Uterus

The uterus is a hollow smooth-muscle organ whose inner mucosal lining — the endometrium — undergoes one of the most dramatic regenerative cycles in human biology. In reproductive-age women, the endometrium grows, differentiates, and sheds roughly 400–500 times across a lifetime, reconstituting the full-thickness functional layer from a thin residual basalis within 4–10 days each cycle ¹. This extraordinary regenerative capacity is sustained by a rare population of endometrial stem and progenitor cells in the basalis layer, making the uterus a compelling model for studying adult tissue regeneration and its failure with age.

After menopause, the twin drivers of endometrial biology — estrogen and progesterone — are withdrawn. The endometrium atrophies, the myometrium loses smooth-muscle tone, and the steroid-dependent pathologies that characterize reproductive life (fibroids, cyclical dysfunction) resolve. A new set of pathological risks emerges in their place: endometrial atrophy, postmenopausal bleeding, and most importantly endometrial cancer, the most common gynecologic malignancy in high-income countries and a disease whose incidence is rising with obesity rates.

Anatomy at a glance

Compartment	Major cell types	Primary function	Aging-relevant change
Endometrium — functionalis	Luminal + glandular epithelial cells, stromal fibroblasts	Implantation; shed at menstruation	Lost post-menopause; atrophic epithelium
Endometrium — basalis	Epithelial progenitors, perivascular mesenchymal stem cells (SUSD2+/CD146+PDGFR-β+)	Regenerative reserve; reconstitutes functionalis each cycle	Persists post-menopause but quiescent; regeneration potential declines
Myometrium	Uterine smooth-muscle cells (uSMCs), interstitial cells	Contractility (labor, menstruation)	Fibrosis; leiomyoma formation and involution
Serosa / perimetrium	Mesothelial cells, sub-serosal connective tissue	Protective outer layer	Largely stable with age

The endometrial stem cell: biology of cyclical regeneration

Clonogenic progenitors in the basalis

Gargett and colleagues established that the endometrium harbors a rare population of clonogenic epithelial and stromal stem/progenitor cells concentrated in the basalis — the layer that survives shedding ²¹. Quantitative clonal analysis showed that only ~0.09% of epithelial cells and ~0.02% of stromal cells initiate large clones, consistent with the rarity expected of true tissue stem cells ².

Stromal stem/progenitor cells in the basalis are marked by the pericyte-identity surface phenotype CD146(+)/PDGFR-β(+) and, more specifically in menstrual blood-accessible populations, SUSD2(+) (sushi domain-containing protein 2). These perivascular endometrial mesenchymal stem/stromal cells (eMSCs) fulfill International Society for Cellular Therapy multipotency criteria and can reconstitute endometrial stroma in xenograft models ³. Epithelial progenitors express N-cadherin and are detectable in menstrual effluent — demonstrating that shed cells include a stem-like subpopulation, not merely terminally differentiated material ⁴.

Hypoxia-Notch axis in stem cell maintenance

The eMSC niche is hypoxic. Zhang et al. 2022 showed that hypoxia activates HIF-1α → Notch signaling in SUSD2(+) label-retaining stromal cells during endometrial breakdown and early repair, enhancing self-renewal and clonogenicity ⁵. This positions the basalis perivascular niche as functionally analogous to the hypoxic bone marrow HSC niche — a recurrent motif in adult stem cell biology.

Postmenopausal fate of endometrial progenitors

Post-menopause, estrogen and progesterone withdrawal silences the cyclical proliferative drive. The endometrium atrophies to a thin, inactive epithelium (typically ≤4 mm on transvaginal ultrasound). Whether the stem/progenitor compartment is lost, persists quiescent, or becomes epigenetically reprogrammed is not fully characterized ⁶. Perimenopausal endometrial stromal fibroblasts show a distinct transcriptome relative to premenopausal counterparts, with dysregulation of cytoskeletal, proliferative, and survival pathways, while eMSCs retain relatively similar signatures — consistent with the interpretation that the stromal mesenchymal stem pool is more resilient to hormonal withdrawal than the differentiated stroma ⁶. needs-human-replication

Dimension	Status
Stem cell pool conserved post-menopause?	partial — eMSCs persist but proliferative drive withdrawn; long-term pool fate unstudied
Regeneration capacity retained?	no (physiological cycling ceases); pharmacological restoration (local estrogen) re-establishes limited proliferative response
Replicated mechanistically in humans?	partial — clonogenic characterization confirmed in humans; postmenopausal niche not prospectively studied

Postmenopausal endometrial atrophy

Following the final menstrual period, circulating estradiol falls to <20 pg/mL (premenopausal follicular phase: 30–400 pg/mL). The endometrium undergoes progressive atrophy: glandular epithelium becomes cuboidal to flattened, glands are sparse and inactive, stroma becomes fibrous, and the endometrium thins to typically 1–3 mm. Atrophic endometrium is the most common cause of postmenopausal bleeding, accounting for approximately 60–80% of cases.

