{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T17:48:12Z","timestamp":1790790492759,"version":"4.1.0"},"reference-count":108,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T00:00:00Z","timestamp":1788307200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Oncol. Rev."],"abstract":"<jats:p>\n                    Primary lung adenocarcinoma is the most common histological subtype of lung cancer. It disproportionately affects female sex, especially never-smokers. The rising incidence among females without a smoking history suggests roles for hormonal, genetic, and environmental factors. We conducted a comprehensive literature review using several databases. We examined global epidemiology data, molecular mechanisms, hormone-related pathways, and new diagnostic and therapeutic approaches. The findings show that estrogen signaling, especially via estrogen receptor beta (ER\u03b2), contributes to oncogenesis. The mechanism involves cross-talk with\n                    <jats:italic>EGFR<\/jats:italic>\n                    and downstream MAPK\/PI3K pathways.\n                    <jats:italic>EGFR<\/jats:italic>\n                    mutations appear more frequently in females. The association between KRAS and other cell cycle drivers is mixed across studies. Non-tobacco exposures, including air pollution and secondhand smoke, further increase risk among females. Diagnostic disparities persist because current screening guidelines focus on smoking. This approach excludes many high-risk never-smoking females. This review aims to narrate and synthesize growing evidence highlighting how female sex is associated with a distinct epidemiological footprint, unique molecular and biological profiles, and tailored therapeutic strategies in lung adenocarcinoma, driven by mechanisms beyond traditional tobacco exposure. Incorporating sex-specific risk assessment, hormonal level modification, and targeted gene therapies into clinical practice may improve screening and outcomes for females with lung adenocarcinoma.\n                  <\/jats:p>","DOI":"10.3389\/or.2026.1813124","type":"journal-article","created":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T07:46:25Z","timestamp":1788335185000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Beyond tobacco: understanding the growing burden of lung adenocarcinoma in women"],"prefix":"10.3389","volume":"20","author":[{"given":"Michael Christian A.","family":"Virata","sequence":"first","affiliation":[{"name":"Department of Pathology, Molecular and Cell-Based Medicine, Icahn School of Medicine at Mount Sinai","place":["New York, NY, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rizal Michael 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