scholarly journals Energy balance and cancer: the role of sex hormones

2001 ◽  
Vol 60 (1) ◽  
pp. 81-89 ◽  
Author(s):  
Timothy J. Key ◽  
Naomi E. Allen ◽  
Pia K. Verkasalo ◽  
Emily Banks

Energy balance can affect the risk for hormone-related cancers by altering sex hormone levels. Energy intake and expenditure are difficult to measure in epidemiological studies, but a chronic excess of intake relative to expenditure leads to a high BMI, which can be accurately measured. In premenopausal women obesity has little effect on the serum concentration of oestradiol, but causes an increase in the frequency of anovular menstrual cycles and thus a reduction in progesterone levels; these changes lead to a large increase in the risk for endometrial cancer, but little change, or a small decrease, in the risk for breast cancer. In post-menopausal women oestradiol levels are not regulated by negative feedback, and obesity causes an increase in the serum concentration of bioavailable oestradiol; this factor causes increases in the risk for both endometrial cancer and breast cancer. The development of ovarian cancer appears to be related more strongly to the frequency of ovulation than to direct effects of circulating levels of sex hormones, and BMI is not clearly associated with the risk for ovarian cancer. In men, increasing BMI has little effect on bioavailable androgen levels, and any effect of obesity on prostate cancer risk is small.

2008 ◽  
Vol 159 (3) ◽  
pp. 197-202 ◽  
Author(s):  
Andreas Mueller ◽  
Louis Gooren

ObjectiveTo assess the risk of development of hormone-related tumors in transsexuals receiving treatment with cross-sex hormones.DesignDescription of cases of transsexuals who have developed a hormone-related malignancy observed in their own clinic or reported in the literature. Recommendations for early diagnosis and prevention are presented.MethodsReview of the literature in PubMed.ResultsIn male-to-female transsexuals receiving estrogen administration, lactotroph adenomas, breast cancer, and prostate cancer have been reported. In female-to-male transsexuals receiving treatment with testosterone, a single case of breast carcinoma and several cases of ovarian cancer have been reported. So far endometrial cancer has not been encountered though it remains a potential malignant development.ConclusionsThere are so far only a few cases of hormone-related cancer in transsexuals. There may be an underreporting. The probability of a hormone-related tumor increases with the duration of exposure to cross-sex hormones and the aging of the population of transsexuals.


2019 ◽  
Vol 29 (2) ◽  
pp. 299-304 ◽  
Author(s):  
Arnold-Jan Kruse ◽  
Henk G ter Brugge ◽  
Harm H de Haan ◽  
Hugo W Van Eyndhoven ◽  
Hans W Nijman

ObjectiveVaginal hysterectomy with bilateral salpingo-oophorectomy may be an alternative strategy for patients with low-risk endometrial cancer and medical co-morbidities precluding laparoscopic or abdominal procedures. The current study evaluates the prevalence of co-existent ovarian malignancy in patients with endometrial cancer and the influence of bilateral salpingo-oophorectomy on survival outcomes in these patients.MethodsMedline and EMBASE were searched for studies published between January 1, 2000 and November 20, 2017 that investigated (1) the prevalence of co-existing ovarian malignancy (either metastases or primary synchronous ovarian cancer in women with endometrial cancer, and (2) the influence of bilateral salpingo-oophorectomy on recurrence and/or survival rates.ResultsOf the pre-menopausal and post-menopausal patients (n=6059), 373 were identified with metastases and 106 were identified with primary synchronous ovarian cancer. Of the post-menopausal patients (n=6016), 362 were identified with metastases and 44 were identified with primary synchronous ovarian cancer. Survival outcomes did not differ for pre-menopausal patients with endometrial cancer with and without bilateral salpingo-oophorectomy (5-year overall survival rates were 89–94.5% and 86–97.8%, respectively).ConclusionBilateral salpingo-oophorectomy during vaginal hysterectomy seems to have a limited impact on disease outcome in patients with endometrial cancer. These results support the view that vaginal hysterectomy alone or with bilateral salpingo-oophorectomy may be an option for patients with endometrial cancer who are not ideal surgical candidates.


