***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    Input: Inflammation and gonadotropins are hypothesized to influence ovarian carcinogenesis . In a prospect i ve study , we evaluated ovarian cancer risk associated with self-reported use of medications that influence inflammation or gonadotropin levels . The Breast Cancer Detection Demonstration Project Follow-Up Study enrolled 61,431 women in 1979 and used telephone interviews and 3 mailed question naires through 1998 to up date risk factor information and identify incident ovarian cancers . The 1992 - 95 question naire ascertained medication use , including duration and frequency of use for aspirin , acetaminophen , other nonsteroidal anti-inflammatory drugs ( NSAIDs ) , tranquilizers and histamine-receptor antagonists . A Poisson regression analysis generated rate ratios ( RRs ) and 95 % confidence intervals ( CIs ) for the 31,364 women who were at risk of ovarian cancer and responded to the question naire that queried regular medication use . One hundred sixteen women developed ovarian cancer  during follow-up . None of the anti-inflammatory medications was associated with ovarian cancer , but the RR for more than 1 aspirin per day for 1 year or longer was 0.56 ( 95 % CI 0.20 - 1.5 ) and the RR for more than 5 years of regular " other NSAID " use was 2.0 ( 95 % CI 0.95 - 4.2 ) . Regular tranquilizer use  was not associated with ovarian cancer , but histamine-receptor antagonists used regularly for more than 5 years ( RR = 3.6 , 95 % CI 1.4 - 9.1 ) or more than once daily ( RR = 3.1 , 95 % CI 1.5 - 6.5 ) appeared to increase risk . In our study , neither anti-inflammatory medications nor anti-psychotic medications were associated with ovarian cancer . Potential associations with histamine-receptor antagonists may warrant further study Objective : We sought to evaluate the association between ovarian cancer risk and use of aspirin and nonsteroidal anti-inflammatories . Methods : We prospect ively assessed use of aspirin , nonsteroidal anti-inflammatories ( NSAIDs ) , and acetaminophen use in relation to ovarian cancer risk among 76,821 participants in the Nurses ' Health Study who had no history of cancer other than non-melanoma skin cancer . Women reported known and suspected ovarian cancer risk factors in biennial mailed question naires from 1976 to 1996 , along with new diagnoses of ovarian cancer . Aspirin use was assessed in 1980 , 1982 , 1984 , and 1988–1994 . We assessed NSAID use in 1980 , and both NSAID and acetaminophen use in 1990 , 1992 , and 1994 . During 16 years of follow-up and 1,222,412 person-years , 333 cases of invasive epithelial ovarian cancer were confirmed . We used pooled logistic regression to control for age , body mass index , oral contraceptive use , smoking history , parity , postmenopausal hormone use , tubal ligation , and other potential ovarian cancer risk factors . Results : Aspirin use was not associated with ovarian cancer risk overall ( RR for users compared with nonusers , 1.00 , 95 % confidence interval ( CI 0.80–1.25 ) . We found no association between  aspirin dose ( in number of weekly tablets ) and ovarian cancer risk ( RR for those taking 15 or more tablets weekly compared with nonusers , 0.98 , 95 % CI 0.63–1.52 ) . Similarly , duration of aspirin use was not associated with risk ( RR for aspirin use of 20 or more years , 0.99 , 95 % CI 0.69–1.43 ) . In separate models assessing the relation between NSAID use and ovarian cancer risk we found a 40 % reduction in risk among NSAID users versus nonusers ( RR 0.60 , 95 % CI 0.38–0.95 ) . However , when we examined this relationship in terms of days of NSAID use per month , we did not observe a dose – response with increasing NSAID use . Conclusions : We observed no association between  aspirin use , dose , or duration and epithelial ovarian cancer risk . Although we found a modest reduction in risk associated with NSAID use , there was no dose – effect Background : Several epidemiologic studies have shown inverse associations between use of nonsteroidal anti-inflammatory drugs ( NSAID ) and incident ovarian cancer , but the results are inconsistent . There have been only a few studies examining possible links between NSAIDs and endometrial cancer risk . We investigated associations between use of NSAIDs and incident ovarian and endometrial cancers in a prospect i ve cohort of about 20,000 women with ages from 58 to 76 years in 1992 . Participants were asked how often they used aspirin and nonaspirin NSAIDs .  