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Related Experiment Video

Updated: Jul 16, 2026

Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants

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Published on: March 6, 2018

Endocrine Disruptors and Gynecological Malignancies.

Dimitris Baroutis¹, Eleni Katsianou², Konstantinos Koukoumpanis¹

¹1st Department of Obstetrics and Gynecology, Alexandra Hospital, National and Kapodistrian University of Athens, 11528 Athens, Greece.

Diagnostics (Basel, Switzerland)

|July 15, 2026

Summary

Endocrine-disrupting chemicals (EDCs) are linked to gynecological cancers like breast and endometrial cancer. Reducing EDC exposure, especially during development, is crucial for prevention and early detection strategies.

Keywords:

biomarkers bisphenol A breast cancer endocrine disruptors endometrial cancer environmental carcinogens gynecological malignancies ovarian cancer phthalates risk stratification

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Published on: April 26, 2018

Area of Science:

Environmental Health
Gynecologic Oncology
Toxicology

Background:

Endocrine-disrupting chemicals (EDCs) disrupt hormonal balance, contributing to gynecological malignancies.
Evidence links EDC exposure to breast, endometrial, ovarian, and cervical cancers.

Purpose of the Study:

Synthesize current evidence on EDC exposure and gynecological cancers.
Examine molecular mechanisms, epidemiology, and clinical implications.
Assess diagnostic and prevention strategies.

Main Methods:

Comprehensive literature review across major databases (PubMed, Embase, Scopus, Cochrane).
Inclusion of systematic reviews, meta-analyses, cohort, and case-control studies.
Quality appraisal using Newcastle-Ottawa Scale, AMSTAR-2, and GRADE framework.

Main Results:

Major EDCs (bisphenols, phthalates, PCBs, pesticides, PFAS) show carcinogenic potential via hormonal and epigenetic pathways.
Strongest evidence links DDT/DDE to increased breast cancer risk (up to 3.7-fold).
Endometrial cancer associated with xenoestrogen mixtures; ovarian and cervical cancers show emerging links.

Conclusions:

EDCs contribute to gynecological cancers through convergent molecular pathways.
Causal inference is limited by observational data and exposure complexity.
Integrate EDC risk into models, use multi-omics biomarkers, and prioritize exposure reduction.