Incomplete pregnancy and risk of ovarian cancer: results from two Australian case–control studies and systematic review

Although full-term pregnancies reduce the risk of ovarian cancer, it has not been conclusively established whether incomplete pregnancies also influence risk. We investigated the relationship between a history of incomplete pregnancy and incident epithelial ovarian cancer among over 4,500 women who participated in two large Australian population-based case–control studies in 1990–1993 and 2002–2005. They provided responses to detailed questions about their reproductive histories and other personal factors. Summary odds ratios (OR) and confidence intervals (CI) derived for each study using the same covariates were aggregated. We found no significant associations between the number of incomplete pregnancies and ovarian cancer, for parous (OR = 0.98, 95% CI: 0.89, 1.08) or nulliparous (OR = 1.06, 95% CI: 0.75, 1.48) women, nor for the number of spontaneous or induced abortions and ovarian cancer for parous women (OR = 0.95, 95% CI 0.82, 1.09; OR = 1.08, 95% CI: 0.86, 1.36) or nulliparous women (OR = 1.2, 95% CI: 0.6, 2.4; OR = 0.8, 95% CI: 0.47, 1.38), respectively. A systematic review of 37 previous studies of the topic confirmed our findings that a history of incomplete pregnancy does not influence a woman’s risk of epithelial ovarian cancer.     

Statin use and risk for ovarian cancer: a Danish nationwide case–control study

Background:

Limited data suggest that statin use reduces the risk for ovarian cancer.

Methods:

Using Danish nationwide registries, we identified 4103 cases of epithelial ovarian cancer during 2000–2011 and age-matched them to 58 706 risk-set sampled controls. Conditional logistic regression was used to estimate adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for epithelial ovarian cancer overall, and for histological types, associated with statin use.

Results:

We observed a neutral association between ever use of statins and epithelial ovarian cancer risk (OR=0.98, 95% CI=0.87–1.10), and no apparent risk variation according to duration, intensity or type of statin use. Decreased ORs associated with statin use were seen for mucinous ovarian cancer (ever statin use: OR=0.63, 95% CI=0.39–1.00).

Conclusions:

Statin use was not associated with overall risk for epithelial ovarian cancer. The inverse association between statin use and mucinous tumours merits further investigation.     

Lifetime recreational moderate-to-vigorous physical activity and ovarian cancer risk: A case–control study

Results of epidemiologic studies of physical activity and ovarian cancer risk are inconsistent. Few have attempted to measure physical activity over the lifetime or in specific age windows, which may better capture etiologically relevant exposures. We examined participation in moderate-to-vigorous recreational physical activity (MVPA) in relation to ovarian cancer risk. In a population-based case–control study conducted in Montreal, Canada from 2011 to 2016 (485 cases and 887 controls), information was collected on lifetime participation in various recreational physical activities, which was used to estimate MVPA for each participant. MVPA was represented as average energy expenditure over the lifetime and in specific age-periods in units of metabolic equivalents (METs)-hours per week. Odds ratios (OR) and 95% confidence intervals (CI) for the relation between average MVPA and ovarian cancer risk were estimated using multivariable logistic regression models. Confounding was assessed using directed acyclic graphs combined with a change-in-estimate approach. The adjusted OR (95% CI) for each 28.5 MET-hr/week increment of lifetime recreational MVPA was 1.11 (0.99–1.24) for ovarian cancer overall. ORs for individual age-periods were weaker. When examined by menopausal status, the OR (95% CI) for lifetime MVPA was 1.21 (1.00–1.45) for those diagnosed before menopause and 1.04 (0.89–1.21) for those diagnosed postmenopausally. The suggestive positive associations were stronger for invasive ovarian cancers and more specifically for high-grade serous carcinomas. These results do not support a reduced ovarian cancer risk associated with MVPA.     

