCC and main measures for the prevention of this neoplasm. © 2014 Elsevier Ltd
Clinical and Genetic Markers of Nonalcoholic Fatty Liver Disease and Prediction of Liver Disease Mortality: Ready for Population Screening?
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Family history and the risk of cancer : genetic factors influencing multiple cancer sites
No full textA number of co-aggregations of cancers at different sites has been reported, including recognized syndromes (e.g., Li-Fraumeni), and aggregations between cancers at breast, stomach and ovary, between cancers at prostate, urinary tract and other sites, as well as between several tobacco-related neoplasms. In a network of case-control studies from Italy and Switzerland, including more than 12,000 cases of 13 different cancers, after controlling for multiple testing, significant associations emerged between oral and pharyngeal cancer and family history of laryngeal cancer (relative risk (RR): 3.3); esophageal cancer and family history of oral and pharyngeal cancer RR: 4.1; breast cancer and family history of colorectal cancer (RR: 1.5) and of hemolymphopoietic cancers (RR: 1.7); ovarian cancer and family history of breast cancer (RR: 2.3); and prostate cancer and family history of bladder cancer (RR: 3.4). Shared exposures to environmental factors within families account for some of the observed aggregations, together with heritable, and hence, genetic factors
A meta-analysis of body mass index and esophageal and gastric cardia adenocarcinoma
No full textBackground: The incidence rates of esophageal and gastric cardia adenocarcinoma (EGCA) have increased over recent years in several countries, and overweight/obesity has been suggested to play a major role in these trends. In fact, higher body mass index (BMI) has been positively associated with EGCA in several studies. Material and methods: We conducted a meta-analysis of case-control and cohort studies on the BMI and EGCA updated to March 2011. We estimated overall relative risks (RRs) and 95% confidence intervals (CI) for BMI between 25 and 30 and BMI ≥ 30 kg/m2, when compared with normo-weight subjects, using random-effects models. Results: We identified 22 studies, including almost 8000 EGCA cases. The overall RR was 1.71 (95% CI 1.50-1.96) for BMI between 25 and 30, and was 2.34 (95% CI 1.95-2.81) for BMI ≥ 30 kg/m2. The continuous RR for an increment of 5 kg/m2 of BMI was 1.11 (95% CI 1.09-1.14). The association was stronger for esophageal adenocarcinoma (RR for BMI ≥ 30 kg/m2 = 2.73, 95% CI 2.16-3.46) than for gastric cardia adenocarcinoma (RR for BMI ≥ 30 kg/m2 = 1.93, 95% CI 1.52-2.45). No substantial differences emerged across strata of sex and geographic areas. Conclusion: Overweight and obesity are strongly related to EGCA, particularly to espophageal adenocarcinoma
Coffee consumption and risk of colorectal cancer : a meta-analysis of case-control studies
No full textA meta-analysis of case-control studies on coffee consumption and colorectal cancer risk was conducted. Twenty-four eligible studies published before May 2010 were identified, including a total of 14,846 cases of colorectal, colon or rectal cancer. Compared to non/occasional drinkers, the odds ratios (OR) for drinkers were 0.83 (95% CI 0.73-0.95) for colorectal, 0.93 (95% CI 0.81-1.07) for colon and 0.98 (95% CI 0.85-1.13) for rectal cancer, with significant heterogeneity among studies; the corresponding ORs for the increment of 1 cup/day were 0.94 (95% CI 0.91-0.98), 0.95 (95% CI 0.92-0.98), and 0.97 (95% CI 0.95-0.99). For the highest coffee drinkers, the ORs were 0.70 (95% CI 0.60-0.81) for colorectal cancer, 0.75 (95% CI 0.64-0.88) for colon cancer and 0.87 (95% CI 0.75-1.00) for rectal cancer, when compared to non/low drinkers. The results of this meta-analysis of case-control studies suggest a moderate favorable effect of coffee consumption on colorectal cancer risk. The reduced risk was consistent across study design (hospital vs. population based), geographic area, and various confounding factors considered. It may reflect a real protection but also partly or largely be due to reverse causation, i.e. decreased coffee consumption among cases following the onset of bowel symptoms
