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  • DKFZ Publication Database  (4)
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  • 1
    Keywords: CANCER ; radiotherapy ; carcinoma ; human ; neoplasms ; DIAGNOSIS ; RISK ; PATIENT ; kidney ; RISK-FACTORS ; CARCINOGENESIS ; colon ; ASSOCIATION ; BREAST ; LYMPHOMA ; AGE ; OVARIAN-CANCER ; risk factors ; CERVICAL-CANCER ; RATES ; cancer risk ; REGISTRATION ; CANCER-PATIENTS ; adenocarcinoma ; TOBACCO ; pancreatic cancer ; LONG-TERM SURVIVORS ; YOUNG ; REGISTRY ; REPRODUCTIVE FACTORS ; ASSOCIATIONS ; ENDOMETRIAL ; PANCREATIC-CANCER ; cancer registries ; TESTICULAR CANCER ; LYMPHOMAS ; cancer registry ; pooled analysis ; RISK-FACTOR ; CANCERS ; REGISTRIES ; CANCER-DIAGNOSIS ; pancreatic neoplasms ; MALIGNANT NEOPLASMS ; neoplasms,second primary
    Abstract: Studies of pancreatic cancer in the setting of second primary malignant neoplasms can provide etiologic clues. An international multicenter study was carried out using data from 13 cancer registries with a registration period up to year 2000. Cancer patients were followed up from the initial cancer diagnosis, and the occurrence of second primary malignant neoplasms was compared with expected values derived from local rates, adjusting for age, sex, and period of diagnosis. Results from individual registries were pooled by use of a fixed-effects model. People were at higher risk of developing pancreatic cancer within 10 years of a diagnosis of cancers of the pharynx, stomach, gallbladder, larynx, lung, cervix, corpus uteri, bladder, and eye and 10 years or later following a diagnosis of cancers of the stomach, colon, gallbladder, breast, cervix, placenta, corpus uteri, ovary, testis, bladder, kidney, and eye, as well as Hodgkin's and non-Hodgkin's lymphomas. Pancreatic cancer was connected with smoking-related cancers, confirming the etiologic role of tobacco. The associations with uterine and ovarian cancers suggest that reproductive factors might be implicated in pancreatic carcinogenesis. The elevated pancreatic cancer risk in young patients observed among several types of cancer implies a role of genetic factors. Radiotherapy is also suggested as a risk factor
    Type of Publication: Journal article published
    PubMed ID: 16421239
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  • 2
    Keywords: CANCER ; carcinoma ; PATHWAY ; PATHWAYS ; RISK ; GENE ; TUMORS ; TIME ; DNA ; kidney ; MECHANISM ; RISK-FACTORS ; colon ; mechanisms ; SKIN ; ASSOCIATION ; LYMPHOMA ; NUMBER ; AGE ; DNA-REPAIR ; REPAIR ; DIETARY ; ADENOCARCINOMAS ; INDIVIDUALS ; SMALL-INTESTINE ; NONPOLYPOSIS COLORECTAL-CANCER ; 2ND PRIMARY NEOPLASMS ; DNA repair ; CLUSTER ; REGISTRY ; pancreas ; ASSOCIATIONS ; cancer registries ; INCREASE ; GLAND ; SMALL-BOWEL ; INTERVAL ; GENDER ; second primary cancers ; rectum ; cancer registry ; pooled analysis ; CANCER INCIDENCE ; registry-based study ; small intestine cancer
    Abstract: Cancer of the small intestine is a rare neoplasm, and its etiology remains poorly understood. Analysis of other primary cancers in individuals with small intestine cancer may help elucidate the causes of this neoplasm and the underlying mechanisms. We included 10,946 cases of first primary small intestine cancer from 13 cancer registries in a pooled analysis. The observed numbers of 44 types of second primary cancer were compared to the expected numbers derived from the age-, gender- and calendar period-specific cancer incidence rates in each registry. We also calculated the standardized incidence ratios (SIR) for small intestine cancer as a second primary after other cancers. There was a 68% overall increase in the risk of a new primary cancer after small intestine carcinoma (SIR = 1.68, 95% confidence interval [CI] = 1.47-1.71), that remained constant over time. The overall SIR was 1.18 (95% CI = 1.05-1.32) after carcinoid, 1.29 (1.01-1.63) after sarcoma, and 1.27 (0.78-1.94) after lymphoma. Significant (p 〈 0.05) increases were observed for cancers of the oropharynx, colon, rectum, ampulla of Vater, pancreas, corpus uteri, ovary, prostate, kidney, thyroid gland, skin and soft (issue sarcomas. Small intestine cancer as a second primary was increased significantly after all these cancers, except after oropharyngeal and kidney cancers. Although some of the excess may be attributable to overdiagnosis, it is plausible that most additional cases of second primary cancers were clinically relevant and were due to common genetic (e.g., defects in mismatch or other DNA repair pathways) and environmental (e.g., dietary) factors. (c) 2005 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16003748
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  • 3
    Keywords: CANCER ; LUNG ; COHORT ; EXPOSURE ; liver ; RISK ; SITE ; SITES ; TISSUE ; RISK-FACTORS ; SKIN ; SUPPRESSION ; ASSOCIATION ; LYMPHOMA ; PATTERNS ; NUMBER ; AGE ; WOMEN ; CIGARETTE-SMOKING ; risk factors ; non-hodgkin's lymphoma ; Hodgkin's lymphoma ; SKIN-CANCER ; CLUSTER ; MALIGNANCY ; RE ; cancer registries ; SUBTYPES ; PRIMARY NEOPLASMS ; second primary cancers