A population-based case–control study of carotenoid and vitamin A intake and ovarian cancer (United States)

Objective: To evaluate the association between dietary intake of carotenoids and vitamin A and the incidence of ovarian cancer. Methods: We conducted a population-based case–control study of ovarian cancer in Massachusetts and Wisconsin. Incident cases diagnosed between 1991 and 1994 were identified through statewide tumor registries. We selected community controls at random from lists of licensed drivers and Medicare recipients; 327 cases and 3129 controls were included in the analysis. Data were collected by telephone interview, which included an abbreviated food and supplement list to quantify typical consumption of carotenoids (lutein/zeaxanthin, alpha-carotene, beta-carotene), retinol and total vitamin A at 5 years prior to diagnosis in cases, or to a comparable reference date in controls. Results were adjusted for age, state, and other risk factors. Results: Participants with the highest dietary intake of lutein/zeaxanthin (24,000 g/week) experienced a 40% lower risk of ovarian cancer (95% CI = 0.36–0.99) compared to those with the lowest intake. Intake of alpha-carotene, beta-carotene, retinol and total vitamin A was unrelated to risk. Among foods, we observed non-significantly lower risks with high consumption of spinach, carrots, skim/lowfat milk and liver. Conclusion: These results support previous findings suggesting an inverse relationship between carotenoid intake and ovarian cancer risk.     

CYP1A1 and GSTP1 gene variations in breast cancer: a systematic review and case–control study

In first part of this study, a systematic review was designed to explore the involvement of CYP1A1 and GSTP1 genes in breast cancerogenesis. Based on systematic review, we designed a study to screen CYP1A1 and GSTP1 genes for mutation and their possible association with breast carcinogenesis. A total of 400 individuals were collected and analyzed by PCR-SSCP. After sequence analysis of coding region of CYP1A1 we identified eleven mutations in different exons of respective gene. Among these eleven mutations, ~3 folds increased breast cancer risk was found associated with Asp82Glu mutation (OR 2.99; 95 % CI 1.26–7.09), with Ser83Thr mutation (OR 2.99; 95 % CI 1.26–7.09) and with Glu86Ala mutation (OR 3.18; 95 % CI 1.27–7.93) in cancer patients compared to controls. Furthermore, ~4 folds increase in breast cancer risk was found associated with Asp347Glu, Phe398Tyr and 5178delT mutations (OR 3.92; 95 % CI 1.35–11.3) in patients compared to controls. The sequence analysis of GSTP1 resulted in identification of total five mutations. Among these five mutations, ~3 folds increase in breast cancer risk was observed associated with 1860G>A mutation, with 1861-1876delCAGCCCTCTGGAGTGG mutation (OR 2.70; 95 % CI 1.10–6.62) and with 1861C>A mutation (OR 2.97; 95 % CI 1.01–8.45) in cancer patients compared to controls. Furthermore, ~5 folds increase in breast cancer risk was associated with 1883G>T mutation (OR 4.75; 95 % CI 1.46–15.3) and ~6 folds increase in breast cancer risk was found associated with Iso105Val mutation (OR 6.43; 95 % CI 1.41–29.3) in cancer patients compared to controls. Our finding, based on systematic review and experimental data suggest that the polymorphic CYP1A1 and GSTP1 genes may contribute to risk of developing breast cancer.     

Hypercholesterolemia and prostate cancer: a hospital-based case–control study

Objective  High levels of serum cholesterol have been proposed to increase the risk of prostate cancer but the epidemiologic evidence is limited. Methods  We conducted a hospital-based case–control study in Fargo, ND, USA, to examine the association between hypercholesterolemia and prostate cancer. Cases were men with incident, histologically confirmed prostate cancer. Controls were men without clinical cancer who were seen at the same hospital for an annual physical exam. Demographic and clinical data were abstracted from patients’ medical charts. Results  From a patient population aged 50 to 74 years old, we obtained data on 312 White cases and 319 White controls. Hypercholesterolemia was defined as total cholesterol greater than 5.17 (mmol/l). Univariate logistic regression showed a significant association between hypercholesterolemia and prostate cancer (odds ratio (OR) = 1.64, 95% confidence interval (CI): 1.19–2.27). This association changed only slightly after adjustment for age, family history of prostate cancer, body mass index, type 2 diabetes, smoking, and multivitamin use (OR = 1.58, 95% CI: 1.11–2.24). A significant association was found between low HDL and prostate cancer (OR = 1.57, 95% CI: 1.04–2.36). High LDL was associated with a 60% increased risk for prostate cancer (OR = 1.60, 95% CI: 1.09–2.34). Compared to never smokers, current smokers had an 84% increased risk for prostate cancer (OR = 1.84, 95% CI: 1.09–3.13). Conclusion  This study adds to recent evidence that hypercholesterolemia may increase the risk of prostate cancer in white men.     