Gastric cancer and allium vegetable intake: A critical review of the experimental and epidemiologic evidence
No full textThere are suggestions of an anticancerogenic effect of allium vegetables and their associated organosulfur components against several cancer types, including gastric cancer, but the issue remains open to discussion and quantification. The present critical review discussed the history, the health properties, the chemistry, the anticancerogenic evidences from experimental studies, and the anticancer mechanisms of allium vegetables. We also summarized findings from epidemiological studies concerning the association between different types of allium vegetables and gastric cancer risk, published up to date. Available data, derived mainly from case-control studies, suggested a favorable role of high intakes of allium vegetables, mainly garlic and onion, in the etiology of gastric cancer. In particular, of 10 studies, 7 suggested a favorable role of high intake of total allium vegetables and gastric cancer. All 14 studies on garlic and most studies on onion (more than 80%) reported a beneficial role of these allium types against gastric cancer. However several limitations, including possible publication bias and the difficulty to establish a dose-risk relationship, suggest caution in the interpretation. Evidences on other types of allium vegetables, as well as on the influence of different gastric cancer anatomical and histological types, are less consistent. © 2014 Copyright © 2014, Taylor & Francis Group, LLC
Exposure to antithyroid drugs and ethylenethiourea and risk of thyroid cancer: a systematic review of the epidemiologic evidence
No full textIntroduction: The thyroid peroxidase inhibiting compounds methimazole, methylthiouracil, propylthiouracil, thiouracil (i.e. 'antithyroid' drugs) and ethylenethiourea have been associated to thyroid tumours in rodents. According to a systematic review by the International Agency for Research on Cancer (IARC) published in 2000, evidence for the human carcinogenicity was inadequate.
Methods: We performed an up-to-date systematic review of human epidemiological studies on the association between such compounds and thyroid cancer incidence or mortality.
Results: The literature research (1999-March 2020) identified four relevant articles. Considering also reports from the previous IARC review, this systematic review considered seven reports (five distinct studies) on antithyroid drugs and two on ethylenethiourea. As for antithyroid drugs, three reports based on different follow-ups gave results from a cohort of patients treated for hyperthyroidism in 1946-1964. In the earlier report, thyroid cancer incidence was higher in patients primarily treated with antithyroid drugs (3.2/1000) than in those originally treated with thyroidectomy (0.34/1000) or radioactive iodine (0.88/1000), which can be explained by the higher frequency of subsequent thyroidectomy, and hence the higher chance of cancer detection, in that group (30 vs. 0.5 and 1.2%). The two subsequent reports found no deaths from thyroid cancer among patients treated exclusively with antithyroid drugs through 1990 and 2014. A nested case-control study found an odds ratio (OR) of thyroid cancer of 2.79 [95% confidence interval (CI), 0.78-10.02, from a 2-year lag analysis] for ≥3 vs. no propylthiouracil prescriptions. The increased risk can be attributed to advanced diagnosis of an underlying cancer, as suggested by the stronger association observed in a no-lag analysis (OR, 8.03). In a historical cohort of newly diagnosed hyperthyroid patients, the hazard ratio for treatment with radioactive iodine vs. thionamides only was 0.45 (95% CI, 0.21-0.99), possibly due to the closer surveillance of patients receiving thionamides only. Two case-control studies did not find any association with the use of antithyroid drugs. As for ethylenethiourea, no thyroid cancer cases were found in a historical cohort of 1929 workers occupationally exposed in a 15-year period and no association with proxies of mancozeb exposure (a fungicide whose main metabolite is ethylenethiourea) was detected in a cohort of >236 000 farmers.
Conclusion: There is no evidence for a relevant role of either antithyroid drugs or ethylenethiourea on thyroid cancer
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