Author(s):  
Allakhyarov D.Z. ◽  
Petrov Yu.A. ◽  
Palieva N.V.

This article presents reviews of literature sources on the issue of assessing the risk of developing gynecological cancer in women after an in vitro fertilization program. Infertility and infertile marriages have now become quite a big problem of modern medicine. Against the background of the unfavorable demographic situation in the Russian Federation, this problem is becoming quite urgent. The main way to solve this situation is assisted reproductive technologies, among which the most common is in vitro fertilization. The in vitro fertilization program is accompanied by a hormonal ovulation stimulation procedure to obtain a female germ cell capable of fertilization. Against the background of the active use of the in vitro fertilization procedure, many patients had concerns related to the risk of developing gynecological cancer after the IVF procedure, which is due to the use of hormonal drugs to stimulate the ovaries. Also of concern is the fact that certain types of cancer, including ovarian cancer, endometrial cancer and breast cancer, are hormone-dependent. In this regard, multiple large-scale studies were conducted, which showed that the risk of developing gynecological cancer is really increased in patients after the in vitro fertilization program. In particular, breast cancer in women after the in vitro fertilization program is more common by 10%, and in women without a history of pregnancy and over the age of 40, it is more common by 31%. The increased risk may be due to age-related vulnerability to the effects of hormones or higher doses of hormones during the IVF procedure. Ovarian cancer and endometrial cancer are also more common in patients after IVF. According to the research results, it is suggested that it is not the IVF procedure itself that causes the development of cancer, but excessive hormonal load of the body, which leads to the launch of carcinogenesis.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 352-352
Author(s):  
Rawiwan Sirirat ◽  
Yessenia Tantamango-Bartley ◽  
Celine Heskey ◽  
Ella Haddad ◽  
Gary Fraser ◽  
...  

Abstract Objectives Breast cancer is the most diagnosed form of cancer among American women. Worldwide, it is second only to lung cancer. Phytosterols are phytochemicals found in plant foods that have potential benefits for breast cancer. Research on phytosterols and cancer associations to date has been limited to breast cancer cell lines and animal studies, and the results have been promising. Our objective is to examine the association between breast cancer incidence and phytosterol intake in the Adventist Health Study-2, a large cohort in North America. Methods The present study estimated the association between phytosterol intake and breast cancer incidence in 52,734 females who were part of the Adventist Health Study 2 (AHS-2) cohort. Breast cancer cases (n = 1050) were ascertained with tumor registries from 2008 to 2014. Phytosterols content in foods was quantified by using USDA 17 and other published sources. These values were used to estimate phytosterol intake from food intake assessed by a self-administered food frequency questionnaires (FFQ). Results Hazard ratios were below the null, but statistically non-significant for β-sitosterol [HR = 0.77, 95%CI (0.44–1.36)], campesterol [HR = 0.84, 95%CI (0.46–1.55)], stigmasterol [HR = 0.76 (0.46–1.26)], and total phytosterol [HR = 0.77, 95%CI (0.43–1.40)]. In premenopausal women, HRs ranged between 0.95–1.72; in postmenopausal women, HRs were below the null, ranging between 0.67–0.83. In both premenopausal and postmenopausal women, HRs were statistically non-significant. Conclusions The inverse association between phytosterol consumption and breast cancer incidence appears uncertain. The uncertainty possibly could be due to lack of power or measurement error. Additional epidemiological studies with a larger number of breast cancer cases, improved phytosterol intake estimates, or both are needed. Funding Sources Unilever Research &Development, Vlaardingen, The Netherlands.


2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 6588-6588
Author(s):  
B. M. Harris ◽  
A. C. Broxson ◽  
L. A. Anderson ◽  
J. G. Engelbrink ◽  
M. A. Zalewski ◽  
...  