Paradoxically, although atrophy is the dominant state, even trace estrogen exposure — from peripheral aromatization or exogenous sources — can stimulate the atrophic epithelium disproportionately. This underlies the clinical imperative to investigate any postmenopausal bleeding even when the endometrium appears thin on ultrasound, because a thin atrophic endometrium and an early neoplastic endometrium can coexist in different uterine regions.

The downstream experience of urogenital atrophy is captured in the related phenotype genitourinary-syndrome-menopause, which encompasses atrophic changes in the vagina, vestibule, and lower urinary tract alongside the endometrial changes discussed here.

Uterine fibroids (leiomyoma)

Epidemiology and natural history

Uterine leiomyomas are benign monoclonal tumors of myometrial smooth-muscle origin and represent the most common solid tumor in women. By age 50, cumulative incidence is estimated at ~70% in White women and ~80% in Black women (by ultrasound diagnosis). The majority are asymptomatic; clinically significant fibroids affect ~25% of reproductive-age women, causing heavy menstrual bleeding, bulk symptoms, and infertility.

A defining feature of fibroids relevant to aging: they are strictly dependent on ovarian steroids. Fibroids invariably shrink after menopause, and postmenopausal growth of a known fibroid should raise concern for leiomyosarcoma rather than benign fibroid growth ⁷.

Pathogenesis: estrogen, progesterone, and ECM

The fundamental growth stimulus for fibroids involves both estrogen and progesterone acting in concert ⁷⁸:

Estradiol upregulates progesterone receptor (PR) expression in leiomyoma cells, amplifying the proliferative response to progesterone.
Progesterone/PR signaling is the dominant mitogenic stimulus: progesterone induces mature leiomyoma cells to release paracrine growth factors (EGF, IGF-1, TGF-β) that drive smooth-muscle proliferation. Clinical evidence: GnRH agonists that suppress both steroids shrink fibroids by 35–65% over 3 months; adding back progesterone attenuates shrinkage.
Extracellular matrix (ECM) accumulation is a hallmark structural feature: fibroids contain 3–5× more collagen, fibronectin, and laminin than normal myometrium. TGF-β and activin-A, both upregulated by progesterone signaling, drive this fibrosis ⁹. The ECM itself likely has a biomechanical role in tumor stiffness and growth.

A stem/progenitor cell origin hypothesis has gained evidence: leiomyoma-initiating cells express CD44, lack estrogen receptor, and are driven to clonal expansion by somatic mutations (most commonly in MED12 exon 2, found in ~70% of fibroids; or HMGA2 overexpression in a minority) before differentiating into the bulk hormone-responsive leiomyoma mass ⁷.

Clinical management and aging context

GnRH agonists (leuprolide) and GnRH antagonists with “add-back” hormone therapy (relugolix + estradiol + norethindrone acetate) achieve substantial bleeding reduction in pre-menopausal women ¹⁰. Menopause achieves the same endpoint naturally. From an aging perspective, fibroids exemplify a class of steroid-dependent pathology that resolves with the hormonal collapse of menopause — the same withdrawal that drives endometrial atrophy.

Endometrial cancer

Epidemiology and framing

Endometrial cancer (uterine corpus endometrial carcinoma, UCEC) is the most common gynecologic cancer in high-income countries, with ~66,000 new cases estimated annually in the United States. It is predominantly a postmenopausal disease (median age at diagnosis ~63 years) and predominantly estrogen-driven (Type I, endometrioid histology, ~80% of cases).

Incidence has been rising, driven principally by the obesity epidemic. This rise is not a mystery of biology — it is a quantitatively predictable consequence of the peripheral aromatization axis: adipose tissue expresses cyp19a1 (aromatase), which converts adrenal androgens (androstenedione, DHEA) to estrogens (estrone, estradiol) without a proportional rise in progesterone. In postmenopausal women without an intact ovarian cycle, this peripheral production creates unopposed estrogen exposure to the endometrium — the central pathogenic mechanism for Type I endometrial cancer.

