Long and irregular menstrual cycles,polycystic ovary syndrome,and ovarian cancer risk in a population‐based case‐control study

Long and irregular menstrual cycles, a hallmark of polycystic ovary syndrome (PCOS), have been associated with higher androgen and lower sex hormone binding globulin levels and this altered hormonal environment may increase the risk of specific histologic subtypes of ovarian cancer. We investigated whether menstrual cycle characteristics and self‐reported PCOS were associated with ovarian cancer risk among 2,041 women with epithelial ovarian cancer and 2,100 controls in the New England Case‐Control Study (1992–2008). Menstrual cycle irregularity, menstrual cycle length, and PCOS were collected through in‐person interview. Unconditional logistic regression models were used to calculate odds ratios (OR) and 95% confidence intervals (95% CIs) for ovarian cancer risk overall, and polytomous logistic regression to evaluate whether risk differed between histologic subtypes. Overall, we observed no elevation in ovarian cancer risk for women who reported periods that were never regular or for those reporting a menstrual cycle length of >35 days with ORs of 0.87 (95% CI = 0.69–1.10) and 0.83 (95% CI = 0.44–1.54), respectively. We observed no overall association between self‐reported PCOS and ovarian cancer (OR = 0.97; 95% CI = 0.61–1.56). However, we observed significant differences in the association with menstrual cycle irregularity and risk of ovarian cancer subtypes (p_{heterogeneity} = 0.03) as well as by BMI and OC use (p_interaction < 0.01). Most notable, menstrual cycle irregularity was associated with a decreased risk of high grade serous tumors but an increased risk of serous borderline tumors among women who had never used OCs and those who were overweight. Future research in a large collaborative consortium may help clarify these associations.     

Menstrual pain and epithelial ovarian cancer risk

Purpose

Menstrual pain is associated with increased production of inflammatory molecules, such as prostaglandins. Inflammation is involved in pathogenesis of several cancers, including ovarian cancer. In this study, we examined the association between menstrual pain and risk of ovarian cancer.

Methods

We conducted a case–control study with 2,028 cases of epithelial ovarian cancer and 2,091 age- and study center-matched controls. Women were asked to report the severity of menstrual pain during their twenties and thirties, when not using oral contraceptives or breastfeeding. We used an unconditional logistic regression to evaluate the association between menstrual pain and epithelial ovarian cancer risk overall, and polytomous logistic regression to evaluate whether the association differed across tumor subtypes.

Results

Risk of ovarian cancer was increased in women with moderate (OR 1.22, 95 % CI 1.05–1.42) and severe pain (OR 1.34, 95 % CI 1.09–1.65) compared to women with no or mild pain during menstrual period. The association differed by histologic subtypes, with significant associations for severe pain with endometrioid (OR 1.64, 95 % CI 1.15–2.34) and clear cell tumors (OR 1.91, 95 % CI 1.11–3.28).

Conclusions

Our data suggest that moderate and severe pain during menstrual period are associated with increased risk of epithelial ovarian cancer. Due to high prevalence of menstrual pain in women of reproductive age, this observation warrants further studies.     

Menstrual pain and risk of epithelial ovarian cancer: Results from the Ovarian Cancer Association Consortium

Menstrual pain, a common gynecological condition, has been associated with increased risk of ovarian cancer in some, but not all studies. Furthermore, potential variations in the association between menstrual pain and ovarian cancer by histologic subtype have not been adequately evaluated due to lack of power. We assessed menstrual pain using either direct questions about having experienced menstrual pain, or indirect questions about menstrual pain as indication for use of hormones or medications. We used multivariate logistic regression to calculate the odds ratio (OR) for the association between severe menstrual pain and ovarian cancer, adjusting for potential confounders and multinomial logistic regression to calculate ORs for specific histologic subtypes. We observed no association between ovarian cancer and menstrual pain assessed by indirect questions. Among studies using direct question, severe pain was associated with a small but significant increase in overall risk of ovarian cancer (OR = 1.07, 95% CI: 1.01–1.13), after adjusting for endometriosis and other potential confounders. The association appeared to be more relevant for clear cell (OR = 1.48, 95% CI: 1.10–1.99) and serous borderline (OR = 1.31, 95% CI: 1.05–1.63) subtypes. In this large international pooled analysis of case‐control studies, we observed a small increase in risk of ovarian cancer for women reporting severe menstrual pain. While we observed an increased ovarian cancer risk with severe menstrual pain, the possibility of recall bias and undiagnosed endometriosis cannot be excluded. Future validation in prospective studies with detailed information on endometriosis is needed.     

