A prospective study of reproductive factors, hormone use, and risk of lung cancer in postmenopausal women

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 1501-1501 ◽  
Author(s):  
C. S. Baik ◽  
G. M. Strauss ◽  
D. Feskanich

1501 Background: There has been increased interest in understanding the role of hormonal factors in lung cancer (LC) in women with the observation that it exhibits different epidemiologic patterns and treatment response when compared to men. However, results of published studies have been inconsistent, possibly due to inadequate smoking adjustment. Methods: We prospectively examined the associations between reproductive factors, exogenous hormone use, and LC incidence in 106,574 postmenopausal women in the Nurses’ Health Study. Participants completed biennial questionnaires which included updated smoking history. We assessed age at menopause, age at menarche, type of menopause, parity, postmenopausal hormone (PMH), and oral contraceptive use. Cox proportional hazards modeling was used to estimate the relative risks (RR) of each exposure, adjusted for smoking status, number of cigarettes, time since quitting, age of initiating smoking, fruit/vegetable intake, body mass index, and environmental smoking exposure. Results: We identified 1,565 LC cases during follow up from 1984 to 2004. Parity was associated with decreased LC risk in never smokers (RR = 0.54, 95% CI 0.31–0.96) but increased risk in current smokers (RR = 1.44, 95% CI 1.03–2.02). No association was seen in former smokers. Also, younger age at menopause was associated with higher LC risk in women with natural menopause (p-trend = 0.016). PMH use was not associated with LC incidence. The RR for current PMH users was 1.01 (95% CI 0.87–1.17) and for past users was 0.95 (95% CI 0.82–1.1). No significant association was seen when assessed by duration of PMH use, time since last use, or type of PMH. However, past use of oral contraceptives for greater than 5 years was associated with increased LC risk (RR = 1.2, 95% CI 1.03–1.41). Conclusions: These results suggest that there may be an association between hormonal factors and LC development, and further suggest that the mechanism may differ in smokers versus lifelong never smokers. No significant financial relationships to disclose.

2010 ◽  
Vol 19 (10) ◽  
pp. 2525-2533 ◽  
Author(s):  
Christina S. Baik ◽  
Gary M. Strauss ◽  
Frank E. Speizer ◽  
Diane Feskanich

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Zhi-bing Hu ◽  
Ze-xiong Lu ◽  
Feng Zhu

Abstract Background The relationship between women’s reproductive characteristics and stroke events is unclear. We aimed to investigate age at menarche, age at menopause and number of reproductive years in relation to fatal stroke occurrence in the Guangzhou Biobank Cohort Study. Methods In total, 16,504 postmenopausal women without stroke, heart disease or a cancer history at baseline were included and followed up for a median of 12.0 years. After review of available records, 222 stroke deaths were recorded. Cox proportional hazards regression was used to assess the associations between the risk of fatal stroke occurrence and age at menarche, age at menopause and number of reproductive years. Results In the whole cohort, compared with those aged 15 years at menarche, an increased risk of fatal stroke among women at menarche showed respectively in those aged 12 years (aHR (adjusted hazard ratio) = 1.86, 95% confidence interval (CI) 0.96–3.60), aged 13 years (aHR = 1.69, 95% CI 0.98–2.92), aged 17 years (aHR = 1.83, 95% CI 1.10–3.05) and aged ≥ 18 years (aHR = 1.66, 95% CI 1.03–2.70), wherein the associations revealed an atypically U-shaped; similar U-shaped association to the cohort of postmenopausal women born before 1940 released a range of incremental risks of fatal stroke in women at menarche aged ≤ 12 years (aHR = 3.68, 95% CI 1.68–8.05), aged 13 years (aHR = 2.11, 95% CI 1.02–4.34), aged 14 years (aHR = 2.07, 95% CI 1.04), aged 17 years (aHR = 2.30, 95% CI 1.20–4.39) and aged 18 years (aHR = 2.50, 95% CI 1.37–4.57), respectively. Compared with menopausal women aged 51–52 years, those aged < 43 years at menopause had an increased risk for fatal stroke among postmenopausal women born in and after 1940 (aHR = 1.64, 95% CI 0.97–2.78) and postmenopausal women born before 1940 (aHR = 1.97, 95% CI 1.05–3.69). Additionally, compared with those with 32–34 reproductive years, women with ≤ 28 reproductive years had an increased risk for fatal stroke in the whole cohort (aHR = 1.91, 95% CI 1.28–2.86) and the cohort of postmenopausal women born before 1940 (aHR = 1.79, 95% CI 1.15–2.80). Conclusions Younger and older age at menarche, younger age at menopause and fewer reproductive ages were related to an increased risk of fatal stroke in postmenopausal women.


