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  • 1
    Keywords: brain ; CANCER ; tumor ; BLOOD ; LUNG ; COHORT ; cohort studies ; cohort study ; DISEASE ; incidence ; liver ; POPULATION ; RISK ; SITE ; PATIENT ; kidney ; colon ; ASSOCIATION ; NO ; meta-analysis ; cancer risk ; ESOPHAGUS ; RELATIVE RISK ; pulmonary embolism ; ORDER ; FEATURES ; MALIGNANCY ; pancreas ; review ; METAANALYSIS ; methods ; EVENTS ; CANCERS ; CANCER-RISK ; ENGLAND ; HUMAN PANCREATIC-CANCER ; PUBLICATION BIAS ; GENERAL-POPULATION ; DEEP-VEIN THROMBOSIS ; EXCESS ; ACUTE PULMONARY-EMBOLISM ; LOWER-LIMBS ; SYSTEMATIC REVIEWS ; TISSUE-FACTOR EXPRESSION ; venous thromboembolic events
    Abstract: Background: Despite a recognized association between venous thromboembolic events (VTE) and cancer, little is known about the strength and the features of this association. We performed a meta-analysis in order to clarify this issue. Methods: We retrieved data from 40 reports published between 1982 and 2007: 12 contained cancer risk estimates for patients with either idiopathic or secondary VTE vs. subjects without VTE and 17 for patients with idiopathic vs. secondary VTE. We also pooled risk estimates from four cohort studies to assess the association between VTE and specific forms of cancer and conducted a proportional incidence study, based on the remaining 28 reports, which did not provide risk estimates. Results: The pooled relative risk (RR) of cancer was 3.2 [95% confidence interval (95% CI) 2.4-4.5] for patients with any form of VTE vs. no VTE, 2.7 (95% CI 1.9-3.9) for patients with idiopathic vs. no VTE and 3.8 (95% CI 2.6-5.4) for patients with idiopathic vs. secondary VTE. In the pooled cohort studies, RRs for VTE vs. no VTE were significantly elevated for cancers of the ovary (RR 7.0), pancreas (RR 6.1), liver (RR 5.6), blood (4.2), brain (RR 3.8), kidney (RR 3.4), lung (3.1), colon (2.9), and esophagus (2.1). In the proportional incidence study, cancers of the pancreas, colon, and blood were significantly more frequently observed than in the general population. Conclusions: Overall we found a 3-fold excess risk of occult cancer in patients with VTE. The risk varies according to tumor site and is highest for cancers of the ovary, pancreas, and liver
    Type of Publication: Journal article published
    PubMed ID: 18284604
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  • 2
    Keywords: CANCER ; Germany ; MODEL ; MODELS ; FOLLOW-UP ; COHORT ; EPIDEMIOLOGY ; HISTORY ; RISK ; TIME ; ASSOCIATION ; HEALTH ; CIGARETTE-SMOKING ; smoking ; cancer risk ; ethanol ; NETHERLANDS ; ALCOHOL ; PROJECT ; ALCOHOL-CONSUMPTION ; CONSUMPTION ; EPIC ; nutrition ; pancreatic cancer ; LIFE-STYLE FACTORS ; pancreas ; PANCREATIC-CANCER ; WEIGHT ; DIETARY-INTAKE MEASUREMENTS ; BEER ; prospective ; CANCER-RISK ; MALE SMOKERS ; BEVERAGE CONSUMPTION ; COFFEE CONSUMPTION
    Abstract: To examine the association of baseline and lifetime ethanol intake with cancer of the pancreas in the European Prospective Investigation into Cancer and Nutrition (EPIC). Included in this analysis were 478,400 subjects, of whom detailed information on the intake of alcoholic beverages at baseline and over lifetime was collected between 1992 and 2000. During a median follow-up time of 8.9 years, 555 non-endocrine pancreatic cancer cases were observed. Multivariate Cox proportional hazard models were used to examine the association of ethanol intake at recruitment and average lifetime ethanol intake and pancreatic cancer adjusting for smoking, height, weight, and history of diabetes. Overall, neither ethanol intake at recruitment (relative risk (RR) = 0.94, 95% confidence interval (CI) 0.69-1.27 comparing 30+ g/d vs. 0.1-4.9 g/d) nor average lifetime ethanol intake (RR = 0.95, 95% CI 0.65-1.39) was associated with pancreatic cancer risk. High lifetime ethanol intake from spirits/liquor at recruitment tended to be associated with a higher risk (RR = 1.40, 95% CI 0.93-2.10 comparing 10+ g/d vs. 0.1-4.9 g/d), but no associations were observed for wine and beer consumption. These results suggest no association of alcohol consumption with the risk of pancreatic cancer