Multiple births and risk of epithelial ovarian cancer

BACKGROUND AND METHODS: Prevailing hypotheses about the causes of ovarian carcinogenesis predict that women with a history of multiple births (twins, triplets, etc.) should be at increased risk of epithelial ovarian cancer. However, the scant available evidence suggests that they may actually be at lower risk. To resolve this issue, we pooled data from eight studies involving 2859 parous women with epithelial ovarian cancer (case patients) and 7434 parous women without ovarian cancer (control women). In addition to assessing their history of multiple births (and the sex of the children, where available), we obtained information on age, parity, oral contraceptive use, and other reproductive factors for each woman. Details of tumor histology were available for all case patients. We estimated the relative risks of various histologic types of ovarian cancers associated with multiple births by using multivariable logistic regression analysis, adjusting for matching and confounding variables. RESULTS: Among these parous women, 73 case patients (2. 6%) and 257 control women (3.5%) had a history of multiple births. The adjusted summary odds ratio (OR) for developing all types of epithelial ovarian cancer that are associated with multiple births was 0.81 (95% confidence interval [CI] = 0.61-1.08). We found no evidence that risks associated with multiple births differed among women with borderline or invasive tumors and among women with same-sex and opposite-sex offspring from multiple births. The risk reductions appeared specific for nonmucinous tumors (n = 2453; summary adjusted OR = 0.71 [95% CI = 0.52-0.98]); in contrast, associations with mucinous tumors (n = 406) were heterogeneous across studies. CONCLUSIONS: Parous women with nonmucinous ovarian cancer are no more likely to have a history of multiple births than other parous women, counter to the predictions of current hypotheses for causes of ovarian cancer.     

Incidence of histologic types of uterine sarcoma in relation to menstrual and reproductive history

To determine whether the occurrence of one or more histologic types of uterine sarcoma is related to events in a woman's reproductive life, a population-based case-control study was conducted. One-hundred sixty-seven women newly diagnosed with uterine sarcoma among residents of 6 geographic regions were compared to 208 women selected at random from the same populations with regard to histories of menstruation, pregnancy and childbearing, and breast feeding, as reported during a telephone interview. Compared to women whose menstrual periods began at age 13, women whose menses began earlier were at increased risk of leiomyosarcoma (OR = 2.0, 95% CI 0.9, 4.3); other histologic types were less strongly associated with early age at menarche. Women with leiomyosarcoma and endometrial stromal sarcoma, but not malignant mixed Müllerian tumors, tended to have ceased menstruating 2-3 years later than controls. None of the histologic types was clearly related to parity or to age at first live birth, but each was inversely related to age at last live birth. Associations were observed between leiomyosarcoma and histories of an induced abortion (OR = 4.2, 95% CI 1.2, 14.2) and of breast feeding after a live birth (OR = 0.5, 95% CI 0.3, 1.0); these relationships were not observed for other morphologic variants. These results suggest possible similarities and differences in menstrual and reproductive risk factors among histologic types of uterine sarcoma, and between these malignancies and the more common breast, endometrial and ovarian carcinomas.     

Inverse association of NSAID use and ovarian cancer in relation to oral contraceptive use and parity

We examined the association between non-steroidal anti-inflammatory drug (NSAID) use and ovarian cancer by potential effect modifiers, parity and oral contraceptive use, in a population-based case-control study conducted in Wisconsin and Massachusetts. Women reported prior use of NSAIDs and information on risk factors in a telephone interview. A total of 487 invasive ovarian cancer cases and 2653 control women aged 20-74 years were included in the analysis. After adjustment for age, state of residence and other covariates, ever use of NSAIDs was inversely associated with ovarian cancer in never users of oral contraceptives (odds ratio (OR)=0.58, 95% confidence interval (CI) 0.42-0.80) but not for ever users (OR=0.98, 95% CI 0.71-1.35) (P-interaction=0.03). A reduced risk with NSAID use was also noted in nulliparous women (OR=0.47, 95% CI 0.27-0.82) but not among parous women (OR=0.81, 95% CI 0.64-1.04) (P-interaction=0.05). These results suggest that use of NSAIDs were beneficial to women at greatest risk for ovarian cancer.     

