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Biomedical subjects

J Chang-Claude

Publications and source records attributed to J Chang-Claude.

At least 19 recordsLinked to original sources
PubMed2006

Does a negative screening colonoscopy ever need to be repeated?

BACKGROUND AND AIMS: Screening colonoscopy is thought to be a powerful and cost-effective tool to reduce colorectal cancer incidence and mortality. Whether and when colonoscopy with negative findings has to be repeated is not well defined. The aim of this study was to assess the long term risk of clinically manifest colorectal cancer among subjects with negative findings at colonoscopy. PATIENTS: 380 cases and 485 controls participating in a population based case-control study in Germany. METHODS: Detailed history and results of previous colonoscopies were obtained by interview and from medical records. Adjusted relative risks of colorectal cancer among subjects with a previous negative colonoscopy compared with those without previous colonoscopy were estimated according to time since colonoscopy. RESULTS: Subjects with previous negative colonoscopy had a 74% lower risk of colorectal cancer than those without previous colonoscopy (adjusted odds ratio (aOR) = 0.26 (95% confidence interval, 0.16 to 0.40)). This low risk was seen even if the colonoscopy had been done up to 20 or more years previously. Particularly low risks were seen for sigma cancer (aOR = 0.13 (0.04 to 0.43)) and for rectal cancer (aOR = 0.19 (0.09 to 0.39)), and after a negative screening colonoscopy at ages 55 to 64 (aOR = 0.17 (0.08 to 0.39)) and older (aOR = 0.21 (0.10 to 0.41)). CONCLUSIONS: Subjects with negative findings at colonoscopy are at very low risk of colorectal cancer and might not need to undergo repeat colonoscopy for 20 years or more, if at all. The possibility of extending screening intervals to 20 years or more might reduce complications and increase the feasibility and cost-effectiveness of colonoscopy based screening programmes.

Adult↗
PubMed2006

Polymorphisms of genes coding for insulin-like growth factor 1 and its major binding proteins, circulating levels of IGF-I and IGFBP-3 and breast cancer risk: results from the EPIC study.

Insulin-like growth factor I (IGF-I) stimulates cell proliferation and can enhance the development of tumours in different organs. Epidemiological studies have shown that an elevated level of circulating IGF-I is associated with increased risk of breast cancer, as well as of other cancers. Most of circulating IGF-I is bound to an acid-labile subunit and to one of six insulin-like growth factor binding proteins (IGFBPs), among which the most important are IGFBP-3 and IGFBP-1. Polymorphisms of the IGF1 gene and of genes encoding for the major IGF-I carriers may predict circulating levels of IGF-I and have an impact on cancer risk. We tested this hypothesis with a case-control study of 807 breast cancer patients and 1588 matched control subjects, nested within the European Prospective Investigation into Cancer and Nutrition. We genotyped 23 common single nucleotide polymorphisms in IGF1, IGFBP1, IGFBP3 and IGFALS, and measured serum levels of IGF-I and IGFBP-3 in samples of cases and controls. We found a weak but significant association of polymorphisms at the 5' end of the IGF1 gene with breast cancer risk, particularly among women younger than 55 years, and a strong association of polymorphisms located in the 5' end of IGFBP3 with circulating levels of IGFBP-3, which confirms previous findings. Common genetic variation in these candidate genes does not play a major role in altering breast cancer risk in Caucasians.

Adult↗
PubMed2005

Lung fibre burden in lung cancer cases employed in the rock and slag wool industry.

OBJECTIVES: To evaluate the relationship between estimated exposure to man-made vitreous fibres (MMVF) and to asbestos fibres and their concentration in the lung tissue of lung cancer cases amongst MMVF production workers. METHODS: Retrospective retrieval of available lung tissue specimens was conducted following a case-control study that assessed estimated occupational exposures of MMVF workers. Fibre recovery and analysis by transmission electron microscopy (TEM) were conducted to determine fibre type, fibre dimension and numbers per gram of dry lung tissue. For cases with detailed exposure data, geometric mean (GM) concentrations were compared across the exposure categories, and regression models were used to investigate the relationship between the lung fibres and the variables of estimated exposure, with and without additional variables that may affect fibre retention. RESULTS: A total of 24 samples from 17 cases of lung cancer were available for analysis: MMVF were detected in all cases. Asbestos fibres were detected in 16. No difference or trend in GM MMVF concentration was observed across the estimated exposure categories. Odds ratio (OR) for MMVF g(-1) dry lung was 0.5 (95% confidence interval: 0.1-2.4) for the second, and 3.5 (0.6-18.9) for the third quartile of index of average exposure to MMVF in industry, compared with the first (lowest exposed) quartile (no cases in the highest quartile). CONCLUSIONS: No observable relationship existed between estimated exposure and directly-measured lung fibres among this sample of cases. Retrospective specimen collection, intra-individual variability in fibre concentration, effect of unknown factors on fibre retention and small sample size militated against this study providing evidence for or against a relationship between estimated exposure and lung fibre concentrations.