    Type of Publication: Journal article published
    PubMed ID: 19145468
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  • 3
    Keywords: CANCER ; EXPRESSION ; carcinoma ; Germany ; DISEASE ; GENE ; TUMORS ; PATIENT ; FREQUENCY ; LESIONS ; MUTATION ; meta-analysis ; PCR ; MUTATIONS ; POLYMERASE-CHAIN-REACTION ; adenocarcinoma ; intraepithelial neoplasia ; K-RAS ; chronic pancreatitis ; ALLELIC LOSS ; K-ras mutation ; pancreatic ductal carcinoma ; molecular ; DUCTAL ADENOCARCINOMA ; KRAS MUTATIONS ; METAANALYSIS ; CODON ; DNA ADDUCT ; duration ; K-RAS MUTATIONS ; KRAS ; GENETIC PROGRESSION ; ONCOGENE ACTIVATION ; pancreatic intraepithelial neoplasia
    Abstract: Molecular analyses have demonstrated mutations in the K-ras gene at codon 12 in the majority of pancreatic ductal adenocarcinomas (PDACs). In order to determine whether the K-ras mutation rate increases parallel to the grade of dysplasia in duct lesions, we performed a meta-analysis of the studies published between 1988 and 2003 that provide information on K-ras mutations in hyperplastic and dysplastic duct lesions in the pancreas. The described duct lesions were reclassified according to the nomenclature for pancreatic intraepithelial neoplasia (PanIN), and the molecular methods for detecting K-ras were reviewed. In PanIN lesions from pancreata of patients with PDAC, there was a stepwise increase in K-ras mutations that correlated with the grade of dysplasia of the PanIN lesion. K-ras mutations were found in 36%, 44%, and 87% of PanIN-1a, 1b, and 2-3 lesions, respectively (trend statistic P 〈 .001). Mutation-enriched polymerase chain reaction (PCR) resulted in higher rates of K-ras mutations in PanIN than plain PCR did. The incidence of K-ras mutations in PanIN lesions associated with chronic pancreatitis (CP) or normal pancreas was low (around 10%). In CP, K-ras mutations were only found after a disease duration of 3 years. The correlation of the incidence of K-ras mutations with the grade of dysplasia in PanIN and the occurrence of these mutations in CP with a duration of more than 3 years underlines the importance of this genetic change for the development of PDAC
    Type of Publication: Journal article published
    PubMed ID: 15720814
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  • 4
    Keywords: CANCER ; tumor ; LUNG ; lung cancer ; LUNG-CANCER ; SUPPORT ; DEATH ; DISEASE ; incidence ; MORTALITY ; RISK ; PATIENT ; primary ; RISK-FACTORS ; ASSOCIATION ; HEALTH ; NUMBER ; AGE ; MUTATION ; etiology ; risk factors ; smoking ; COUNTRIES ; MUTATIONS ; adenocarcinoma ; pancreatic cancer ; EUROPE ; ONCOLOGY ; PANCREATIC-CANCER ; PATTERN ; development ; biomarker ; pancreatic ; USA ; CANCER INCIDENCE ; cancer research ; RISK-FACTOR ; GENETIC ALTERATION ; CANCER-MORTALITY ; YOUNGER ; AGE-OF-ONSET
    Abstract: Pancreatic cancer ranks 4th as a cause of cancer mortality and in similar to 5% to 10% of patients, this lethal tumor develops before age 50. We used age-, sex-, and country-specific cancer incidence and mortality data to describe the burden of early onset pancreatic cancer (EOPC) worldwide. We also reviewed the current published evidence on smoking and genetic factors associated with EOPC. We found an excess of EOPC resulting in a substantial number of years-of-life-lost in countries from Central and Eastern Europe. Worldwide, the proportion of EOPC is strongly correlated with lung cancer mortality (R-2 = 0.53), suggesting that approximately half of the variation in the proportion of EOPC could be explained by smoking. The unusual pattern of the incidence of pancreatic cancer by gender and race supports the primary role of smoking in the etiology of EOPC: the excess male-to-female rate ratio, attributable mainly to smoking, gradually approaches unity with increasing age. Moreover, male-to-female rate ratios are greater in blacks than in whites only in younger patients. Published studies also identified genetic alterations involved either alone or in association with smoking in the development of EOPC. In conclusion, EOPC constitutes only 1% to 5% of the total deaths from pancreatic cancer worldwide, but is responsible for 20% to 30% of the total number of years-of-life-lost caused by the disease. Smoking and genetic mutations are the major identified risk factors and seem to be even more important for EOPC than for PC in. older age groups