The obesity-aromatase-estrogen axis

Adipose tissue aromatase activity is the dominant source of circulating estrogens in postmenopausal women. Simpson et al. 2003 established that local estrogen concentrations in adipose-rich tissues can reach levels an order of magnitude higher than circulating levels — relevant to local endometrial exposure ¹¹. Obesity upregulates CYP19A1 expression in adipose tissue via inflammatory mediators (IL-6, TNF-α, PGE2), linking adipose dysfunction directly to elevated estrogen production ¹².

Quantitative evidence from the Women’s Health Initiative:

Serum unconjugated estradiol showed the strongest association with endometrial cancer among all estrogen metabolites tested: OR 6.19 (95% CI 2.95–13.03, fifth vs first quintile, p=0.0001) in postmenopausal women in the WHI nested case-control study ¹³. Note: a 2025 meta-analysis of 16 studies (Zhu et al., PMID 40300286; n=292,695) found a pooled OR of 2.14 for unconjugated estradiol — the WHI estimate may reflect superior assay sensitivity (HPLC/MS-MS) or study-specific characteristics; both are significant and directionally consistent.
Adiposity-mediated endometrial cancer risk operates partly through estradiol but also through leptin, insulin, and C-reactive protein (CRP) pathways — the obesity-cancer link is multi-mediated, not purely estrogenic ¹⁴.
Bariatric surgery (weight loss) reduces endometrial cancer risk with RR 0.38 (95% CI 0.26–0.55) in a systematic review and meta-analysis of 32 studies — confirming that the adiposity-driven risk is reversible ¹⁵.

Tamoxifen and SERM uterine agonism

selective-estrogen-receptor-modulators (SERMs) illustrate the tissue-specificity of estrogen signaling in the uterus. Tamoxifen, used as adjuvant therapy in ER+ breast cancer, acts as an estrogen receptor antagonist in breast tissue but as a partial agonist in the endometrium via ESR1 esr1. Long-term tamoxifen use (>5 years) in postmenopausal women is associated with a 2–3-fold increase in endometrial cancer risk compared to non-users; this risk is not observed in premenopausal users, consistent with a modulating effect of background estrogen on endometrial sensitivity ¹⁶. Endometrial polyps, hyperplasia, and uterine enlargement are also tamoxifen-associated effects. This tissue-specific partial agonism reflects the coactivator environment of uterine endometrium (high SRC-3/AIB1 expression) contrasting with the breast corepressor environment on which tamoxifen’s antagonism depends.

The newer SERM bazedoxifene (combined with conjugated estrogens in the “TSEC” combination) avoids endometrial stimulation through antagonist activity in the uterus while preserving estrogenic effects on bone and vasomotor symptoms — demonstrating that SERM uterine selectivity is pharmacologically tractable.

Type I vs Type II endometrial cancer in the aging context

Feature	Type I (endometrioid)	Type II (serous, clear cell, carcinosarcoma)
Frequency	~80%	~20%
Estrogen-driven	yes — unopposed estrogen via obesity, anovulation, exogenous use	no — arises on atrophic endometrium
Precursor lesion	endometrial hyperplasia / EIN	serous endometrial intraepithelial carcinoma (SEIC)
Key mutations	PTEN, KRAS, microsatellite instability, CTNNB1	TP53, HER2, CCNE1
Prognosis	generally favorable (70–80% Stage I)	aggressive; often advanced at diagnosis
Aging pattern	obesity + postmenopausal estrogen excess	primarily older postmenopausal women; risk not estrogen-dependent

Type II tumors arise de novo on an atrophic endometrial background — not via hyperplasia — and are associated with aging hallmarks beyond estrogen excess: genomic-instability (TP53 mutation in ~90%), cellular-senescence escape, and a generally worse prognosis because of late presentation and aggressive biology.