Adult↗
PubMed2005

Alcohol dehydrogenase 1B (ADH1B) genotype, alcohol consumption and breast cancer risk by age 50 years in a German case-control study.

In a population-based study of 613 cases and 1082 controls, alcohol dehydrogenase 1B (ADH1B) genotype was not an independent risk factor for breast cancer, although the possibility was raised that it modifies risk associated with high levels of alcohol consumption (OR 1.1, 95% confidence interval (CI) 0.8-1.6 for ADH1B*1/*1 genotype vs 0.2, 95% CI 0.1-1.0 for ADH1B*2 carriers).

Adult↗
PubMed2005

SDMinP: a program to control the family wise error rate using step-down minP adjusted P-values.

SDMinP is an easy-to-use program for fast calculation of empirical and adjusted P-values for correlated and uncorrelated hypotheses in multiple testing experiments. It is based on the Free Step-Down Resampling Method for controlling the family wise error rate, and implements a variation of an efficient algorithm, which reduces the originally required re-sampling effort considerably and makes the method computationally feasible. The program is independent of the underlying test statistic and works with provided observed and permutation test statistics.

Algorithms↗
PubMed2005

Haplotype sharing analysis using mantel statistics.

OBJECTIVE: The potential value of haplotypes has attracted widespread interest in the mapping of complex traits. Haplotype sharing methods take the linkage disequilibrium information between multiple markers into account, and may have good power to detect predisposing genes. We present a new approach based on Mantel statistics for spacetime clustering, which is developed in order to improve the power of haplotype sharing analysis for gene mapping in complex disease. METHODS: The new statistic correlates genetic similarity and phenotypic similarity across pairs of haplotypes for case-only and case-control studies. The genetic similarity is measured as the shared length between haplotypes around a putative disease locus. The phenotypic similarity is measured as the mean-corrected cross-product based on the respective phenotypes. We analyzed two tests for statistical significance with respect to type I error: (1) assuming asymptotic normality, and (2) using a Monte Carlo permutation procedure. The results were compared to the chi(2) test for association based on 3-marker haplotypes. RESULTS: The results of the type I error rates for the Mantel statistics using the permutational procedure yielded pointwise valid tests. The approach based on the assumption of asymptotic normality was seriously liberal. CONCLUSION: Power comparisons showed that the Mantel statistics were better than or equal to the chi(2) test for all simulated disease models.

Case-Control Studies↗
PubMed2005

[Smoking as potential confounder in german epidemiological studies: standardization of assessment, quantification, and analysis].

Tobacco smoking is one of the most frequently examined risk factors in epidemiological studies due to the high frequency of smoking in the population and its high risk potential. This paper discusses the issue of standardization of the assessment of tobacco exposure in German epidemiological studies based on a suggestion of the working group "Epidemiological methods" of the German Society of Epidemiology (DGEpi), the German Society of Social Medicine and Prevention (DGSMP), and German Society of Medical Informatics, Biometry and Epidemiology (GMDS) together with the working group "Epidemiology in the workplace" of the DGEpi and the German Society of Occupational and Environmental Medicine (DGAUM). The main element is a short questionnaire for German adults for the assessment of tobacco smoking in epidemiological studies where smoking is a potential confounder. In addition, information on the consideration of intermittent periods of non-smoking, a very short questionnaire for medical examinations in the workplace or non-responder interviews as well as the quantification and statistical modelling of smoking are presented. A brief discussion of scientific problems and questionnaires related to the exposure to environmental tobacco smoke is given.

Bias↗
PubMed2005

Anthropometric factors and the risk of premenopausal breast cancer in Germany.

Studies have shown fairly consistent results regarding an inverse relationship between overweight and premenopausal breast cancer risk, but reported effects of weight changes have been inconsistent. Data was analysed on weight, weight changes, height and body build for 558 premenopausal women with breast cancer and 1116 controls below 51 years who participated in a population-based case-control study in Germany from 1992 to 1995. Larger body build at menarche conferred a protective effect, when compared with smaller build [odds ratio (OR) 0.69, 95% confidence interval (CI) 0.49, 0.96]. In comparison with the lowest quartile, higher quartiles of weight gain from the lowest adult weight to current weight conferred a significant protective effect to those who attained their lowest adult weight after but not before the (median) age of 21, with OR and 95% CI of 0.52 (0.32, 0.83), 0.50 (0.30, 0.81), 0.56 (0.34, 0.94) for second, third and fourth quartiles respectively. Our findings are consistent with studies that found weight gain to be protective against premenopausal breast cancer and suggest that this effect may be more pronounced for women who were lean in adolescence and early adulthood.