    Type of Publication: Journal article published
    PubMed ID: 17855711
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  • 5
    Keywords: CANCER ; GENE ; SAMPLE ; SAMPLES ; TISSUE ; SURGERY ; PATIENT ; INFECTION ; TISSUES ; NO ; IDENTIFICATION ; MUTATION ; colorectal cancer ; etiology ; COLORECTAL-CANCER ; PATHOGENESIS ; PCR ; MUTATIONS ; CANCER-PATIENTS ; adenocarcinoma ; pathology ; PREVALENCE ; CANCER PATIENTS ; HELICOBACTER-PYLORI ; BIOPSY ; GENE-MUTATIONS ; prospective studies ; colonoscopy ; analysis ; methods ; K-RAS MUTATIONS ; prospective ; prospective study ; correlation ; SPECIMENS ; Helicobacter pylori ; correlates ; GENE MUTATION ; PCR DETECTION ; COLONIC MUCOSA ; DETECT ; CORRELATE
    Abstract: The aim of this study was to detect Helicobacter pylori (H. pylori) in colorectal cancer tissue specimens and relate the possible role of this microorganism in the etiology of colorectal cancer. PATIENTS AND METHODS: From February 2002 to April 2003 83 CRC patients (55 male, 28 female) and 40 control patients (19 male, 21 female) entered the prospective study. The biopsy samples of CRC tissue and normal mucosa were obtained during open surgery on CRC patients. In the control patients biopsy samples were taken during colonoscopy. Pathology confirmed adenocarcinoma in all the CRC patients. The existence of genetic material of H. pylori was determined by detection of the ureA gene by nested PCR. K-ras PCR was also performed on all patients. RESULTS: H. pylori PCR was positive in 1 case (1.2%) of CRC in the tumour tissue and in all 5 samples (6.0%) of the normal colonic mucosa in the cancer patients. The control patients were PCR positive to H. pylori in 13 samples (32.5%). According to Chi-square test, there is no statistical correlation between H. pylori infection and CRC (x2 = 2.9395; p 〉 0.05) but there is a significant prevalence of H. pylori infection in controls compared to CRC (x2 = 15.5625; p 〈 0.01). The K-ras PCR showed gene mutations in 19 tumour tissues of CRC (31.6%) and in 2 cases (3.4%) of normal colonic mucosa of CRC patients . In controls K-ras PCR showed one gene mutation (3.0%). There is a significant statistical correlation between K-ras mutation and CRC (x2 = 16.0694; p 〈 0.01). CONCLUSION: Our established PCR for H. pylori is feasible for CRC tissue as well. However, H. pylori is not considered to play an important role in the pathogenesis of CRC. The identification of K-ras mutations in routine PCR analysis correlates with the presence of CRC
    Type of Publication: Journal article published
    PubMed ID: 18356777
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1569-8041
    Keywords: epidemiology ; gallbladder ; neoplasms ; pancreas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Tumors arising in the pancreatico-biliary system arise from the same embryological source and share several similar clinical features. For both sites, the mortality rate is high and early diagnosis is difficult. Despite these similarities, there are clear epidemiologic differences between cancers of the biliary tract and cancers of the pancreas. Gallbladder cancer is more frequent in females, whereas pancreatic cancer is more frequent in males. High-risk populations for gallbladder cancer include Native American Indians and Hispanic Americans. Black populations are at high risk for pancreatic cancer. Gallstones are causally related to gallbladder cancer, but for pancreatic cancer, smoking is the major known risk factor. The increasing frequency of cholecystectomy in persons with gallstones should result in a reduction in the incidence of gallbladder cancer. For pancreatic cancer, public health efforts to reduce smoking offers the best chance for prevention.
    Type of Medium: Electronic Resource
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