Reproductive factors, oral contraceptive use, and human papillomavirus infection: pooled analysis of the IARC HPV prevalence surveys.

High parity, early age at first full-term pregnancy (FTP), and long-term oral contraceptive (OC) use increase cervical cancer risk, but it is unclear whether these variables are also associated with increased risk of acquisition and persistence of human papillomavirus (HPV) infection, the main cause of cervical cancer. Information on reproductive and menstrual characteristics and OC use were collected from 14 areas worldwide, among population-based, age-stratified random samples of women aged 15 years or older. HPV testing was done using PCR-based enzyme immunoassay. Unconditional logistic regression was used to estimate the odds ratios (OR) of being HPV-positive according to reproductive and menstrual factors and corresponding 95% confidence intervals (CI). When more than two groups were compared, floating CIs (FCI) were estimated. A total of 15,145 women (mean age, 40.9 years) were analyzed. Women with >or=5 FTPs (OR, 0.90; 95% FCI, 0.76-1.06) showed a similar risk of being HPV-positive compared with women with only one FTP (OR, 1.00; 95% FCI, 0.86-1.16). However, nulliparous women showed an OR of 1.40 (95% CI, 1.16-1.69) compared with parous women. Early age at first FTP was not significantly related to HPV positivity. HPV positivity was similar for women who reported >or=10 years of use of OCs (OR, 1.16; 95% FCI, 0.85-1.58) and never users of OCs (OR, 1.00; 95% FCI, 0.90-1.12). Our study suggests, therefore, that high parity, early age at first FTP, and long-term OC use are not associated with HPV prevalence, but rather these factors might be involved in the transition from HPV infection to neoplastic cervical lesions.     

Timing of pregnancy and the risk of epithelial ovarian cancer.

Recent animal studies suggest that progestagen-induced apoptosis of transformed ovarian surface epithelial cells may underlie the observed protective effect of pregnancy on the risk of ovarian cancer. Assuming that increasing numbers of cells are transformed with advancing age, we postulated that the benefits of pregnancy would be greater for older than younger women and tested this hypothesis in a population-based case-control study. We conducted interviews with 620 parous women, ages 18-79 years, with histologically confirmed incident ovarian cancer and 723 parous controls of the same age. Detailed information was collected on reproductive history, as well as hormonal exposures, smoking, medical history, and other factors. We estimated the relative risk of ovarian cancer associated with births at different ages through multiple logistic regression models. After adjusting for parity, older age at first and last births, and shorter time since last birth were all associated with significantly reduced risks of ovarian cancer. Age at first birth and time since last birth were not associated with ovarian cancer when adjusted for each other, whereas age at last birth remained strongly protective [odds ratio (OR), 0.57; 95% confidence interval (CI), 0.36-0.90] among women >35 years versus women less than 25 years. The effect was independent of total parity (per year of age among women with one birth: OR, 0.93; 95%CI, 0.87-1.01; among women with four or more births: OR, 0.96; 95%CI, 0.90-1.02). Our finding that ovarian cancer risk is reduced by pregnancy at older ages is further evidence that pregnancy confers a benefit beyond anovulation and is consistent with the theory that ovarian surface epithelial cell apoptosis induced by pregnancy hormones may be the underlying protective mechanism.     