Adolescent↗
PubMed2005

Postmenopausal serum androgens, oestrogens and breast cancer risk: the European prospective investigation into cancer and nutrition.

Considerable experimental and epidemiological evidence suggests that elevated endogenous sex steroids - notably androgens and oestrogens - promote breast tumour development. In spite of this evidence, postmenopausal androgen replacement therapy with dehydroepiandrosterone (DHEA) or testosterone has been advocated for the prevention of osteoporosis and improved sexual well-being. We have conducted a case-control study nested within the European Prospective Investigation into Cancer and Nutrition. Levels of DHEA sulphate (DHEAS), (Delta4-androstenedione), testosterone, oestrone, oestradiol and sex-hormone binding globulin (SHBG) were measured in prediagnostic serum samples of 677 postmenopausal women who subsequently developed breast cancer and 1309 matched control subjects. Levels of free testosterone and free oestradiol were calculated from absolute concentrations of testosterone, oestradiol and SHBG. Logistic regression models were used to estimate relative risks of breast cancer by quintiles of hormone concentrations. For all sex steroids -the androgens as well as the oestrogens - elevated serum levels were positively associated with breast cancer risk, while SHBG levels were inversely related to risk. For the androgens, relative risk estimates (95% confidence intervals) between the top and bottom quintiles of the exposure distribution were: DHEAS 1.69 (1.23-2.33), androstenedione 1.94 (1.40-2.69), testosterone 1.85 (1.33-2.57) and free testosterone 2.50 (1.76-3.55). For the oestrogens, relative risk estimates were: oestrone 2.07 (1.42-3.02), oestradiol 2.28 (1.61-3.23) and free oestradiol (odds ratios 2.13 (1.52-2.98)). Adjustments for body mass index or other potential confounding factors did not substantially alter any of these relative risk estimates. Our results have shown that, among postmenopausal women, not only elevated serum oestrogens but also serum androgens are associated with increased breast cancer risk. Since DHEAS and androstenedione are largely of adrenal origin in postmenopausal women, our results indicated that elevated adrenal androgen synthesis is a risk factor for breast cancer. The results from this study caution against the use of DHEA(S), or other androgens, for postmenopausal androgen replacement therapy.

Aged↗
PubMed2002

Alcohol, tobacco and breast cancer--collaborative reanalysis of individual data from 53 epidemiological studies, including 58,515 women with breast cancer and 95,067 women without the disease.

Alcohol and tobacco consumption are closely correlated and published results on their association with breast cancer have not always allowed adequately for confounding between these exposures. Over 80% of the relevant information worldwide on alcohol and tobacco consumption and breast cancer were collated, checked and analysed centrally. Analyses included 58,515 women with invasive breast cancer and 95,067 controls from 53 studies. Relative risks of breast cancer were estimated, after stratifying by study, age, parity and, where appropriate, women's age when their first child was born and consumption of alcohol and tobacco. The average consumption of alcohol reported by controls from developed countries was 6.0 g per day, i.e. about half a unit/drink of alcohol per day, and was greater in ever-smokers than never-smokers, (8.4 g per day and 5.0 g per day, respectively). Compared with women who reported drinking no alcohol, the relative risk of breast cancer was 1.32 (1.19-1.45, P<0.00001) for an intake of 35-44 g per day alcohol, and 1.46 (1.33-1.61, P<0.00001) for >/=45 g per day alcohol. The relative risk of breast cancer increased by 7.1% (95% CI 5.5-8.7%; P<0.00001) for each additional 10 g per day intake of alcohol, i.e. for each extra unit or drink of alcohol consumed on a daily basis. This increase was the same in ever-smokers and never-smokers (7.1% per 10 g per day, P<0.00001, in each group). By contrast, the relationship between smoking and breast cancer was substantially confounded by the effect of alcohol. When analyses were restricted to 22 255 women with breast cancer and 40 832 controls who reported drinking no alcohol, smoking was not associated with breast cancer (compared to never-smokers, relative risk for ever-smokers=1.03, 95% CI 0.98-1.07, and for current smokers=0.99, 0.92-1.05). The results for alcohol and for tobacco did not vary substantially across studies, study designs, or according to 15 personal characteristics of the women; nor were the findings materially confounded by any of these factors. If the observed relationship for alcohol is causal, these results suggest that about 4% of the breast cancers in developed countries are attributable to alcohol. In developing countries, where alcohol consumption among controls averaged only 0.4 g per day, alcohol would have a negligible effect on the incidence of breast cancer. In conclusion, smoking has little or no independent effect on the risk of developing breast cancer; the effect of alcohol on breast cancer needs to be interpreted in the context of its beneficial effects, in moderation, on cardiovascular disease and its harmful effects on cirrhosis and cancers of the mouth, larynx, oesophagus and liver.