Over 15 years , 311 endometrial and 167 ovarian incident malignancies were identified .  Multivariate-adjusted hazard ratios were estimated using Cox proportional regression . Results : Compared with women who reported no use of aspirin , the relative risks for ovarian cancer for those who used aspirin < 2 , 2 to 5 times , and ≥6 times per week were 0.83 , 0.77 , and 0.61 , respectively ( P trend = 0.04 ) . We did not observe any association  between nonaspirin NSAIDs use and ovarian cancer risk . Neither did we find associations  between aspirin or nonaspirin NSAIDs use and risk for endometrial cancer . Conclusions : Our results suggest a possible inverse association between frequency of aspirin use and risk for ovarian cancer . Cancer Epidemiol Biomarkers Prev ; 19(2 ) ; Background : Previous studies have suggested that use of aspirin or other nonsteroidal anti-inflammatory drugs ( NSAIDs ) may be associated with reduced risk of lung cancer , but the data are inconsistent and are limited particularly with respect to the effects of aspirin , separate from other NSAIDs . Methods : The Iowa Women 's Health Study is a prospect i ve cohort of 41,836 Iowa women ages 55 to 69 years old at baseline in 1986 .  NSAID use was assessed in 1992 . Over 10 years of follow-up , 403 incident cases of lung cancer were identified . The association of incident lung cancer with current use of aspirin or non-aspirin NSAIDs was analyzed after adjustment for lung cancer risk factors . Hazard ratios ( HR ) were estimated using multivariate COX proportional hazards regression . Results : There were 27,162 women in the analytic cohort . After controlling for age , education , alcohol intake , pack-years , smoking status , body mass index , and total fruit intake , the RR of women taking six or more  aspirin  weekly was 1.21 ( 95 % confidence interval , 0.92 - 1.59 ) . The HR was 1.23 for women taking six or more non-aspirin NSAIDs weekly ( 95 % confidence interval , 0.92 - 1.65 ) . There was no statistically significant trend by frequency of use for either aspirin ( Ptrend = 0.22 ) or non-aspirin NSAIDs ( Ptrend = 0.53 ) . Analyses by histologic type and smoking status yielded similar null results . Information on dosage and duration of use were not available for this analysis . Conclusion : These findings do not suggest that aspirin or other NSAIDs reduce risk of lung cancer  in this cohort of postmenopausal women . ( Cancer Epidemiol Biomarkers Prev 2006;15(11):2226–31 Inflammation is postulated to play an important role in ovarian carcinogenesis . Prostagl and in endoperoxide synthase 2 ( PTGS2 ) is responsible for the conversion of arachidonic acid to prostagl and ins in response to inflammation . In a pooled analysis of two population -based studies , the Hawaii Ovarian Cancer Case – Control Study and the New Engl and Case – Control Study , including 1,025 women with invasive ovarian carcinoma and 1,687 cancer-free controls , the association of ovarian cancer risk with the PTGS2 rs5275 polymorphism and the use of nonsteroidal antiinflammatory drugs ( NSAIDs ) were examined . Odds ratios ( ORs ) and 95 % confidence intervals ( CIs ) were estimated using unconditional logistic regression . In the pooled analysis , the CC genotype was associated with a reduced risk of nonserous ovarian carcinoma ( OR = 0.66 ; CI : 0.44–0.98 ) . In addition , the lowest risk was observed among carriers of the CC genotype who were users of only nonaspirin NSAIDs ( OR = 0.43 ; CI:0.20–0.93 ) in all women combined . The association of PTGS2 rs5275 with nonserous ovarian carcinoma and possible effect modification by NSAID use needs further validation , preferably in prospect i ve studies BACKGROUND Epidemiological evidence suggests that chronic inflammation may influence ovarian carcinogenesis . The study objective was to examine the association between the commonly used anti-inflammatory drug aspirin and  epithelial ovarian cancer .  