Showing papers by "Petra H.M. Peeters published in 2003"
TL;DR: Dietary fibre in foods was inversely related to incidence of large bowel cancer, with the protective effect being greatest for the left side of the colon, and least for the rectum.
1,070 citations
University of Turin1, University of Naples Federico II2, Lund University3, Umeå University4, University of Oxford5, Medical Research Council6, German Cancer Research Center7, Aarhus University8, Utrecht University9, Institut Gustave Roussy10, National and Kapodistrian University of Athens11, University of Tromsø12, International Agency for Research on Cancer13
TL;DR: Findings from this large study support the causal relation between smoking and gastric cancer in this European population and should be added to the burden of diseases caused by smoking.
Abstract: Smoking has recently been recognised as causally associated with the development of gastric cancer (GC). However, evidence on the effect by sex, duration and intensity of smoking, anatomic subsite and cessation of smoking is limited. Our objective was to assess the relation between tobacco use and GC incidence in the European Prospective Investigation into Cancer and Nutrition (EPIC). We studied data from 521,468 individuals recruited from 10 European countries taking part in the EPIC study. Participants completed lifestyle questionnaires that included questions on lifetime consumption of tobacco and diet in 1991-1998. Participants were followed until September 2002, and during that period 305 cases of stomach cancer were identified. After exclusions, 274 were eligible for the analysis, using the Cox proportional hazard model. After adjustment for educational level, consumption of fresh fruit, vegetables and preserved meat, alcohol intake and body mass index (BMI), there was a significant association between cigarette smoking and gastric cancer risk: the hazard ratio (HR) for ever smokers was 1.45 (95% confidence interval [CI] = 1.08-1.94). The HR of current cigarette smoking was 1.73 (95% CI = 1.06-2.83) in males and 1.87 (95% CI = 1.12-3.12) in females. Hazard ratios increased with intensity and duration of cigarette smoked. A significant decrease of risk was observed after 10 years of quitting smoking. A preliminary analysis of 121 cases with identified anatomic site showed that current cigarette smokers had a higher HR of GC in the cardia (HR = 4.10) than in the distal part of the stomach (HR = 1.94). In this cohort, 17.6 % (95% CI = 10.5-29.5 %) of GC cases may be attributable to smoking. Findings from this large study support the causal relation between smoking and gastric cancer in this European population. Stomach cancer should be added to the burden of diseases caused by smoking.
263 citations
TL;DR: The data do not support an association between postmenopausal circulating levels of IGF‐I, IGFBP‐1, ‐2, 3, C‐peptide and post menopausal breast cancer.
Abstract: Higher levels of circulating Insulin-like Growth Factor (IGF)-I may be associated with higher risks for premenopausal breast cancer. We investigate the associations between circulating levels of IGF-I, its binding proteins (IGFBPs) -1, -2, -3, C-peptide and postmenopausal breast cancer. This is a prospective study nested in 2 Dutch cohorts. The study population included women who were postmenopausal at baseline. Breast cancer cases were identified through linkage with cancer registries. Controls were matched to cases by cohort, age, date of blood donation and place of residence. In total, 149 breast cancer cases and 333 healthy controls were included. Plasma levels of IGF-I, IGFBP-1, -2, -3 and C-peptide were measured by radioimmunoassays. Estimates of the relative risk for breast cancer associated with the quartiles of the peptides' circulating levels were obtained by conditional logistic regression. Models were adjusted for BMI, age at menarche and age at first full-term delivery. For IGF-I, the adjusted OR (95% CI) of the top vs. bottom quartile was 1.1 (0.6; 2.1); for IGFBP-1 it was 0.7 (0.3; 1.3); for IGFBP-2, 1.1 (0.5; 2.4); for IGFBP-3, 1.6 (0.7; 3.5), for C-peptide, 1.3 (0.7; 2.7) and for IGF-I/IGFBP-3 ratio, 1.0 (0.5; 1.8). Our data do not support an association between postmenopausal circulating levels of IGF-I, IGFBP-1, -2, -3, C-peptide and postmenopausal breast cancer.