Adult↗
PubMed2002

Estimating the sensitivity of a genetic test using gene-carrier probability estimates and its application in genetic counselling.

BACKGROUND: The estimation of the sensitivity of a genetic test is of practical importance. If a 'gold standard' (an exact test) is not available, an estimate of the probability of being a gene carrier may be useful for an individual. This information could be based on individual pedigree and family-history data, and a known genetic model for the disease of interest. METHODS: We develop a maximum-likelihood estimate of the sensitivity of a genetic test that may be applied in a situation without a 'gold standard', in which an estimate of the probability of being a gene carrier for an individual is available. RESULTS: A maximum-likelihood estimate for the sensitivity can be obtained through an iterative algorithm. We demonstrate the method using data from a project on familial breast cancer. We further present disease-risk estimates incorporating results from a genetic test with different values of sensitivity, and compare these with disease-risk estimates that are solely based on family-history data. DISCUSSION: We provide a systematic methodology to obtain an estimate of sensitivity of a genetic test when only gene-carrier probability estimates from a genetic model are available. Given a negative result from a genetic test, predictions for lifetime and age-specific disease-risk, accounting for test sensitivity, can then be provided in genetic counselling.

Algorithms↗
PubMed2001

Low-dose oral contraceptives: protective effect on ovarian cancer risk.

Low-dose oral contraceptive (OC) formulations containing 35 microg or less ethinyl estradiol have preferably been prescribed in the last decade, however, few data exist on its relation to ovarian cancer risk. We determined the effects of low-dose OC on the risk of ovarian cancer in a population-based case-control study, including 282 patients ages 20-75 years at diagnosis of incident primary invasive ovarian cancer or borderline tumour between 1993-1996 and 533 control subjects individually matched by age and study area to each case. Analysis excluded women who had undergone a bilateral ovariectomy or had a previous diagnosis of either ovarian cancer or borderline tumour. The association of OC use by ethinyl estradiol dose and ovarian cancer risk was assessed by odds ratios (OR), adjusting simultaneously for the other OC types and determinants of ovarian cancer risk. Ovarian cancer risk was significantly reduced by 52% for ever use of any type of OC. The reduction in risk was 7% per year of use (OR = 0.93, 95% confidence interval [CI] = 0.90-0.96) and was more evident in first-use subjects younger than 25 years. Risk reduction for ovarian cancer was substantial for use of low-dose OC, the odds ratios being 0.86 (95% CI = 0.77-0.94), 0.91 (95% CI = 0.83-1.00), and 0.95 (95% CI = 0.91-0.99) per year of using OC containing <35 microg, 35-<50 microg, and >or=50 microg ethinyl estradiol, respectively. Our study provides evidence that low-dose oral contraceptives confer substantial protection against the development of ovarian cancer.

Adult↗
PubMed2001

Low-to-moderate alcohol consumption and breast cancer risk by age 50 years among women in Germany.

Studies of the association between alcohol drinking and breast cancer show a tendency towards an increase in risk for high consumption levels but yield less consistent results for low-to-moderate levels, particularly among premenopausal women. In a population-based case-control study in Germany, the authors determined the effect of alcohol consumption at low-to-moderate levels on breast cancer risk among women up to age 50 years. The study included 706 case women whose breast cancer had been newly diagnosed in 1992-1995 and 1,381 residence- and age-matched controls. In multivariate conditional logistic regression analysis, the adjusted odds ratios for breast cancer were 0.71 (95% confidence interval (CI): 0.54, 0.91) for average ethanol intake of 1-5 g/day, 0.67 (95% CI: 0.50, 0.91) for intake of 6-11 g/day, 0.73 (95% CI: 0.51, 1.05) for 12-18 g/day, 1.10 (95% CI: 0.73, 1.65) for 19-30 g/day, and 1.94 (95% CI: 1.18, 3.20) for > or = 31 g/day. The association with high daily ethanol intake of > or = 19 g was modified by educational level, such that odds ratios were 3.7, 1.6, and 0.7 for women with low, moderate, and high levels of education, respectively. These data suggest that low-level consumption of alcohol does not increase breast cancer risk in premenopausal women.

