# Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) and Risk of Gynecologic Cancer: A Nationwide Cohort Study

**Authors:** Min Jin Jeong, Yong Seok Lee, Youn Jin Choi, Kyung Do Han

PMC · DOI: 10.3390/cancers18060894 · 2026-03-10

## TL;DR

This study shows that liver disease linked to metabolic issues increases the risk of gynecologic cancers in women, regardless of menopause status.

## Contribution

The study is the first to demonstrate a nationwide association between MASLD and gynecologic cancers in a large Korean cohort.

## Key findings

- MASLD increases the risk of cervical, endometrial, and ovarian cancers in premenopausal women.
- MASLD similarly elevates the risk of these cancers in postmenopausal women.
- MASLD is identified as a modifiable risk factor for gynecologic malignancies.

## Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a systemic condition that influences cancer development beyond the liver. While its impact on various metabolic disorders is well-documented, the specific relationship between MASLD and gynecologic cancers has not been fully explored in large-scale populations. In this study, we demonstrated that MASLD significantly increases the risk of cervical, endometrial, and ovarian cancers regardless of menopausal status, using a comprehensive nationwide database of over 2 million individuals. Our findings suggest that MASLD serves as a critical, modifiable risk factor for gynecologic malignancies. Consequently, integrating liver health assessments into routine gynecologic cancer screening could provide a proactive strategy for early prevention and risk management in women with metabolic dysfunction.

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is now widely identified as a multisystem disorder with oncogenic implications that extend beyond liver-specific outcomes. Nonetheless, the link between MASLD and gynecologic cancers remains insufficiently characterized in robust, well-powered population studies. We investigated this association by menopausal status in a large cohort of Korean women. Methods: We performed a longitudinal cohort study utilizing data from a nationwide Korean cohort of over 2 million women, with a median observation period of 12.3 years. MASLD, including its subtypes metabolic alcohol-associated liver disease (MetALD), and alcohol-related liver disease (ALD) with metabolic dysfunction were identified using the most recent diagnostic standards. Adjusted hazard ratios (aHR) for gynecologic cancers were estimated with Cox models, accounting for metabolic, reproductive, and lifestyle factors. Results: In premenopausal women, MASLD was associated with increased risks of cervical (aHR, 1.13, 95% CI, 1.01–1.26), endometrial (aHR, 1.63, 95% CI, 1.50–1.79) and ovarian cancer (aHR, 1.22, 95% CI, 1.12–1.33). In postmenopausal women, MASLD similarly conferred elevated risks across all three cancers: cervical (aHR, 1.12, 95% CI, 1.05–1.20), endometrial (aHR, 1.42, 95% CI, 1.32–1.54) and ovarian cancer (aHR, 1.14, 95% CI, 1.08–1.20). Conclusions: MASLD should be considered an independent and modifiable risk determinant for gynecologic cancers. These data underscore the necessity of including hepatic steatosis in risk assessment protocols for cancer prevention. Early recognition and directed screening among metabolically susceptible women may provide important avenues for proactive cancer risk reduction.

## Linked entities

- **Diseases:** Metabolic dysfunction-associated steatotic liver disease (MONDO:0013209), MASLD (MONDO:0013209), cervical cancer (MONDO:0002974), endometrial cancer (MONDO:0002447), ovarian cancer (MONDO:0005140)

## Full-text entities

- **Diseases:** metabolic dysfunction (MESH:D008659), cervical (MESH:D002575), ALD (MESH:D008108), Gynecologic Cancer (MESH:D009369), endometrial (MESH:D014591), MASLD (MESH:D008107), ovarian cancer (MESH:D010051), hepatic steatosis (MESH:D005234)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13025304/full.md

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Source: https://tomesphere.com/paper/PMC13025304