Dietary inflammatory index and ovarian cancer risk in a large Italian case–control study

Background

While inflammation has been shown to play an important etiologic role in ovarian carcinogenesis, little is known about the association between inflammatory properties of diet and ovarian cancer risk.

Methods

We explored the association between the dietary inflammatory index (DII) and ovarian cancer risk in a multicentric Italian case–control study conducted between 1992 and 1999. Cases were 1,031 women with incident, histologically confirmed ovarian cancer from four areas in Italy. Controls were 2,411 women admitted to the same network of hospitals as the cases for acute, non-malignant and non-gynecological conditions, unrelated to hormonal or digestive-tract diseases or committed to long-term modifications of diet. DII scores were computed based on 31 nutrients and food items assessed using a reproducible and validated 78-item food frequency questionnaire. Odds ratios (ORs) were estimated through logistic regression models adjusting for age, total energy intake and other recognized confounding factors.

Results

Subjects in the highest quartile of DII scores (i.e., with the most pro-inflammatory diets) had a higher risk of ovarian cancer compared to subjects in the lowest quartile (i.e., with an anti-inflammatory diet) (OR_Quartile4vs1 1.47, 95% confidence interval, CI, 1.07, 2.01; p _trend = 0.009). When analyses were carried out using continuous DII, a significant positive association with ovarian cancer was observed: the OR for one-unit increment in DII score (corresponding to approximately 8 % of its range in the current study, +6.0 to ?6.20) was 1.08 (95% CI 1.02, 1.14).

Conclusion

A pro-inflammatory diet as indicated by higher DII scores is associated with increased ovarian cancer risk.

     

Leukocyte telomere length in a population-based case–control study of ovarian cancer: a pilot study

Objectives

Telomeres are structures at chromosome ends that contribute to maintaining genomic integrity. Telomere shortening with repeated cell divisions may lead to genomic instability and carcinogenesis. Studies suggest that shorter telomeres in constitutional DNA are associated with bladder, breast, lung, and renal cancer. Ovarian cancer tissues also have shortened telomeres and increased telomerase activity, suggesting that telomere abnormalities may be related to ovarian cancer.

Methods

We investigated leukocyte telomere length in 99 women with serous ovarian adenocarcinoma and 100 age-matched cancer-free controls enrolled in a population-based case–control study.

Results

Cases tended to have shorter telomeres than controls (P _wilcoxon = 0.002). Compared to subjects with telomere lengths in the longest tertile, those in the middle and shortest tertiles showed respective age-adjusted odds ratios (95% confidence intervals) of 2.69 (1.23–5.88) and 3.39 (1.54–7.46) (P _trend = 0.002). Strongest associations were found for subjects with poorly differentiated carcinomas (OR = 4.89, 95% CI 1.93–12.34).

Conclusions

This study shows that short leukocyte telomeres are associated with serous ovarian adenocarcinoma. These findings should be confirmed in large, prospective studies.     

Statins and pancreatic cancer risk: a nested case–control study

Objective  

To investigate the relationship between statin use and pancreatic cancer risk.     

Fiber intake and pancreatic cancer risk: a case–control study

BackgroundScanty and inconsistent studies are available on the relation between dietary fiber intake and pancreatic cancer. A case–control study was carried out in northern Italy to further investigate the role of various types of dietary fibers in the etiology of pancreatic cancer.Patients and methodsCases were 326 patients with incident pancreatic cancer, excluding neuroendocrine tumors, admitted to major teaching and general hospitals during 1991–2008. Controls were 652 patients admitted for acute, nonneoplastic conditions to the same hospital network of cases. Information was elicited using a validated food frequency questionnaire. Odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) were estimated for intake quintiles of different types of fiber after allowance for total energy intake and other potential confounding factors.ResultsTotal fiber intake was inversely related to risk of pancreatic cancer (OR = 0.4 for highest versus lowest quintile of intake; 95% CI 0.2–0.7). An inverse association emerged between pancreatic cancer and both soluble (OR = 0.4; 95% CI 0.2–0.7) and total insoluble fiber (OR = 0.5; 95% CI 0.3–0.8), particularly cellulose (OR = 0.4; 95% CI 0.3–0.7) and lignin (OR = 0.5; 95% CI 0.3–0.9). Fruit fiber intake was inversely associated with pancreatic cancer (OR = 0.5; 95% CI 0.3–0.8), whereas grain fiber was not (OR = 1.2; 95% CI 0.7–2.0).ConclusionsThis study suggests that selected types of fiber and total fiber are inversely related to pancreatic cancer.     