METHODS The authors conducted a case-control study based in the New York University Women 's Health Study cohort enrolled between 1985 and 1991 in New York City . After a median follow-up period of 12 years , 68 incident cases of epithelial ovarian cancer were identified . Data about regular aspirin use were collected during the 1994 - 1996 follow-up question naire . Using a case-control study design , 10 controls per case were r and omly selected among study participants who matched the case by age and menopausal status . Conditional logistic regression analysis was used to study the relationships between  aspirin  and epithelial ovarian cancer by generating odds ratios ( ORs ) and 95 % confidence intervals ( CIs ) . RESULTS Relative to no aspirin use , the OR for epithelial ovarian cancer among women who reported  aspirin use three or more times per week for a period of at least 6 months was 0.60 ( 95 % CI 0.26 , 1.38 ) , after adjustment for age at menarche , parity , oral contraceptive use , and first-degree family history of breast cancer before age 50 . Among recent , within the previous 5 years , users of aspirin , the adjusted OR was 0.36 ( 95 % CI 0.11 , 1.18 ) . CONCLUSION Although confidence intervals included unity , the observed risk estimates seem to be compatible with previous studies suggesting that regular aspirin use could be inversely associated with risk of epithelial ovarian cancer Chronic inflammation may play an etiologic role in endometrial cancer .  Nonsteroidal anti-inflammatory drugs ( NSAIDs ) reduce inflammatory activity by inhibiting the proinflammatory cyclooxygenase enzymes and , therefore , may decrease cancer risk . However , few studies have examined the association between NSAID use and endometrial cancer  . We conducted a prospect i ve study among 72,524 women in the NIH-AARP Diet and Health Study . Women completed a question naire in 1996–1997 on lifestyle and health-related factors , including type and frequency of NSAID use within the past year , and were followed through 2003 by linkages to cancer registries and vital status data bases . During 488,261 person-years of follow-up , there were 732 incident endometrial cancers . NSAID use , compared with nonuse of NSAIDs , was not significantly associated with endometrial cancer risk [ relative risk ( RR ) , 0.90 ; 95 % confidence interval ( 95 % CI ) , 0.74–1.09 ] . Null associations were also observed by type of NSAID use [ aspirin only : RR , 0.88 ; 95 % CI , 0.70–1.11 ; nonaspirin NSAID ( NA-NSAID ) only : RR , 1.01 ; 95 % CI , 0.79–1.29 ; both aspirin and NA-NSAIDs : RR , 0.85 ; 95 % CI , 0.68–1.06 ] . Generally , results were not statistically significant by frequency of use for aspirin or NA-NSAIDs . Results did not change when women with a history of heart disease , hypertension , or diabetes were excluded to minimize the potential for confounding by indication . Overall , our data do not support an association between aspirin or NA-NSAID use and endometrial cancer risk To date , no prospect i ve studies have explored the relationship between the use of aspirin , other nonsteroidal anti-inflammatory medications ( NSAID ) , and acetaminophen and endometrial adenocarcinoma . Of the 82,971 women enrolled in a prospect i ve cohort study , 747 developed medical record-confirmed invasive endometrial cancer over a 24-year period . Use of aspirin was ascertained from 1980 to  
    Output:
    
The studies reported conflicting results or no statistically significant associations between the use of non-aspirin NSAIDs and risk of lung , ovary , bladder , prostate , skin , and head and neck cancers .
We did not find sufficient evidence to support the use of the non-aspirin NSAIDs for the primary chemoprevention of a wide variety of non-gastrointestinal cancers .