Parity and Pancreatic Cancer Risk: A Dose-Response Meta-Analysis of Epidemiologic Studies

Guan, Hongyan; Wu, Lang; Wu, Qi‐Jun; Zhu, Jingjing; Gong, Ting-Ting

doi:10.1371/journal.pone.0092738

Cited by 37 publications

(35 citation statements)

References 56 publications

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“…Data extracted from each study included: the first author's last name, year of publication, study region, study design, characteristics of study population (sample size, age, length of follow‐up, measures and numbers of parity, and effect sizes). If multiple estimates of the association for the same outcome were reported, we extracted the estimate that adjusted for the most appropriate covariates, like previous studies . In cases when only unadjusted estimates were presented, we included the crude estimates.…”

Section: Methodsmentioning

confidence: 99%

Parity and thyroid cancer risk: a meta‐analysis of epidemiological studies

Zhu

et al. 2015

Cancer Medicine

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Although observational studies have assessed the relationship between parity and thyroid cancer risk, the findings are inconsistent. To quantitatively assess the association, we conducted a systematic review and meta‐analysis. PubMed and Embase were searched up to January 2015. Prospective or case–control studies that evaluated the association between parity and thyroid cancer risk were included. We used the fixed‐effects model to pool risk estimates. After literature search, 10 prospective studies, 12 case‐control studies and 1 pooled analysis of 14 case‐control studies including 8860 patients were identified. The studies had fair methodological quality. Pooled analysis suggested that there was a significant association between parity and risk of thyroid cancer (RR for parous versus nulliparous: 1.09, 95% CI 1.03‐1.15; I2=33.4%). The positive association persisted in almost all strata of subgroup analyses based on study design, location, study quality, type of controls, and confounder adjustment, although in some strata statistical significance was not detected. By evaluating the number of parity, we identified that both parity number of 2 versus nulliparous and parity number of 3 versus nulliparous demonstrated significant positive associations (RR=1.11, 95% CI 1.01‐1.22; I2=31.1% and RR=1.16, 95% CI 1.01‐1.33; I2=19.6% respectively). The dose‐response analysis suggested neither a non‐linear nor linear relationship between the number of parity and thyroid cancer risk. In conclusion, this meta‐analysis suggests a potential association between parity and risk of thyroid cancer in females. However, the lack of detection of a dose‐response relationship suggests that further studies are needed to better understand the relationship.

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Section: Methodsmentioning

confidence: 99%

Parity and thyroid cancer risk: a meta‐analysis of epidemiological studies

Zhu

et al. 2015

Cancer Medicine

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“…Motivated by these observations, and under the hypothesis that greater exposure to female sex hormones (through early menarche, later menopause, high number of pregnancies, and having a history of hormone use) decreases the risk of PC, several epidemiological studies have examined possible risk associations with menstrual and reproductive factors, and hormone use, but with inconsistent results. A review paper on reproductive factors and PC 13 , two meta-analyses on parity 14,15 , and a recent meta-analysis 16 attempted to make clear the relations between these factors and PC risk. Comparing and summarizing previous evidence, however, is not a simple task.…”

Section: Introductionmentioning

confidence: 99%

Menstrual and Reproductive Factors, Hormone Use, and Risk of Pancreatic Cancer

et al. 2016

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Objectives We aimed to evaluate the relation between menstrual and reproductive factors, exogenous hormones, and risk of pancreatic cancer (PC). Methods Eleven case-control studies within the International Pancreatic Cancer Case-Control Consortium (PanC4) took part in the present study, including in total 2,838 case and 4,748 control women. Pooled estimates of odds ratios (ORs) and their 95% confidence intervals (CIs) were calculated using a two-step logistic regression model and adjusting for relevant covariates. Results An inverse OR was observed in women who reported having had hysterectomy (ORyesvs.no 0.78, 95%CI 0.67–0.91), remaining significant in post-menopausal women and never-smoking women, adjusted for potential PC confounders. A mutually-adjusted model with the joint effect for hormone replace therapy (HRT) and hysterectomy showed significant inverse associations with PC in women who reported having had hysterectomy with HRT use (OR 0.64, 95%CI 0.48–0.84). Conclusion Our large pooled analysis suggests that women who have had a hysterectomy may have reduced risk of PC. However, we cannot rule out that the reduced risk could be due to factors or indications for having had a hysterectomy. Further investigation of risk according to HRT use and reason for hysterectomy may be necessary.

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“…Estradiol activation of ERs inhibits apoptotic death of β cells in case of inflammatory insult [77]. Estradiol promotes β cell recovery after pancreatic injury [80]. In rodent models of type 2 diabetes, estrogen treatment reduced lipid synthesis and prevented β cell failure in pancreatic islets [79].…”

Section: Pancreasmentioning

confidence: 99%

“…In rodent models of type 2 diabetes, estrogen treatment reduced lipid synthesis and prevented β cell failure in pancreatic islets [79]. Correlations between parity and pancreatic cancer risk were studied in a meta-analysis of epidemiologic studies and the findings suggest that higher parity is associated with a decreased risk of pancreatic cancer [80].…”

Section: Pancreasmentioning

confidence: 99%

Crossroad between Obesity and Cancer: A Defective Signaling Function of Heavily Lipid-Laden Adipocytes

Suba¹

2020

Understanding the Molecular Crosstalk in Biological Processes

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Obesity and its comorbidities exhibit a gender-related dimorphism. Obese males tend to accrue more visceral fat leading to abdominal adiposity, which shows a strong correlation with serious obesity-associated comorbidities, cardiovascular diseases and cancers. In contrast, obese females accumulate excessive fatty tissue predominantly subcutaneously enjoying strong protection from the obesity-related diseases. The health advantage of obese women as compared with obese men may be attributed to their higher estrogen production and an increased transactivation of estrogen receptors (ERs). The recently clarified intracrine, paracrine, and endocrine functions of adipose tissue illuminate that concentrations of estrogens and the suitable expression and activity of ERs strongly define all regulatory functions in both men and women. All well-known cancer risk factors are in correlation with defects of estrogen signaling in partnership with glucose intolerance as estrogen regulates all steps of glucose uptake. In central obesity, increased secretions of cytokines and growth factors are not causal factors of developing insulin resistance, and unrestrained cell proliferation, but rather, they are compensatory processes so as to increase estrogen synthesis and ER transactivation. In conclusion, a causal therapy against obesity and obesity-related diseases aims to improve estrogen signaling in both men and women.

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Parity and Pancreatic Cancer Risk: A Dose-Response Meta-Analysis of Epidemiologic Studies

Cited by 37 publications

References 56 publications

Parity and thyroid cancer risk: a meta‐analysis of epidemiological studies

Parity and thyroid cancer risk: a meta‐analysis of epidemiological studies

Menstrual and Reproductive Factors, Hormone Use, and Risk of Pancreatic Cancer

Crossroad between Obesity and Cancer: A Defective Signaling Function of Heavily Lipid-Laden Adipocytes

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