2003 ◽  
Vol 99 (5) ◽  
pp. 848-853 ◽  
Author(s):  
Balraj S. Jhawar ◽  
Charlie S. Fuchs ◽  
Graham A. Colditz ◽  
Meir J. Stampfer

Object. The goal of this study was to investigate the risk of meningioma in relation to exogenous and endogenous sex hormones. Methods. The study participants were female registered nurses from 11 US states who were between 30 and 55 years of age when they enrolled in the Nurses' Health Study cohort. These women completed biennial questionnaires between 1976 and 1996. All participants were free from cancer and other major medical illness at the onset of the study. The primary endpoint was meningioma as self-reported in biennial and supplemental questionnaires. During 1,213,522 person-years of follow-up review, 125 cases of meningioma were confirmed. After adjusting for age and body mass index (BMI), compared with postmenopausal women who had never used postmenopausal hormones, the relative risk (RR) for premenopausal women was 2.48 (95% confidence interval [CI] 1.29–4.77; p = 0.01) and the RR for postmenopausal women who received hormone therapy was 1.86 (95% CI 1.07–3.24; p = 0.03). The authors found no excess risk associated with past hormone use. In models that additionally controlled for hormone use and menopausal status, the authors found that, compared with women whose menarche occurred before they were 12 years of age, the RR for women whose menarche occurred at ages 12 through 14 years was 1.29 (95% CI 0.86–1.92; p = 0.21) and the RR for women whose menarche occurred after age 14 years was 1.97 (95% CI 1.06–3.66; p = 0.03). The authors also observed a tendency, albeit nonsignificant, for increased risk of meningioma in parous as opposed to nulliparous women (multivariate RR = 2.39, 95% CI 0.76–7.53; p = 0.14). A trend toward an increasing risk of meningioma with increasing BMI was also noted (p for trend = 0.06). No association was found for past or current use of oral contraceptives. Conclusions. The risk for meningiomas was increased among women exposed to either endogenous or exogenous sex hormones. An unexpected relationship with increasing age at menarche was also noted; this remains unexplained.


2021 ◽  
Author(s):  
Zhi-bing Hu ◽  
Ze-xiong Lu ◽  
Feng Zhu

Abstract Background The relationship between women’s reproductive characteristics and stroke events is unclear. We aimed to investigate age at menarche, age at menopause and number of reproductive years in relation to fatal stroke occurrence in the Guangzhou Biobank Cohort Study. Methods In total, 16504 postmenopausal women without stroke, heart disease or a cancer history at baseline were included and followed up for a median of 12.0 years. After review of available records, 222 stroke deaths were recorded. Cox proportional hazards regression was used to assess the associations between the risk of fatal stroke occurrence and age at menarche, age at menopause and number of reproductive years. Results In the whole cohort, compared with those aged 15 years at menarche, women aged 17 years at menarche had an increased risk for fatal stroke (adjusted hazard ratio [aHR] = 1.83, 95% confidence interval (CI) 1.10–3.05) and fatal haemorrhagic stroke (HR = 2.65, 95% CI 1.14–6.18), and women aged ≥ 18 years at menarche had an increased risk for fatal stroke (HR = 1.66, 95% CI 1.03–2.70) and fatal ischaemic stroke (HR = 2.01, 95% CI 1.01–3.99). Among postmenopausal women born before 1940, women aged < 43 years at menopause had an increased risk for fatal stroke (HR = 1.97, 95% CI 1.05–3.69) compared with those aged 51–52 years at menopause. Additionally, in the whole cohort, women with ≤ 28 reproductive years had an increased risk for fatal stroke (HR = 1.91, 95% CI 1.28–2.86) and fatal ischaemic stroke (HR = 2.26, 95% CI 1.26–4.05) compared with those with 32–34 reproductive years; postmenopausal women born before 1940 had a similar risk for fatal stroke and fatal ischaemic stroke. Conclusions Older age at menarche, younger age at menopause and fewer reproductive ages were related to an increased risk of fatal stroke in postmenopausal women.