Occupation and keratinocyte cancer risk: a population-based case–control study

Objective The aim of our study was to identify occupations associated with increased risk of basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). Methods We conducted a population-based case–control study of BCC and SCC in New Hampshire. Cases (n = 599 BCC, n = 290 SCC) and controls (n = 524) completed a self-administered residence and work history questionnaire and personal interview regarding major risk factors for skin cancer. Reported jobs were coded using the Standardized Occupational Classification system (SOC). Odds ratios (ORs) and confidence intervals (CIs) for BCC and SCC were calculated for men and women separately using unconditional logistic regression models taking into account age, education, skin reaction to sun, history of painful sunburns, time spent outdoors, and for SCC, smoking. Results Among men, we observed elevated risks of both BCC and SCC among groundskeepers and gardeners, except farm (SOC 5622). We also found that garage and service station-related occupations (SOCs 873) and to some extent food/beverage preparation/service occupations (SOC 521) were associated with BCC risk among men. Women in health services occupations (SOC 523) had elevated risks for both tumors, especially for BCC. Additionally, administrative support (SOC 46/47) occupations were related to BCC risk among women. Other occupations were associated with excess risks, but without consistent trends by duration of employment. Conclusion We observed several occupations associated with elevated BCC and SCC risk. These results resemble reported findings for cutaneous melanoma and are generally consistent with the few available studies on keratinocyte cancers.     

Lifetime body size and prostate cancer risk in a population-based case–control study in Sweden

Purpose

The role of body size in prostate cancer etiology is unclear and potentially varies by age and disease subtype. We investigated whether body size in childhood and adulthood, including adult weight change, is related to total, low–intermediate-risk, high-risk, and fatal prostate cancer.

Methods

We used data on 1,499 incident prostate cancer cases and 1,118 population controls in Sweden. Body figure at age 10 was assessed by silhouette drawings. Adult body mass index (BMI) and weight change were based on self-reported height and weight between ages 20 and 70. We estimated odds ratios (ORs) with 95 % confidence intervals (CIs) by unconditional logistic regression.

Results

Height was positively associated with prostate cancer. Overweight/obesity in childhood was associated with a 54 % increased risk of dying from prostate cancer compared to normal weight, whereas a 27 % lower risk was seen in men who were moderately thin (drawing 2) in childhood (P _trend = 0.01). Using BMI <22.5 as a reference, we observed inverse associations between BMI 22.5 to <25 at age 20 and all prostate cancer subtypes (ORs in the range 0.72–0.82), and between mean adult BMI 25 to <27.5 and low–intermediate-risk disease (OR 0.75, 95 % CI 0.55–1.02). Moderate adult weight gain increased the risk of disease in men with low BMI at start and in short men.

Conclusions

Our comprehensive life-course approach revealed no convincing associations between anthropometric measures and prostate cancer risk. However, we found some leads that deserve further investigation, particularly for early-life body size. Our study highlights the importance of the time window of exposure in prostate cancer development.     

Alcohol and endometrial cancer risk: a case–control study and a meta-analysis

To evaluate the association between alcohol consumption and endometrial cancer risk, we analyzed data from a hospital-based case–control study, conducted in Italy between 1992 and 2006, on 454 endometrial cancer cases and 908 controls, and performed a meta-analysis updated to October 2009. Compared to never alcohol drinkers, the odds ratio was 1.03 (95% confidence interval, CI, 0.76–1.41) for ≤7, 1.27 (95% CI 0.86–1.87) for 8–14, and 1.19 (95% CI 0.80–1.77) for ≥15 drinks/week, with no trend in risk. No association emerged for wine, beer, and spirit consumption analyzed separately. The meta-analysis included 20 case–control and seven cohort studies, for a total of 13,120 cases. Compared to non/low drinkers, the pooled relative risks for drinkers were 0.90 (95% CI 0.80–1.01) for case–control studies, 1.01 (95% CI 0.90–1.14) for cohort studies, and 0.95 (95% CI 0.88–1.03) overall, with no heterogeneity between study design (p = 0.156). The overall estimate for heavy versus non/low drinkers was 1.12 (95% CI 0.87–1.45). The results were consistent according to selected study characteristics, including geographic area, definition of alcohol drinkers, and type of controls in case–control studies. Our findings provide evidence that alcohol drinking is not associated with endometrial cancer risk, although a weak positive association for very high drinkers cannot be excluded.     