Cigarette smoking and risk of epithelial ovarian cancer (Australia)

Objectives: We studied the association between cigarette smoking and ovarian cancer in a population-based case–control study. Methods: A total of 794 women with histologically confirmed epithelial ovarian cancer who were aged 18–79 years and resident in one of three Australian states were interviewed, together with 855 controls aged 18–79 years selected at random from the electoral roll from the same states. Information was obtained about cigarette smoking and other factors including age, parity, oral contraceptive use, and reproductive factors. We estimated the relative risk of ovarian cancer associated with cigarette smoking, accounting for histologic type, using multivariable logistic regression to adjust for confounding factors. Results: Women who had ever smoked cigarettes were more likely to develop ovarian cancer than women who had never smoked (adjusted odds ratio (OR) = 1.5; 95% confidence interval (CI) = 1.2–1.9). Risk was greater for ovarian cancers of borderline malignancy (OR = 2.4; 95% CI = 1.4–4.1) than for invasive tumors (OR = 1.7; 95% CI = 1.2–2.4) and the histologic subtype most strongly associated overall was the mucinous subtype among both current smokers (OR = 3.2; 95% CI = 1.8–5.7) and past smokers (OR = 2.3; 95% CI = 1.3–3.9). Conclusions: These data extend recent findings and suggest that cigarette smoking is a risk factor for ovarian cancer, especially mucinous and borderline mucinous types. From a public health viewpoint, this is one of the few reports of a potentially avoidable risk factor for ovarian cancer.     

Effects of Menstrual and Reproductive Factors on the Risk of Breast Cancer: Meta-analysis of the Case-Control Studies in Japan

To elucidate the magnitude of the effect of menstrual and reproductive factors on breast cancer occurrence among Japanese women, we reviewed eight case-control studies previously conducted in Japan and used a quantitative method (meta-analysis) to summarize the data. While individual studies have different methods and populations, the estimated odds ratios (ORs) in the studies were statistically homogeneous for all study variables. It was confirmed that early age at menarche, late age at first birth, and premenopausal status are significantly associated with risk of breast cancer; an estimated combined OR of 0.68 (95% confidence interval (CI): 0.59-0.77) was obtained for women with onset of menstruation after age 16 compared to those before age 14. Nulliparous women had higher risk than women with first birth before age 25 (OR=1.56 95%, CI: 1.27-1.91). The OR for women with first birth after age 35 was 2.26 (95% CI: 1.85-2.77) compared to women at first birth before age 25. Premenopausal women had a higher risk than women with menopause before age 50 (OR=2.21, 95% CI: 1.53-3.20). We also found a significant protective effect of high parity after controlling for age at first birth and the other menstrual factors. The OR estimate for 3 or more births compared to nulliparity was 0.68 (95% CI: 0.54-0.86). The meta-analysis provided quantitative estimates of breast cancer risk among Japanese women with improved precision.     

Preterm delivery is associated with an increased risk of epithelial ovarian cancer among parous women

Epithelial ovarian cancer is a fatal disease of largely unknown etiology. Higher parity is associated with reduced risk of ovarian cancer. However, among parous women, the impact of pregnancy‐related factors on risk is not well understood. This population‐based case–control study included all parous women with epithelial ovarian cancer in Denmark, Finland, Norway and Sweden during 1967–2013 (n = 10,957) and up to 10 matched controls (n = 107,864). We used conditional logistic regression to estimate odds ratios (ORs) with 95% confidence intervals (CIs) for pregnancy‐related factors and ovarian cancer risk by histological subtype. Preterm delivery was associated with an increased risk [pregnancy length (last pregnancy) ≤30 vs. 39–41 weeks, OR 1.33 (95% CI 1.06–1.67), adjusted for number of births]; the OR increased as pregnancy length decreased (p for trend < 0.001). Older age at first and last birth was associated with a decreased risk [first birth: 30–39 vs. <25 years: adjusted OR 0.76 (95% CI 0.70–0.83); last birth 30–39 vs. <25 years: adjusted OR 0.76 (95% CI 0.71–0.82)]. Increasing number of births was protective [≥4 births vs. 1; OR 0.63 (95% CI 0.59–0.68)] for all subtypes, most pronounced for clear‐cell tumors [OR 0.30, (95% CI 0.21–0.44), p_{heterogeneity} < 0.001]. No associations were observed for multiple pregnancies, preeclampsia or offspring size. In conclusion, in addition to high parity, full‐term pregnancies and pregnancies at older ages were associated with decreased risk of ovarian cancer. Our findings favor the cell clearance hypothesis, i.e. a recent pregnancy provides protection by clearing of precancerous cells from the epithelium of the ovary/fallopian tubes, mediated by placental or ovarian hormones.     