2020 ◽  
Vol 49 (2) ◽  
pp. 599-607 ◽  
Author(s):  
Mohammad Abufaraj ◽  
Shahrokh Shariat ◽  
Marco Moschini ◽  
Florian Rohrer ◽  
Kyriaki Papantoniou ◽  
...  

Abstract Background With three out of four new bladder cancer (BCa) cases occurring in men, an apparent gender disparity exists. We aimed to investigate the role of hormonal and reproductive factors in BCa risk using two large female US prospective cohorts. Methods Our study population comprised 118 256 and 115 383 female registered nurses who were recruited in the Nurses' Health Study (NHS) and NHS II, respectively. Reproductive and hormonal factors and other relevant data were recorded in biennial self-administered questionnaires. Cox-regression analyses were performed to estimate age- and multivariable-adjusted incidence risk ratios (IRRs) and 95% confidence intervals (CIs). Inverse-variance-weighted meta-analysis was used to pool estimates across cohorts. Results During up to 36 years of follow-up, 629 incident BCa cases were confirmed. In the NHS, 22 566 women (21.3%) were postmenopausal at baseline, compared with 2723 women (2.4%) in the NHS II. Among women in the NHS, younger age at menopause (≤45 years) was associated with an increased risk of BCa (IRR: 1.41, 95% CI: 1.11–1.81, Ptrend = 0.01) compared with those with menopause onset at age 50+ years, particularly among ever-smokers (IRR for age at menopause ≤45 years: 1.53, 95% CI: 1.15–2.04; PIntx = 0.16). Age at menarche and first birth, parity, oral-contraceptive use and postmenopausal hormone use were not associated with BCa risk. Conclusions Overall, we found little support for an association between female reproductive factors and BCa risk in these prospective cohort studies. Earlier age at menopause was associated with a higher risk of BCa, particularly among smokers, indicating the potential for residual confounding.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 62.2-63
Author(s):  
Y. Eun ◽  
J. E. Yoo ◽  
K. D. Han ◽  
D. H. Kim ◽  
J. Lee ◽  
...  