Breast cancer risk in women with a primary ovarian cancer—a case–control study

Register-based studies show that women with ovarian cancer are at increased risk of developing breast cancer. Primary suggested explanations are heredity factors and a common hormonal aetiology. However, clinical surveillance that is provided for cancer patients during, and after, treatment of their primary malignancies together with possible mistakes in the registering procedures could affect the risk estimates. In order to examine these factors in women registered with ovarian cancer who develop subsequent breast cancer, a case–control study was performed. Using a regional Swedish cancer registry including 5060 women registered with ovarian cancer, 89 cases of breast cancer were found. After corrections for discrepancies in the registered and recorded information, 75 cases remained, of which 72 cases were included in the study. Information concerning possible risk factors were extracted from hospital records and compared with 177 matched controls. Suggested risk factors such as parity (relative risk (RR)=1.41), late age at menopause (52–61 years; RR=1.61) and heredity for breast and/or ovarian cancer (RR=1.50) were all connected with a non-significant increased risk of subsequent breast cancer. In all, 43% of the breast cancer cases were revealed without preceding symptoms at clinical follow-up, indicating that increased clinical surveillance is a factor of importance when explaining the increased risk. The fact that only 75 (missing records included) out of the 89 registered breast cancer cases could be linked to the preceding ovarian cancer indicates that the actual risk of developing breast cancer is smaller than previously described. The clinical implications from these findings could be that, beside general screening programmes and health controls offered to women in cancer-prone families, additional mammography examinations based on the assumption of an increased risk of breast cancer are not warranted in ovarian cancer patients.     

Flavonoid intake and liver cancer: a case–control study in Greece

In the context of a case–control study undertaken in Greece, we examined the role of six flavonoid classes in the etiology of hepatocellular carcinoma (HCC), by viral status, and of cholangiocarcinoma (CAC). Data and blood samples were collected between 1995 and 1998. Information about dietary intakes and covariates, including chronic infection with hepatitis B (HBV) and C (HCV) virus, were available for 250 HBV and/or HCV positive HCC cases, 83 HBV and HCV negative HCC cases, six CAC cases, and 360 hospital controls. In logistic regression models including gender, age, education, tobacco smoking, and total energy intake, there were no distinct patterns with respect to either HCC virus positive and HCC virus negative in relation to total flavonoids or any class of flavonoids, with the exception of flavones. Flavone intake, mostly derived from spinach and peppers, was inversely associated with both virus positive (P-trend, 0.049) and virus negative (P-trend, 0.084) HCC. There was also a suggestion of an inverse association of CAC with flavan-3-ols, anthocyanidins, and total flavonoids which, however, has to be taken with due caution on account of the small number of cases of this rare tumor. We conclude that flavones may be inversely associated with HCC risk, irrespective of its dominant etiology (viral or non viral).     

Male infertility and prostate cancer risk: a nested case–control study

The pathogenesis of prostate cancer is unclear, although experimental evidence implicates androgens as playing an important role. Infertile men frequently suffer from some degree of hypogonadism and may hence be hypothesized to be at lower risk of developing prostate cancer than fertile men. To test this hypothesis, we conducted a case–control study nested within “the Malmö Diet and Cancer Study” cohort in Sweden, inviting 661 prostate cancer cases and 661 age-matched controls to participate. Of the 975 (74%) respondents, we excluded 84 childless men with unknown fertility status. Thus, 891 men were included, providing 445 prostate cancer cases and 446 controls. Of these, 841 (94%) men were biological fathers and 50 (6%) men were infertile. Logistic regression showed that the infertile men were at significantly lower risk of being diagnosed with prostate cancer than the fertile men (odds ratio, 0.45; 95% confidence interval, 0.25–0.83). Conditional and unconditional multivariate models, adjusting for socioeconomic, anthropometric, and health-status-related factors, provided similar estimates. We conclude that enduring male infertility is associated with a reduced prostate cancer risk, thus corroborating the theory that normal testicular function, and hence most probably sufficient steroidogenesis, is an important contributing factor to the later development of this malignancy.     