6588 Background: Antiestrogen therapy has dramatically improved breast cancer survival rates but weight gain may be problematic. Studies evaluating antiestrogen therapy-related weight gain have yielded mixed results. Our primary objective was to evaluate weight changes in female breast cancer survivors (BCS) who received adjuvant anti-estrogen therapy for stage 0-III breast cancer. Methods: A retrospective chart review was conducted to evaluate weight changes in female chemo naive BCS receiving anti-estrogen therapy. Weights at initiation of hormonal therapy and at 6, 12, 24, and 36 months of follow-up were recorded. Median weight changes were calculated and were compared with Wilcoxon's signed rank test or the Kurskall-Wallis test. Results: A total of 622 women were included. The majority were white (77%), had stage I disease (78%), and were postmenopausal (82%). The median age at diagnosis was 59 years (range, 26–87). Median weight at initiation of hormonal therapy among premenopausal women was 65 kg (range 45.4–122.9). Median weight gain in this group was 0.4 kg (p = 0.009), 0.7 kg (p = 0.013), 1.9 kg (p = 0.0001), and 2.4 kg (p < 0.0001) at 6, 12, 24, and 36 months respectively. Among post-menopausal women, median weight at initiation of therapy was 71.7 kg (range 41.5–152.0) and median weight gain was 0.5 kg (p < 0.0001), 1 kg (p < 0.0001), 0.85 kg (p = 0.001), and 0.85 kg (p = 0.004) at 6, 12, 24, and 36 months respectively. Premenopausal patients had significantly more weight gain at 24 (p = 0.041) and 36 months (p = 0.005), as compared to postmenopausal patients. Among premenopausal women, 110/111 were treated with tamoxifen. Among post-menopausal women (n = 510), hormonal therapy was as follows: unknown n = 28 patients, tamoxifen n = 312, and AI n = 170. Overall, BCS treated with tamoxifen vs an AI had significantly more weight gain at 24 (p = 0.003) and 36 months (p = 0.009). Conclusions: Premenopausal patients are at higher risk for weight gain than postmenopausal patients. Further prospective research is warranted examining weight gain as a long-term side effect of anti-estrogen therapy in BCS. No significant financial relationships to disclose.


2021 ◽  
Author(s):  
Bryony L Hayes ◽  
Timothy Robinson ◽  
Siddhartha P. Kar ◽  
Katherine S Ruth ◽  
Konstantinos K Tsilidis ◽  
...  