111 citations
TL;DR: A thorough histopathological and radiological review of all DCIS underestimates, including a histological comparison with core biopsy specimens of 32 true DCIS cases, concluded that approximately half of these are potentially avoidable.
Abstract: Background: For the evaluation of nonpalpable lesions of the breast, image-guided 14-gauge automated needle biopsy is increasingly replacing wire-localized excision. When ductal carcinoma-in-situ (DCIS) is diagnosed at core biopsy, invasive cancer is found in approximately 17% of excision specimens. These so-called DCIS underestimates pose a problem for patients and surgeons, because they generally cause extension of treatment. We evaluated DCIS underestimates in detail to assess reasons for missing the invasive component at core biopsy. This evaluation also included a histological comparison with true DCIS (DCIS at core biopsy and excision).
88 citations
TL;DR: Support is provided for the view that women who smoke and who have a genetically determined reduced inactivation of carcinogens (GSTM1 null genotype or slow NAT2 genotype) are at increased risk of breast cancer.
Abstract: N-acetyltransferase (NAT) 1 and 2 and glutathione S-transferase (GST) M1 and T1 are phase II enzymes that are important for activation and detoxification of carcinogenic heterocyclic and aromatic amines, as present in cigarette smoke. We studied whether genetic polymorphisms in these genes modifies the relationship between smoking and breast cancer. A nested case-control study was conducted among participants in a Dutch prospective cohort. Breast cancer cases (n = 229) and controls (n = 264) were frequency-matched on age, menopausal status and residence. Compared to never smoking, smoking 20 cigarettes or more per day increased breast cancer risk statistically significant only in postmenopausal women [odds ratio (OR) = 2.17; 95% confidence interval (Cl) 1.04-4.51]. Neither NAT1 slow genotype, or GSTT1 null genotype, alone or in combination with smoking, affected breast cancer risk. However, compared to individuals with rapid NAT2 genotype, women with the very slow acetylator genotype (NAT2*5), who smoked for 20 years showed an increased breast cancer risk (OR = 2.29; 95% Cl 1.06-4.95). Similarly, the presence of GSTM1 null genotype combined with high levels of cigarette smoking (OR = 3.00; 95% Cl 1.46-6.15) or long duration (OR = 2.53; 95% Cl 1.24-5.16), increased rates of breast cancer. The combined effect of GSTM1 null genotype and smoking high doses was most pronounced in postmenopausal women (OR = 6.78; 95% Cl 2.31 -19.89). In conclusion, our results provide support for the view that women who smoke and who have a genetically determined reduced inactivation of carcinogens (GSTM1 null genotype or slow NAT2 genotype (especially very slow NAT2 genotype)) are at increased risk of breast cancer.
78 citations
TL;DR: It is suggested that caloric restriction decreases age at natural menopause, and early childhood seems to be a particularly sensitive age period for this effect.
Abstract: Objective: To assess the effect of caloric restriction, as endured during the 1944-1945 Dutch famine, on the age at which natural menopause occurs and to identify specific vulnerable age periods in which caloric restriction has the largest effect. Design: This was a population-based cohort study conducted in Utrecht, the Netherlands. Between 1983 and 1986, 9,471 women aged 40 to 73 years at the time of interview were classified regarding their exposure to the famine. Age at natural menopause was obtained from all available data, retrospectively as well as prospectively. We estimated differences in mean age at natural menopause between famine exposure categories (not, moderately, and severely exposed), with adjustment for smoking, parity, socioeconomic status, body mass index, age at menarche, and year of birth. Results: Women experienced natural menopause on average 0.36 years earlier (95% CI: �0.60, �0.11) when severely exposed to the famine and 0.06 years earlier (95% CI: �0.22, 0.09) when moderately exposed compared with the unexposed women. This effect was particularly pronounced in those severely exposed from 2 to 6 years of age: �1.83 years (95% CI: �3.03, �0.63). Conclusions: Our findings suggest that caloric restriction decreases age at natural menopause. Early childhood seems to be a particularly sensitive age period for this effect.