Background:Previous studies on the link between female reproductive factors and osteoarthritis (OA) have shown conflicting results.Objectives:This study attempted to explore the association between reproductive factors and joint replacement arthroplasty of knee (TKRA) and hip (THRA) in a large nationwide population-based cohort of postmenopausal women.Methods:1,218,257 subjects who participated in national health examination in 2009 were included in the study. The study outcomes is incident THRA or TKRA due to severe hip or knee OA. The association of reproductive factors and THRA or TKRA was evaluated using a multivariate-adjusted proportional hazards model.Results:During the mean follow-up duration of 8.2 years, 1,733 incident THRA cases and 65,108 incident TKRA cases were observed. Later age at menarche (aHR 1.12 in 13-14 years; aHR 1.24 in 15-16 years; aHR 1.32 in ≥ 17 years), longer breastfeeding (aHR 1.24 in < 6 months; aHR 1.24 in 6-12 months; aHR 1.50 in ≥ 12 months), HRT (aHR 1.06 in < 2 years; aHR 1.11 in 2-5 years; aHR 1.21 ≥ 5 years) and OC use (aHR 1.11 in < 1 year; aHR 1.17 ≥ 1 year) was associated with increased risk of TKRA for severe knee OA, while later age at menopause (aHR 0.93 in 45-49 years; aHR 0.89 in 50-54 years), longer reproductive span (aHR 0.91 in 30-34 years; aHR 0.87 in 35-39 years; aHR 0.91 in ≥ 40 years) was associated with decreased risk. With regard to THRA for severe hip OA, later menarche (aHR 1.21 ≥ 17 years), longer breastfeeding (aHR 1.39 in < 6 months; aHR 1.31 in ≥ 12 months), and HRT more than 5 years (aHR 1.49) were associated with higher risk. The association between reproductive factors and severe OA was more pronounced in underweight and younger subjects.Conclusion:Our study found that shorter estrogen exposure was associated with higher risk of joint replacement therapy due to severe OA, and such association was more pronounced in underweight and younger subjects.Disclosure of Interests:None declared


2019 ◽  
Vol 78 (3) ◽  
pp. 438-448 ◽  
Author(s):  
Yashvee Dunneram ◽  
Darren C. Greenwood ◽  
Janet E. Cade

Menopause, the permanent cessation of the menstrual cycle, marks the end of a woman's reproductive lifespan. In addition to changes in sex hormone levels associated with menopause, its timing is another predictor of future health outcomes such as duration of the presence of vasomotor symptoms (VMS) and the risk of hormone-related cancers. With ageing of the population, it is estimated that worldwide 1·2 billion women will be menopausal by the year 2030. Previously the effects of reproductive factors (e.g. parity, age at menarche, pregnancy) and socio-demographic factors on intermediate and long-term health outcomes of menopause have been widely documented. However, little is known about whether diet could have an impact on these. Therefore, we review current evidence on the associations of diet with menopause, presence of VMS and the risk of hormone-related cancers such as ovarian, endometrial and breast cancer. Dietary factors could influence the lifespan of the ovaries and sex-hormones levels, hence the timing of natural menopause. Few studies reported an association between diet, in particular soya consumption, and a reduced risk of VMS. Sustained oestrogen exposure has been associated with a higher risk of hormone-related cancers and thus high-fat and meat diets have been linked with an increased risk of these cancers. However, to better understand the mechanistic pathways involved and to make stronger conclusions for these relationships, further studies investigating the associations of dietary intakes and dietary patterns with menopause, presence of VMS and the risk of hormone-related cancers are required.


2011 ◽  
Vol 26 (4) ◽  
pp. 234-240
Author(s):  
Renata G. Paleari ◽  
Raquel M.R. Peres ◽  
Juliana O. Florentino ◽  
Juliana K. Heinrich ◽  
Welbe O. Bragança ◽  
...  

Objective To evaluate the prevalence of the C825T polymorphism in the GNB3 gene in women with and without breast cancer and its possible association with clinical or pathological features of breast disease. Subjects and methods We included 134 women with breast cancer and a control group of 129 healthy women. The case group responded to a questionnaire on lifestyle, reproductive factors and family history. Clinical data were also evaluated. The risk for cancer was calculated and PCR was carried out for the detection of the polymorphism. Statistical analysis was performed using the package R Environment, with confidence intervals of 95% and a significance level of 5% (P<0.05). Results The frequency of the TT genotype was significantly greater in women of the control group (30.2%) than women with breast cancer (14.9%) (p=0.02). The polymorphism was not associated with clinical features, age at diagnosis (p=0.07), age at menarche (p=0.17), and age at menopause (p=0.60). The TT genotype did not have a higher frequency in patients with high BMI (p=0.98). The risk for cancer showed no correlation with the presence of the polymorphism. Conclusions Our data indicate that the C825T polymorphism in the GNB3 gene has no relationship to the risk for breast cancer or the characteristics of the disease.