BACKGROUND Previous research has demonstrated that a morning-preference chronotype is protective against both breast and prostate cancer. Sex hormones have been implicated in relation to both chronotype and the development of both cancers. This study aims to assess whether sex hormones confound or mediate the effect of chronotype on breast and prostate cancer risk using a Mendelian Randomization (MR) framework. METHODS We obtained genetic variants strongly (p<5x10-8) associated with chronotype and sex hormones (total testosterone, bioavailable testosterone, sex hormone binding globulin (SHBG), and oestradiol from previously published genome-wide association studies (GWAS) that had been undertaken in UK Biobank and 23andMe (n=244,207 females and n=205,527 males). These variants were used to investigate causal relationships with risk of breast and prostate cancer using summary data from the largest available consortia in breast (nCases/nControls=133,384/ 113,789) and prostate cancer (nCases/nControls=79,148/61,106). This was achieved using a series of MR approaches: univariable, bidirectional and multivariable. Results Overall, we found evidence for a protective effect of genetically predicted tendency towards morning preference on both breast (OR=0.93, 95% CI:0.88, 1.00) and prostate (OR=0.90, 95% CI:0.83, 0.97) cancer risk. There was evidence that an increased tendency to morning preference reduces bioavailable testosterone levels in both females (mean SD difference=-0.08, 95% CI:-0.12, -0.05) and males (mean SD difference=-0.06, 95% CI:-0.09, -0.03), and reduces total testosterone levels in females (mean SD difference=-0.07, 95% CI:-0.10, -0.03). We also found evidence to support higher total and bioavailable testosterone increasing the risk of breast cancer (OR=1.15, 95% CI:1.07, 1.23, OR=1.10, 95% CI:1.01, 1.19 respectively) and higher bioavailable testosterone increasing prostate cancer risk (OR=1.22, 95% CI:1.08, 1.37). While findings from univariable and bidirectional MR analyses indicated that testosterone may lie on the causal pathway between chronotype and cancer risk, there was evidence for a bidirectional association between chronotype and testosterone in females, implicating testosterone as both a confounder and mediator of the chronotype effect on breast cancer risk. However, the effects of chronotype remained largely unchanged when accounting for testosterone in multivariable MR, suggesting that any confounding or mediating effect is likely to be minimal. Conclusions This study has extended previous findings regarding the protective effect of chronotype on breast cancer and found evidence to suggest that morning preference also reduces prostate cancer risk in men. While testosterone levels were found to be closely linked with both chronotype and cancer risk, there was inconsistent evidence for the role of testosterone in mediating the effect of morning preference chronotype on both breast and prostate cancer. Findings regarding the potential protective effect of chronotype on both breast and prostate cancer risk are clinically interesting. However, this may not serve as a direct target for intervention, since it is difficult to modify someone's morning/evening preference. Given this, further studies are needed to investigate the mechanisms underlying this effect and to identify other potential modifiable intermediates.


2021 ◽  
Vol 9 (Suppl 3) ◽  
pp. A562-A562
Author(s):  
Ira Winer ◽  
Akhila Wimalasingham ◽  
Joaquina Baranda ◽  
Armando Santoro ◽  
Kristen Spencer ◽  
...  

BackgroundCabozantinib, a multiple receptor tyrosine kinase inhibitor, promotes an immune-permissive environment which might enhance the activity of immune checkpoint inhibitors. COSMIC-021 (NCT03170960), a multicenter phase 1b study, is evaluating the combination of cabozantinib with atezolizumab in advanced solid tumors; here we present efficacy and safety results in patients with triple negative breast cancer (TNBC), ovarian cancer (OC), and endometrial cancer (EC).MethodsEligible patients had locally advanced or metastatic TNBC, OC, or EC and had radiographically progressed on prior systemic anticancer therapy. One or two lines of prior therapy were permitted. Patients with OC were platinum resistant or refractory. Prior treatment with anti-PD-1 or anti-PD-L1 agents was allowed for patients with TNBC. Patients received cabozantinib, 40 mg PO QD, plus atezolizumab, 1200 mg IV Q3W. The primary endpoint was objective response rate (ORR) per RECIST 1.1 as assessed by investigator. Other endpoints included safety, duration of response (DOR), progression free survival (PFS), and overall survival (OS). CT/MRI scans were performed Q6W for the first year and Q12W thereafter.ResultsAs of February 19, 2021, 30–32 patients were enrolled in each of the cohorts. 47% of patients with TNBC, 47% with OC, and 40% with EC had received 2 lines of prior therapy. Median follow-up was 18.7 months, 20.8 months, and 19.0 months for the TNBC, OC, and EC cohorts, respectively. Grade 3/4 treatment-related adverse events occurred in 33% of patients with TNBC, 56% with OC, and 37% with EC. One Grade 5 treatment-related adverse event of pulmonary hemorrhage occurred in the TNBC cohort and one of encephalitis occurred in the OC cohort. Cabozantinib plus atezolizumab demonstrated clinical activity in all three tumor cohorts (table 1).Abstract 531 Table 1ConclusionsCabozantinib in combination with atezolizumab demonstrated encouraging clinical activity in patients with previously treated advanced cancers.AcknowledgementsMedical writing support provided by Suvajit Sen, PhD (Exelixis, Inc.)Trial RegistrationNCT03170960Ethics ApprovalYesConsentYes


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