76 citations
TL;DR: The findings support the view that fertility problems are frequently followed by early menopause, and both are an expression of accelerated ovarian ageing.
Abstract: BACKGROUND: The aim of the study was to explore the extent to which accelerated ovarian ageing may lead to subfertility early in reproductive life and eventually cause early menopause. METHODS: The population studied (n = 2393) never used oral contraceptives, hormone replacement therapy or an intrauterine device. Logistic regression analyses were performed using age at menopause as proxy for accelerated ovarian ageing. Measures of ovarian ageing and subfertility were menstrual cycle irregularity, ever consulted a physician for fertility problems, nulliparity, uniparity, miscarriage(s) and time interval >5 years between birth of first and second child. RESULTS: For every 5 years later menopause, the probability of reporting menstrual cycle irregularity was reduced by 26% (OR = 0.74, 95% CI: 0.63‐0.86); the probability of ever consulting a physician for fertility problems was reduced by 18% (OR = 0.82, 95% CI: 0.71‐0.95); the probability of staying nulliparous was reduced by 22% (OR = 0.78, 95% CI: 0.64‐0.96); the probability of being uniparous was reduced by 22% (OR = 0.78, 95% CI: 0.66‐0.91); the probability of having a miscarriage was reduced by 11% (OR = 0.89, 95% CI: 0.79‐1.01); the probability of a large time interval between birth of first two children was reduced by 27% (OR = 0.73, 95% CI: 0.61‐0.89). CONCLUSIONS: Fertility problems are frequently followed by early menopause. The findings support the view that both are an expression of accelerated ovarian ageing.
50 citations
TL;DR: The interobserver agreement for the diagnosis of large-core needle biopsies between the general and experts pathologists was excellent, and the risk of benign/malignant inconsistencies between general pathologists and experts was approximately 1 in 55 for both needle and open biopsy specimens.
42 citations
TL;DR: It was found that the factor V Leiden mutation was related, but not statistically significant, to an earlier age at menopause; smoking possibly enhances this effect.
Abstract: Objective: Smoking is consistently associated with a younger age for menopause. Although this may be because of the direct toxic effects of tobacco smoke on follicles, we hypothesize that there may also be a relationship between smoking and a vascular origin of early menopausal onset. Several lifestyle factors have been investigated, but never factors of the clotting cascade. The objective of this study, then, was to determine the effect of factor V Leiden mutation and smoking with respect to age at menopause. Design: Data were used from a subset of 373 postmenopausal participants of a Dutch populationbased cohort, born between 1911 and 1925. All women had experienced natural menopause, without use of hormone replacement therapy. Results: Female carriers of the factor V Leiden mutation (n = 14) reported the onset of menopause at an earlier age than noncarriers (n = 359; difference, 3.1 years; 95% CI: 0.3, 5.9). Smoker carriers (n = 5) were 4.3 years younger at menopause than smoker noncarriers (n = 92; 95% CI: 0.9,7.6). In nonsmokers, this relationship was less strong. Conclusions: We found that the factor V Leiden mutation was related, but not statistically significant, to an earlier age at menopause; smoking possibly enhances this effect. The mutation can be one of the genetic determinants of menopausal age operating through a vascular mechanism.
40 citations
Journal Article•
TL;DR: The classification of aMT6S concentrations in first morning voids from postmenopausal women appears to be sufficiently reproducible to justify its use as a marker for long-term exposure to melatonin in epidemiological studies.
Abstract: To assess the appropriateness of a single measurement of urinary 6-sulfatoxymelatonin (aMT6S) as a marker for long-term exposure to endogenous melatonin in epidemiological studies, we examined the reproducibility of aMT6S in first morning urine voids collected from 40 postmenopausal women. Urine specimens were collected on three different occasions, and the mean time between the first and the third urine sample was 5.1 years. Urinary aMT6S levels were measured by radioimmunoassay and adjusted for creatinine. The intraclass correlation for aMT6S adjusted for creatinine was 0.56 (95% confidence interval, 0.39-0.73). The classification of aMT6S concentrations in first morning voids from postmenopausal women appears to be sufficiently reproducible to justify its use as a marker for long-term exposure to melatonin in epidemiological studies.