    Abstract: An analysis of other primary cancers in individuals with non-Hodgkin's lymphoma (NHL) can help to elucidate this cancer aetiology. In all, 109 451 first primary NHL were included in a pooled analysis of 13 cancer registries. The observed numbers of second cancers were compared to the expected numbers derived from the age-, sex-, calendar period- and registry-specific incidence rates. We also calculated the standardised incidence ratios for NHL as a second primary after other cancers. There was a 47% (95% confidence interval 43 - 51%) overall increase in the risk of a primary cancer after NHL. A strongly significant (P〈0.001) increase was observed for cancers of the lip, tongue, oropharynx*, stomach, small intestine, colon*, liver, nasal cavity*, lung, soft tissues*, skin melanoma*, nonmelanoma skin*, bladder*, kidney*, thyroid*, Hodgkin's lymphoma*, lymphoid leukaemia* and myeloid leukaemia. Non-Hodgkin's lymphoma as a second primary was increased after cancers marked with an asterisk. Patterns of risk indicate a treatment effect for lung, bladder, stomach, Hodgkin's lymphoma and myeloid leukaemia. Common risk factors may be involved for cancers of the lung, bladder, nasal cavity and for soft tissues, such as pesticides. Bidirectional effects for several cancer sites of potential viral origin argue strongly for a role for immune suppression in NHL
    Type of Publication: Journal article published
    PubMed ID: 15970927
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  • 4
    Keywords: CANCER ; carcinoma ; DIAGNOSIS ; FOLLOW-UP ; RISK ; GENE ; GENES ; ACCURACY ; DNA ; INFECTION ; MARKER ; CARCINOGENESIS ; ASSOCIATION ; POLYMORPHISMS ; VARIANTS ; TRIAL ; LESIONS ; PROGRESSION ; EXPERIENCE ; DIFFERENCE ; RATES ; POLYMERASE-CHAIN-REACTION ; STOMACH ; INDIVIDUALS ; CHAIN-REACTION ; chemoprevention ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; BIOPSY ; CHAIN ; ONCOLOGY ; REGRESSION ; RE ; VARIANT ; INCREASE ; polymerase chain reaction ; gastric cancer ; development ; INTERVAL ; methods ; GENOTYPE ; TESTS ; STRAINS ; USA ; odds ratio ; SPECIMENS ; Helicobacter pylori ; BIOPSIES ; LOGISTIC-REGRESSION ; CAGA ; gastric ; HIGH-RISK POPULATION ; VENEZUELA
    Abstract: Background Helicobacter pylori infection is associated with the development of gastric cancer. Although infection with an H. pylori strain containing the cytotoxin-associated (cag A) gene (a marker for a pathogenicity island) may increase the risk of atrophic gastritis and gastric cancer, the relationship of variants in pathogenic H. pylori genes to the severity and progression of precancerous lesions is not well defined. Methods Gastric biopsy specimens were obtained at enrollment from 2145 participants in a chemoprevention trial in Tachira State, Venezuela, and examined histologically to determine the severity of precancerous lesions. The presence of H. pylori DNA in gastric biopsies and the strain type according to presence or absence of the cagA gene were detected by polymerase chain reaction and specific probes. The relationship between H. pylori DNA and histologic diagnosis was analyzed by polytomous logistic regression. Rates of progression and regression of precancerous lesions were determined from biopsies from additional annual gastroscopies (mean follow-up = 3.5 years). All statistical tests were two-sided. Results At enrollment, there was a strong association between cagA-positive H. pylori infection and the severity of gastric precancerous lesions, but cagA-negative H. pylori was associated only with chronic gastritis. Using individuals with normal mucosa or superficial gastritis as control subjects, the odds ratio for dysplasia was 15.5 (95% confidence interval [CI] = 6.42 to 37.2) in cagA-positive individuals compared with uninfected individuals and 0.90 (95% CI = 0.37 to 2.17) for individuals infected with cagA-negative H. pylori compared with uninfected individuals. Individuals infected with cagA-positive H. pylori appeared more likely to experience progression (and less likely to experience regression) of precancerous lesions than those infected with cagA-negative H. pylori, but the differences did not attain statistical significance. Conclusions This large epidemiologic study shows a strong relationship between the presence of H. pylori DNA in gastric biopsies and the severity of precancerous lesions that is specific to cagA-positive strains. The association between H. pylori and gastric carcinoma may have been previously underestimated due to the poor accuracy of serologic H. pylori markers and lack of discrimination by cagA genotype
    Type of Publication: Journal article published
    PubMed ID: 17728213
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