Hallmark connections

Hallmark	Uterine mechanism
stem-cell-exhaustion	Endometrial basalis eMSC pool is the regenerative substrate for cyclical repair; post-menopausal arrest of the cycle represents functional exhaustion of the hormonal drive rather than loss of the pool per se, but the pool’s postmenopausal fate is incompletely characterized
altered-intercellular-communication	Hormonal signaling (estrogen/progesterone paracrine axes between stroma and epithelium) is the dominant intercellular communication system in the endometrium; menopause disrupts this bidirectional crosstalk; adipokine + inflammatory cytokine signaling from dysfunctional adipose tissue substitutes peripherally and drives malignant transformation
cellular-senescence	Senescent cells accumulate in aging myometrium and stromal fibroblasts; SASP contributes to fibroid ECM accumulation and to postmenopausal endometrial inflammatory tone
chronic-inflammation	Menopausal hormonal shift increases systemic inflammatory tone; local endometrial macrophage activation shifts toward an M1 phenotype; relevant to atrophic symptoms, cancer risk, and fibroid biology
genomic-instability	Somatic MED12 mutations drive clonal fibroid initiation; TP53 and microsatellite instability are Type II and Type I endometrial cancer drivers respectively; aging accumulates somatic mutation burden in endometrial tissue even without cyclical selection

Limitations and gaps

#gap/needs-human-replication — The long-term fate of endometrial eMSCs post-menopause has not been prospectively characterized in humans; it is unknown whether the pool depletes, enters deep quiescence, or undergoes epigenetic silencing.
#gap/no-mechanism — The mechanism by which perimenopausal endometrial stromal fibroblasts acquire a distinct transcriptome (dysregulated cytoskeletal/proliferative pathways per Erikson 2017) while eMSC signatures remain relatively stable is not established.
#gap/needs-replication — The quantitative contribution of local vs circulating aromatase-derived estrogen to postmenopausal endometrial cancer risk is not fully decomposed; mediation analyses (e.g., Dashti 2022) provide structural estimates but cannot distinguish local vs systemic estrogen fractions.
#gap/long-term-unknown — The safety profile of long-term local low-dose vaginal estrogen therapy in women with prior endometrial cancer or hyperplasia; current evidence is limited by short follow-up in randomized trials.
#stub — Cell-type pages endometrial-epithelial-cells, endometrial-stromal-cells, endometrial-mesenchymal-stem-cells, uterine-smooth-muscle-cells are implicit stubs; primary mechanistic claims should ultimately be delegated to those atomic pages.
#stub — leiomyoma as a distinct phenotype page does not yet exist; current coverage is embedded here. A dedicated phenotype page would allow richer Dataview querying by phenotype.

Cross-references

ovary — the steroid-producing organ whose endocrine output governs the entire uterine lifecycle; follicle pool depletion drives the menopause cascade that produces endometrial atrophy
menopause — the phenotype of ovarian follicle exhaustion; the hormonal context for postmenopausal endometrial pathology
genitourinary-syndrome-menopause — the broader atrophic phenotype encompassing vaginal, vestibular, and lower urinary tract changes alongside endometrial atrophy
estradiol — primary ovarian estrogen; the principal driver of endometrial proliferation; peripheral adipose aromatization remains the dominant postmenopausal source
progesterone — the anti-proliferative, differentiation-promoting counterweight in the endometrium; its withdrawal is the immediate trigger of menstruation and the long-term basis for postmenopausal atrophy; co-driver (with estradiol) of fibroid growth
esr1 — estrogen receptor alpha; mediates estrogen’s endometrial proliferative effects; the target through which tamoxifen exerts its paradoxical uterine agonism
cyp19a1 — aromatase enzyme; peripheral expression in adipose tissue produces the unopposed estrogen that drives Type I endometrial cancer in postmenopausal women
selective-estrogen-receptor-modulators — SERM class page; tamoxifen’s uterine agonism and bazedoxifene’s uterine antagonism illustrate tissue-selective ER pharmacology
reproductive-system — parent organ-system MOC
stem-cell-exhaustion — hallmark; endometrial eMSC pool as regenerative substrate
altered-intercellular-communication — hallmark; estrogen/progesterone paracrine axis disruption at menopause
cellular-senescence — hallmark; myometrial and stromal senescence + SASP
chronic-inflammation — hallmark; inflammaging in postmenopausal uterine tissue
genomic-instability — hallmark; somatic mutation accumulation driving fibroid and cancer initiation