An association study of established breast cancer reproductive and lifestyle risk factors with tumour subtype defined by the prognostic 70-gene expression signature (MammaPrint®)

BackgroundReproductive and lifestyle factors influence both breast cancer risk and prognosis; this might be through breast cancer subtype. Subtypes defined by immunohistochemical hormone receptor markers and gene expression signatures are used to predict prognosis of breast cancer patients based on their tumour biology. We investigated the association between established breast cancer risk factors and the 70-gene prognostication signature in breast cancer patients.Patients and methodsStandardised questionnaires were used to obtain information on established risk factors of breast cancer from the Dutch patients of the MINDACT trial. Clinical-pathological and genomic information were obtained from the trial database. Logistic regression analyses were used to estimate the associations between lifestyle risk factors and tumour prognostic subtypes, measured by the 70-gene MammaPrint^® signature (i.e. low-risk or high-risk tumours).ResultsOf the 1555 breast cancer patients included, 910 had low-risk and 645 had high-risk tumours. Current body mass index (BMI), age at menarche, age at first birth, age at menopause, hormonal contraceptive use and hormone replacement therapy use were not associated with MammaPrint^®. In parous women, higher parity was associated with a lower risk (OR: 0.75, [95% confidence interval {CI}: 0.59–0.95] P = 0.018) and longer breastfeeding duration with a higher risk (OR: 1.03, [95% CI: 1.01–1.05] P = 0.005) of developing high-risk tumours; risk estimates were similar within oestrogen receptor–positive disease. After stratifying by menopausal status, the associations remained present in post-menopausal women.ConclusionUsing prognostic gene expression profiles, we have indications that specific reproductive factors may be associated with prognostic tumour subtypes beyond hormone receptor status.     

Reproductive factors and risk of meningioma and glioma

Female sex hormones have previously been suggested as possible risk factors for brain tumors, but published studies have reported conflicting results. We conducted a population-based case-control study of glioma (n=626) and meningioma (n=906) cases and randomly selected controls stratified on age and geographic region (n=1,774) in Denmark, Finland, Norway, Sweden, and the United Kingdom. Unconditional logistic regression was used to estimate odds ratios (OR) for glioma and meningioma in relation to reproductive factors. A decreased glioma risk was associated with ever-pregnancy compared with never-pregnancy [OR, 0.8; 95% confidence interval (95% CI), 0.6-1.0]. Meningioma risk among women ages <50 years was increased in relation to number of pregnancies leading to a live birth (OR, 1.8; 95% CI: 1.1-2.8 for giving birth to 3 children compared with nulliparous women; P(trend) among parous women=0.01). This relation was not found for older women. Breast-feeding among parous women increased the glioma risk (OR, 2.2; 95% CI, 1.3-3.9 for breast-feeding 36 months or more compared with breast-feeding 3 months or less). Menopausal status and age at menopause were not associated with meningioma or glioma risk. Our findings imply that reproductive hormones may influence the occurrence of meningioma and glioma.     

Genetic polymorphisms in the Paraoxonase 1 gene and risk of ovarian epithelial carcinoma