Adolescent↗
PubMed2001

Exploring haplotype sharing methods in general and isolated populations to detect gene(s) of a complex genetic trait.

We applied a new haplotype sharing method to the simulated Genetic Analysis Workshop 12 data for both isolated and general populations without knowledge of the disease model, using affection status as phenotype and three different sample sizes. The highest peak for the mean sharing of the haplotypes was found in the isolated population for the markers D06G034 and D06G035, which flank the candidate genes located on chromosome 6, with -log10(p) values of 2.9 and 7.0 in the moderate and large study samples, respectively. The whole genome screen detected three further loci with -log10(p) values of 3.0, which turned out to be false positives. None of the true gene loci were detected in the general population even in the largest sample. The test of linkage disequilibrium based on excess haplotype sharing over the linkage equilibrium expectation revealed z-values one order of magnitude higher in the isolated than in the general population. This approach appears to be promising for mapping genes of complex diseases depending on population characteristics.

Chromosome Mapping↗
PubMed2001

Identification of a recurrent BRCA1 mutation in German breast-cancer and/or ovarian-cancer families.

Specific BRCA1 mutations have been reported to be common within particular populations. We have investigated German breast- and/or ovarian-cancer families and detected a recurrent carboxy-terminal BRCA1 mutation, 5622C > T, using PCR-based restriction assay and haplotype analysis. Unrelated families carrying this BRCA1 mutation shared two different disease-associated haplotypes, indicating two independent mutation events.

Breast Neoplasms↗
PubMed2001

The contribution of cigarette smoking to bladder cancer in women (pooled European data).

BACKGROUND: Using a combined analysis of 11 case-control studies from Europe, we have investigated the relationship between cigarette smoking and bladder cancer in women. METHODS: Available smoking information on 685 female bladder cancer cases and 2416 female controls included duration of smoking habit, number of cigarettes smoked per day, and time since cessation of smoking habit for ex-smokers. RESULTS: There was an increasing risk of bladder cancer with increasing duration of smoking, ranging from approximately a two-fold increased risk for a duration of less than 10 years (odds ratio (OR) = 1.9, 95% confidence interval (CI) 1.1-3.1) to over a four-fold increased risk for a duration of greater than 40 years (OR = 4.1, 95% CI 3.0-5.5). A dose-response relationship was observed between number of cigarettes smoked per day and bladder cancer up to a threshold limit of 15-20 cigarettes per day, OR = 3.8 (95% CI 2.7-5.4), after which no increased risk was observed. An immediate decrease in risk of bladder cancer was observed for those who gave up smoking. This decrease was over 30% in the immediate 1-4 years after cessation, OR = 0.68 (95% CI 0.38-1.2). However, even after 25 years the decrease in risk did not reach the level of the never-smokers, OR = 0.27 (95% CI 0.21-0.35). CONCLUSION: The proportion of bladder cancer cases among women attributable to ever smoking was 0.30, (0.25-0.35) and to current smoking was 0.18 (0.14-0.22). These attributable proportions are less than those observed among men, although they are likely to increase in the future as the smoking-related disease epidemic among women matures.

Adult↗
PubMed2001

Cigar, pipe, and cigarette smoking and bladder cancer risk in European men.

OBJECTIVE: Estimating the risk of bladder cancer from cigar and pipe smoking is complicated by a small number of non-cigarette smokers included in most relevant studies. METHODS: We undertook a pooled analysis of the data on men from six published case-control studies from Denmark, France, Germany, and Spain, to assess the association between pipe and cigar smoking and bladder cancer, and to compare it with the risk from cigarette smoking. Complete history of tobacco smoking was ascertained separately for cigarettes, cigars, and pipe. Odds ratios (ORs) were estimated after adjusting for age, study, and employment in high-risk occupations. RESULTS: The pooled data set comprised 2279 cases and 5268 controls, of whom 88 cases and 253 controls smoked only cigars or pipe. The OR for pure cigarette smoking was 3.5 (95% confidence interval [CI] 2.9-4.2), that for pure pipe smoking was 1.9 (95% CI 1.2-3.1) and that for pure cigar smoking was 2.3 (95% CI 1.6-3.5). The increase in the OR of bladder cancer that was observed with duration of smoking was non-significantly lower for cigars than for cigarettes. CONCLUSION: Our results suggest that smoking of cigars and pipe is carcinogenic to the urinary bladder, although the potency might be lower than for cigarettes.

Case-Control Studies↗