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Life sciences · Journal article
BMC Cancer · September 12, 2026
Reinforces what was already believed, rather than introducing something new.
This meta-analysis of 27 observational studies found no significant association between oral contraceptive use, menopausal hormone therapy, or estrogen therapy with pancreatic cancer risk in adjusted analyses. The evidence quality was rated very-low to low by GRADE criteria, and wide prediction intervals suggest heterogeneity across populations; a modest inverse association with estrogen–progestin therapy was noted but relies on low-certainty evidence from only 5 studies.
Systematic review and random-effects meta-analysis of observational studies. Women with hormone use (oral contraceptives, menopausal hormone therapy, estrogen therapy, or estrogen–progestin therapy) from observational studies reporting association with pancreatic cancer.. Intervention: Oral contraceptive pills (OCP) use, menopausal hormone therapy (MHT), estrogen therapy (ET), or estrogen–progestin therapy (EPT). Compared with: Non-use of the respective hormone therapies.
OCP use: RR = 0.99 (95% CI: 0.86–1.14) in 20 studies; very-low-certainty evidence MHT use: RR = 0.92 (95% CI: 0.79–1.06) in 18 studies; very-low-certainty evidence ET use: RR = 0.82 (95% CI: 0.63–1.07) in 6 studies; very-low-certainty evidence
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
Clinicians can reassure patients that use of oral contraceptives, menopausal hormone therapy, or estrogen therapy is not associated with increased pancreatic cancer risk based on current observational evidence, though the evidence quality is very-low to low. The modest inverse association with estrogen–progestin therapy should not yet guide clinical practice given limited and low-certainty evidence.
A rigorous systematic review and meta-analysis of 27 observational studies that confirms the absence of a clinically meaningful association between oral contraceptives and menopausal hormone therapy with pancreatic cancer risk, with very-low to low certainty evidence.
As stated by the source record.
Quoted from the source exactly as published.
Clinicians can reassure patients that use of oral contraceptives, menopausal hormone therapy, or estrogen therapy is not associated with increased pancreatic cancer risk based on current observational evidence, though the evidence quality is very-low to low. The modest inverse association with estrogen–progestin therapy should not yet guide clinical practice given limited and low-certainty evidence.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Pancreatic cancer has a poor prognosis, and hormonal factors have been proposed as potential modifiers of risk. However, the association between exogenous female hormone use and pancreatic cancer remains uncertain. We conducted a comprehensive systematic review and meta-analysis to evaluate the relationship between menopausal hormone therapy (MHT), estrogen therapy (ET), estrogen–progestin therapy (EPT), and oral contraceptive pills (OCPs) use and pancreatic cancer risk. We systematically searched PubMed, Scopus, and Embase for observational studies up to July 2026. Random-effects meta-analyses of adjusted and crude effect estimates were performed to estimate pooled relative risks (RRs) for adjusted analyses and ORs for crude analyses. Linear and non-linear dose–response meta-analyses were performed. Heterogeneity was assessed using the I 2 statistic, and publication bias was evaluated using Egger’s and Begg’s tests. Study quality was assessed using the Newcastle–Ottawa Scale, and certainty of evidence was evaluated using GRADE. Twenty-seven reports were included in the review. In the adjusted analyses, neither OCPs use (20 studies; RR = 0.99, 95% CI: 0.86–1.14; 95% prediction interval (PI): 0.62–1.59; I 2 = 61.4%; very-low-certainty evidence) nor MHT use (18 studies; RR = 0.92, 95% CI: 0.79–1.06; 95% PI: 0.54–1.56; I 2 = 75.9%; very-low-certainty evidence) was significantly associated with pancreatic cancer risk. ET use was also not significantly associated with risk (6 studies; RR = 0.82, 95% CI: 0.63–1.07; 95% PI: 0.54–1.26; I 2 = 41.9%; very-low-certainty evidence). In contrast, EPT use was associated with a modest inverse association (5 studies; RR = 0.85, 95% CI: 0.78–0.93; 95% PI: 0.77–0.94; I 2 = 0%; low-certainty evidence). In secondary crude analyses, lower odds of pancreatic cancer were observed for OCP use (OR = 0.70, 95% CI: 0.61–0.81; 95% PI: 0.42–1.17) and EPT use (OR = 0.55, 95% CI: 0.34–0.91; 95% PI: 0.16–1.97); however, both analyses showed substantial heterogeneity. Dose–response analyses showed no significant association per 5-year increase in OCP use (RR = 1.07, 95% CI: 0.98–1.17; p = 0.158) or MHT use (RR = 0.84, 95% CI: 0.67–1.05; p = 0.128), and no significant non-linear associations were identified. Adjusted evidence did not show a consistent association between OCP, MHT, or ET use and pancreatic cancer risk. Although EPT use was associated with a modest inverse association, this finding was based on low-certainty observational evidence. Wide prediction intervals for OCP and MHT indicate that associations may vary across populations and settings. Further large prospective studies are warranted to clarify long-term hormonal effects on pancreatic carcinogenesis.
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