Oxidative stress during successive ovulations increases the opportunity for DNA damage to ovarian epithelial cells and the potential for malignant transformation. Paraoxonase 1 (PON1) is an endogenous free radical scavenger that reduces oxidative stress. The association of two common functional single nucleotide polymorphisms (SNP), rs854560 T>A and rs662 A>G, with the risk of epithelial ovarian cancer was examined in a population-based case-control study in Hawaii. A personal interview and blood specimens were collected from 274 women with histologically confirmed, primary ovarian cancer and 452 controls frequency matched on age and ethnicity. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated by unconditional logistic regression. Both PON1 SNPs were significantly associated with ovarian cancer risk. The ORs were 0.53 (95% CI, 0.35-0.79; P for allele-dose effect = 0.01) for women carrying the rs854560 T allele compared with women with the AA genotype and 0.65 (95% CI, 0.44-0.95; P for allele-dose effect = 0.03) for women carrying the rs662 A allele compared with women with the GG genotype. The association of the rs854560 T genotype with risk was stronger among smokers (OR, 0.33; 95% CI, 0.17-0.64; P for allele-dose effect = 0.0007) than among nonsmokers (OR, 0.68; 95% CI, 0.40-1.18; P for allele-dose effect = 0.53). The decreased risk associated with the rs854560 T allele was also stronger among obese women (OR, 0.19; 95% CI, 0.06-0.55; P for allele-dose effect = 0.007) than among nonobese women (OR, 0.62; 95% CI, 0.40-0.98; P for allele-dose effect = 0.16). Our study provides evidence for an association of two PON1 SNPs with the risk of epithelial ovarian cancer. Possible effect modification of these associations by tobacco smoking and obesity needs confirmation in other studies.     

Determinants of risk of invasive cervical cancer in young women.

We analysed determinants of risk of cervical cancer in women aged less than 45 years using data from a case-control study conducted in Italy. Cases were 261 women aged < 45 years with histologically confirmed invasive cervical cancer. Controls were 257 women aged < 45 years, with acute, non-neoplastic conditions, judged to be unrelated to any of the known or suspected risk factors for cervical cancer. In comparison with women reporting one or no sexual partner, the multivariate odds ratio (OR) of cervical cancer was 2.4 (95% confidence interval, CI, 1.3-4.6), for women reporting two or more sexual partners, and, in comparison with women reporting their first intercourse at 17 years of age or before, the multivariate OR was 0.5 (95% CI 0.3-0.9) in women aged > or =23 years at first intercourse. The risk of cervical cancer was higher in parous women and increased with number of births (OR = 8.1 for three or more births). Among parous women the risk tended to increase with later age at last birth; in comparison with parous women reporting their last birth before age 25, the OR was 1.9 in those reporting their last birth at > or =35 years. No clear association emerged between oral contraceptive use, smoking, education, social class and risk of cervical cancer.     

Alcohol, wine, and risk of epithelial ovarian cancer.

Moderate alcohol intake can influence sex hormone levels and affect ovarian function as well as increasing breast cancer risk. This suggests that alcohol might also influence ovarian cancer risk. We have evaluated this among 696 Australian women with histologically confirmed epithelial ovarian cancer and 786 cancer-free control women, selected at random from the electoral roll. Sociodemographic information and a detailed reproductive history were collected in a face-to-face interview, and information about diet and alcohol consumption was obtained from a food frequency questionnaire. Logistic regression was used to calculate adjusted odds ratios (OR) and 95% confidence intervals (95% CI). Overall, 59% of women drank <1 standard drink/week and only 5% of cases and 8% of controls drank an average of > or =2 standard drinks/day. Compared with nondrinkers, the OR for women who drank an average of > or =2 standard drinks/day was 0.49 (95% CI = 0.30-0.81). This effect did not vary for the different subtypes but was restricted to wine (OR = 0.56, 95% CI = 0.33-0.93 for > or =1 glass/day versus nondrinkers) with no effect for beer (OR = 1.26, 95% CI = 0.65-2.46) or sherry/spirits (OR = 1.07, 95% CI = 0.59-1.95). Combining our results with the six previous population-based studies gave a pooled OR of 0.72 (95% CI = 0.54-0.97) for the highest alcohol intake group versus nondrinkers. These data suggest that alcohol does not increase risk of ovarian cancer. In this Australian population, the inverse association with alcohol was due solely to wine consumption and so may be a consequence of antioxidants and/or phytoestrogens in wine rather than the alcohol itself.     