Urinary tract diseases and bladder cancer risk: a case–control study

Objective The role of urinary tract diseases in bladder cancer (BC) etiology is not well established. To gain more insight on the role of urinary tract diseases in bladder cancer risk, we analyzed data from a large case–control study of bladder cancer. Methods Epidemiological data were collected via in-person interview. Logistic regression analyses were used to estimate BC risk in association with prior history of urinary tract diseases. Results A total of 659 BC patients and 689 age-, gender-, -ethnicity matched controls were included in the analyses. Increased bladder cancer risk was associated with history of cystitis (OR = 1.52, 95% CI: 1.12, 2.06), however, the risk was attenuated for infections diagnosed >1 year from the time of BC diagnosis or interview. In contrast, a history of four or more kidney infections was associated with a significant decreased risk of BC (OR=0.17, 95% CI: 0.04, 0.69), and there was a significant dose-response relationship between number of episode and BC risk (P for trend = 0.002). The joint effect of smoking with cystitis, kidney infection, bladder stone, kidney stone, and prostate infection was studied but revealed no significant interaction between smoking and these urinary tract diseases. Conclusion This study does not support the concept that urinary tract infections play a major role in the development of BC. Our study has the strength of collecting diagnosis time data of urinary tract diseases to allow analyzing the impact of timing of diagnosis between cancer and urinary tract diseases. This enables us to effectively address the issue of detection bias in case–controls studies of prior urinary diseases and BC.     

Accuracy of self-reported family history of cancer in a large case–control study of ovarian cancer

OBJECTIVE: To evaluate the reliability of self-reported family history of cancer in first-degree female relatives and to examine possible determinants of accurate reporting. METHODS: Women with ovarian cancer and controls were recruited between 1995 and 1999 and interviewed. The study comprised 579 cases and 1,564 controls with 6,265 first-degree female relatives. Self-reported familial cancer diagnoses were validated from registry data. Sensitivity, specificity, and kappa were calculated, and possible determinants were examined by logistic regression. RESULTS: The sensitivity of self-reporting ranged from 0.78 to 0.90 for all cancers but was lower for self-reporting of most site-specific cancers, ranging from 0.29 to 0.94. The specificity of self-reporting ranged from 0.91 to 0.99 for cancer in general and from 0.99 to 1.00 for site-specific cancers. Type of relative, age at interview, and length of education influenced the sensitivity and specificity significantly. The odds ratio for ovarian cancer was higher when based on registry data than on self-reported data and was significant (OR = 2.58 vs. 1.56). CONCLUSIONS: Cancer diagnoses in first-degree relatives are not always accurately reported by patients with ovarian cancer or by controls. The results indicate that studies of associations with family cancer history should validate self-reported family cancer diagnoses as carefully as possible.     

Dietary habits and risk of pancreatic cancer: an Italian case–control study

Objective  

To investigate the association between dietary habits and pancreatic cancer.     

Dietary fiber and stomach cancer risk: a case–control study from Italy

Objective  Fiber intake has been inversely related to stomach cancer risk, although this issue is still controversial. Methods  A case–control study was conducted in Italy between 1997 and 2007, including 230 cases with incident, histologically confirmed stomach cancer, and 547 controls with acute, non-neoplastic diseases. Dietary habits were investigated through a validated food frequency questionnaire. Results  Compared with the lowest quintile of intake, the multivariate odds ratios (ORs, including terms for major recognised confounding factors and total energy intake) for the highest quintile were 0.47 (95% confidence interval (CI): 0.28–0.79) for total fiber, 0.50 (95% CI: 0.30–0.85) for soluble non-cellulose polysaccharides (NCP), 0.39 (95% CI: 0.23–0.66) for total insoluble fiber, 0.54 (95% CI: 0.32–0.91) for insoluble NCP, 0.37 (95% CI: 0.22–0.64) for cellulose, and 0.59 (95% CI: 0.36–0.98) for lignin. With reference to the sources of fiber, an inverse association was found for fiber from vegetable (OR = 0.42, 95% CI: 0.24–0.72), and to a lesser extent from fruit (OR = 0.65, 95% CI: 0.38–1.10), but not for fiber from grain (OR = 1.25, 95% CI: 0.77–2.03). Conclusions  This study found an inverse relationship between stomach cancer risk and various types of fiber, derived, in particular, from vegetables and fruit.