2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 10594-10594
Author(s):  
S. Carrera ◽  
G. López-Vivanco ◽  
B. Calvo ◽  
U. Aresti ◽  
M. S. Jangi ◽  
...  

10594 Background: Telomerase adds hexameric TTAGGG nucleotide repeats onto the ends of chromosomal DNAs to compensate for losses of each cell replication. In several tumors, telomerase is expressed in a way that tumoral cell proliferates indefinitely. Correlation between telomerase level expression, clinico-pathological characteristics and survival of lung cancer is not well established in NSCLC. Methods: We studied 149 consecutive patients (140 men/9 women) with resected NSCLC: 37.6% adenocarcinoma, 59 % squamous cell, and 3.4% large cell carcinoma. Pathological stage: I (36.9%), II (32.3%) and III (30.8%). Reverse transcription-polymerase chain reaction (RT-PCR) analysis was used for the detection hTERT expression in lung cancer tissues immediately snap-frozen in liquid nitrogen at -80 °C. Results: Median and mean values of hTERT mRNA were 18.27 and 475.29 (SE 309.76). There were no significant differences on expression according to sex, histology, smoking history and pathological stage (ANOVA). Patients with highest values of hTERT mRNA expression (percentile 95, cut-off value >353) had worse median progression free survival (PFS) (p=0.024) and overall survival (OS) (p=0.020), using Kaplan-Meier method. Multivariate analysis by Cox regression yielded that hTERT level > 353 independently predicted a worse PFS (HR=0.39; 95% CI 0.17–0.93, p=0.034) and OS (HR=0.32; 95% CI 0.12–0.82, p=0.017). Conclusions: A high level of telomerase expression in tumoral tissue is strongly associated with increased risk of recurrence and mortality in resected NSCLC. The level of hTERT mRNA would predict the prognosis of lung cancer patients. No significant financial relationships to disclose.


2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 9600-9600
Author(s):  
David Alan Bond ◽  
Gregory Alan Otterson ◽  
Neil Dunavin

9600 Background: In a multi-institutional, retrospective study of 1976 patients treated for Hodgkin's lymphoma (HL) from 1969-2007, 55 patients developed second primary lung cancers a median of 19.5 years after treatment. Of these 55 cases, 32 were identified as lung adenocarcinoma (ACA). The development of targeted therapies in recent years has made the detection of specific genomic alterations important for disease prognosis and treatment in lung ACA. The prevalence of certain genomic alterations (EGFR, ALK, and KRAS) is highly correlated with smoking history. We hypothesize that the prevalence of genomic alterations also may differ in patients with a significant exposure to radiation. Methods: This observational retrospective case series includes 6 patients treated with mediastinal radiation for HL who subsequently developed lung ACA. All patients were treated at Ohio State University Wexner Medical Center. Patients were identified by searching billing diagnosis codes in the electronic medical record and by query of the physicians in the department of thoracic oncology at our institution. IRB approval was obtained. Results: The average age at diagnosis of HL was 25 years (range 18-46) and the average age at diagnosis of lung cancer was 58 (range 52-73). All patients were treated with radiation therapy; two patients were treated additionally with chemotherapy. None of the patients received HDT-ASCT. The average time from diagnosis of HL to diagnosis of lung cancer was 33 years. Of our six cases, 2 were positive for EGFR mutations and the other four were triple negative (-EGFR, -ALK, -KRAS). Three were never smokers, one had a 1.5 pack year history, and two had 10 pack year histories. Lung cancer stages at diagnosis were 1B (n=2), 2B (n=1), 3A (n=2), 4 (n=1). Conclusions: To our knowledge, this is the first report of mutational status of second primary lung ACA following radiation therapy for Hodgkin disease. Although the number of patients is small, the higher prevalence of the EGFR mutation in this sample suggests that ACA related to radiation therapy may have a similar mutational profile to that of never smokers. Further investigation is needed to define the disease characteristics of lung ACA in HL survivors.


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