Menstrual and reproductive factors and endometrial cancer risk: Results from a population-based case-control study in urban Shanghai

The purpose of our study was to evaluate the association of menstrual and reproductive factors with the risk of endometrial cancer. In a population-based case-control study conducted in urban Shanghai, in-person interviews were completed for 833 women aged 30-69 years and an equal number of controls frequency-matched to cases by age. All cases were newly diagnosed with endometrial cancer between January 1, 1997 and December 31, 2001. The unconditional logistic regression model was employed to derive the adjusted odds ratios (ORs) of endometrial cancer and 95% confidence intervals (CIs) in relation to menstrual and reproductive factors. Earlier menarche age, particularly among premenopausal women, and later menopausal age were associated with an elevated risk of endometrial cancer. A clear dose-response relation between endometrial cancer risk and years of menstruation was observed (p for trend < 0.01). Compared to women ever having a pregnancy and women ever having had a live birth, respectively, nulligravity and nulliparity were both associated with a more than one-fold elevated risk of endometrial cancer. Both completed (OR = 3.02, 95% CI 1.10-8.32 for women never having a complete pregnancy) and incomplete pregnancy (OR = 0.69, 95%CI 0.55-0.87) conferred a protective effect against endometrial cancer, and the protective effect appeared to increase with total number of pregnancies (p for trend = 0.01). The effect of pregnancy on endometrial cancer remained unchanged with increasing time since the last pregnancy. Stillbirth and age at first pregnancy was unrelated to endometrial cancer risk. Our study suggests that prolonged menstruation was related to an increased risk of endometrial cancer while pregnancy, including induced abortion, reduced the risk of endometrial cancer.     

Anthropometry and the risk of epithelial ovarian cancer

BACKGROUND: The association between anthropometric factors and ovarian cancer risk was investigated using data from 762 cases and 1348 controls participating in a population-based case-control study in the Delaware Valley from 1994-1998. Because factors such as oral contraceptive (OC), hormone therapy (HT), and parity may affect weight and hormone levels, the associations were examined in women with and without these characteristics. METHODS: Unconditional logistic regression was used to calculate odds ratios and 95% confidence intervals while controlling for age, race, parity, family history of ovarian cancer, tubal ligation, and OC use. RESULTS: Compared with controls, cases were taller and heavier in recent years and at age 18. Results did not differ by OC or HT use. However, anthropometric associations differed significantly based on parity, as increasing anthropometric measures were associated with increased ovarian cancer risk among nulliparous women only. Adjusted OR for recent body mass index (BMI) quartile 4 compared with quartile 1 for nulliparous women was 2.53 (95% confidence interval [CI]: 1.39, 4.61) compared with 0.96 (95% CI: 0.70, 1.31) for parous women. Additionally, adult weight gain was significant only for nulliparous women. Adjusted OR for weight change (recent to age 18) quartile 4 compared with quartile 1 for nulliparous women was 3.73 (95% CI: 1.88, 7.42) versus 1.09 (95% CI: 0.78, 1.51) for parous women. CONCLUSIONS: BMI and weight in women's adult lifetime may be positively associated with ovarian cancer risk. Observations were most apparent for nulliparous women, possibly reflecting an interaction between local inflammation caused by incessant ovulation and increased estrogen exposure on ovarian epithelium.     

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.     

A population-based case-control study of endometrial cancer in Shanghai, China

A case-control study of 268 patients with endometrial cancer and 268 population controls was conducted during 1988-1990 in Shanghai, China, to evaluate etiologic factors in a population whose risk had not been substantially altered by the use of exogenous estrogens. In spite of this, the major risk factors resembled those found in other studies. The risk of endometrial cancer was significantly elevated among nulligravidas (OR = 5.4, 95% CI = 2.0-14.6) and decreased with number of pregnancies (p less than 0.01). Late age at menopause was associated with increased risk, while early age at menarche was unrelated. Use of oral contraceptives for more than 2 years was associated with a reduction in endometrial cancer risk (OR = 0.4, 95% CI = 0.1-1.2), while short-term use of oral contraceptives and other methods of contraception were unrelated. Obesity was a strong predictor of risk, with women in the highest quartile of weight having 2.5 times the risk of those in the lowest quartile. In contrast to many other studies, cigarette smokers were at elevated risk (OR = 1.7, 95% CI = 0.9-3.0). Risk was also elevated among women reporting a history of gall-bladder disease, polycystic ovaries, menstrual symptoms, and non-estrogen hormone use.