34 citations
Journal Article•
TL;DR: Cigarette smoke contains potent carcinogenic compounds, including polycyclic aromatic hydrocarbons, heterocyclic amines, and nitrosamines, which could cause cancer when entering the body.
Abstract: Cigarette smoke contains potent carcinogenic compounds, including polycyclic aromatic hydrocarbons, heterocyclic amines, and nitrosamines. When entering the body, cigarette carcinogens have relatively weak mutagenic potential. After being metabolized, more potent mutagens are formed, which could
TL;DR: The Cys282Tyr mutation is not associated with an increased risk for colorectal cancer in postmenopausal women, although in combination with smoking a slightly increased risk cannot be excluded.
Abstract: Background & Aims: Heterozygosity for the Cys282Tyr transition in the HFE-gene is associated with slightly increased iron levels and may therefore be a potential risk factor for colorectal cancer. Methods: We studied the relationship between Cys282Tyr-heterozygosity and colorectal cancer using a case-control design. The 240 colorectal cancer cases and 635 controls in our study were derived from a prospective cohort study of 12,242 postmenopausal women, who were invited for an experimental breast cancer screening program in Utrecht, the Netherlands. The women were age 51-69 at time of inclusion and were followed for a period of 20 years. HFE genotyping was performed by PCR and allele-specific oligonucleotide (ASO) hybridization. Results: The risk of colorectal cancer was higher for women who were heterozygous for the Cys282Tyr mutation, than for those who were Cys282Tyr-wildtypes, although this was not statistically significant (Age-adjusted OR = 1.2, 95% CI: 0.6-2.2). Cys282Tyr-heterozygotes who smoked seemed to be at higher risk of colorectal cancer, although the p-value for interaction was not significant (p-value 0.42). Conclusions: The Cys282Tyr mutation is not associated with an increased risk for colorectal cancer in postmenopausal women, although in combination with smoking a slightly increased risk cannot be excluded.
Journal Article•
TL;DR: Findings do not provide evidence for an important role of the V89L polymorphism in the etiology of breast cancer, however, in breast cancer patients, the LL genotype may be associated with unfavorable prognosis.
Abstract: Women with high androgen levels appear to be at increased risk for breast cancer. The 5--reductase type 2 enzyme (SRD5A2) is an important mediator of local androgen actions. The SRD5A2 gene contains a polymorphism leading to a valine to leucine change in codon 89 (V89L). The Leu allele has been associated with lower SRD5A2 activity and might be protective for breast cancer. At the same time, among breast cancer patients, the Leu allele has been associated with lower prostatespecific antigen expression, indicating poor prognosis. Within a cohort of breast cancer screening participants in the Netherlands (DOM-cohort) we examined whether the V89L polymorphism is associated with the risk and prognosis of breast cancer. We studied 295 postmenopausal breast cancer cases and a randomly selected reference group from the baseline cohort (n 382). The genotype distribution in the reference group was: VV 52%; VL 40%; and LL 8%. Compared with women with the VV genotype, adjusted breast cancer rate ratios for women with VL and LL genotypes were 1.5 (95% confidence interval 1.0 –2.2) and 1.1 (95% confidence interval 0.5–2.1), respectively. Compared with breast cancer patients with VV or VL genotypes, those with the LL genotype showed larger tumors (proportion with size > 2c m is 26versus 55%, respectively; P 0.07), a higher frequency of positive lymph nodes (28 versus 55%, respectively; P 0.09), and a higher tumor-node-metastasis stage (proportion with stage III/IV: 6 versus 25%, respectively; P 0.04). The LL genotype is also associated with shorter survival than the VV and VL genotypes (P 0.10). In conclusion, our findings do not provide evidence for an important role of the V89L polymorphism in the etiology of breast cancer.