Footnotes

doi:10.1093/humupd/dmv051 · Gargett CE, Schwab KE, Deane JA · “Endometrial stem/progenitor cells: the first 10 years” · Human Reproduction Update 22(2):137–163 · 2016 · review · key finding: CD146(+)/PDGFR-β(+) and SUSD2(+) perivascular cells are the best-characterized eMSC populations; side-population cells reconstitute endometrium in xenograft; menstrual-blood eMSCs accessible non-invasively · archive: pending (OA not confirmed) ↩ ↩²
doi:10.1111/j.1479-828X.2006.00582.x · Gargett CE · “Identification and characterisation of human endometrial stem/progenitor cells” · Australian & New Zealand Journal of Obstetrics & Gynaecology 46(3):250–253 · 2006 · in-vitro (clonal analysis, human endometrial biopsy) · key finding: ~0.09% of epithelial and ~0.02% of stromal cells clonogenic in human endometrium — functional definition of the stem-cell tier · archive: not_oa ↩ ↩²
doi:10.3389/fcell.2020.00497 · Bozorgmehr M, Gurung S, Darzi S et al. · “Endometrial and Menstrual Blood Mesenchymal Stem/Stromal Cells: Biological Properties and Clinical Application” · Frontiers in Cell and Developmental Biology 8:497 · 2020 · review · key finding: eMSC and MenSC fulfill ISCT multipotency criteria; serum-free protocols maintain clonogenic SUSD2(+) populations for clinical translation · archive: pending ↩
doi:10.1016/j.rbmo.2021.04.008 · Masuda H, Schwab KE, Filby CE et al. · “Endometrial stem/progenitor cells in menstrual blood and peritoneal fluid of women with and without endometriosis” · Reproductive Biomedicine Online 43(4):767–779 · 2021 · observational (human; menstrual blood + peritoneal fluid) · key finding: SUSD2(+) eMSCs and N-cadherin(+) epithelial progenitors detected in menstrual blood; clonogenic cells found in peritoneal fluid of 62.5% of endometriosis patients during menses · archive: pending ↩
doi:10.3390/ijms23094613 · Zhang S, Chan RWS, Ng EHY, Yeung WSB · “Hypoxia Regulates the Self-Renewal of Endometrial Mesenchymal Stromal/Stem-like Cells via Notch Signaling” · International Journal of Molecular Sciences 23(9):4613 · 2022 · in-vitro + in-vivo (human eMSC) · key finding: basalis label-retaining eMSCs reside in a hypoxic niche; HIF-1α → Notch axis enhances self-renewal and clonogenicity during endometrial breakdown/repair · archive: pending (OA likely) ↩
doi:10.1093/biolre/iox092 · Erikson DW, Barragan F, Piltonen TT, Chen JC, Balayan S, Irwin JC, Giudice LC · “Stromal fibroblasts from perimenopausal endometrium exhibit a different transcriptome than those from the premenopausal endometrium” · Biology of Reproduction 97(6):852–864 · 2017 · observational (human; perimenopausal vs premenopausal endometrial biopsies) · key finding: perimenopausal stromal fibroblasts show dysregulated cytoskeletal/proliferative/survival pathways; eMSC transcriptomes relatively similar across menopausal status · archive: pending ↩ ↩²
doi:10.1056/NEJMra1209993 · Bulun SE · “Uterine Fibroids” · New England Journal of Medicine 369(14):1344–1355 · 2013 · review · key finding: estradiol upregulates PR in leiomyoma cells; progesterone/PR axis is the dominant mitogenic driver via paracrine growth factors; MED12 exon 2 mutations in ~70% of fibroids; leiomyoma-initiating cells are ER-negative CD44+ stem-like cells · archive: not_oa — no-fulltext-access; quantitative claims (MED12 ~70%, progesterone-dominant-mitogen) accepted per broad secondary-literature consensus but not PDF-verified against this source ↩ ↩² ↩³
doi:10.1016/j.bpobgyn.2015.11.015 · Reis FM, Bloise E, Ortiga-Carvalho TM · “Hormones and pathogenesis of uterine fibroids” · Best Practice & Research Clinical Obstetrics & Gynaecology 34:13–24 · 2016 · review · key finding: steroid hormones drive pathogenesis through autocrine/paracrine mechanisms; GnRH agonist-induced suppression confirms in-vivo steroid dependence; SERMs and progesterone receptor modulators are mechanistically grounded therapeutic targets · archive: not_oa ↩
doi:10.1093/humupd/dmx032 · Islam MS, Ciavattini A, Petraglia F et al. · “Extracellular matrix in uterine leiomyoma pathogenesis: a potential target for future therapeutics” · Human Reproduction Update 24(1):59–85 · 2018 · review · key finding: fibroids contain 3–5× more collagen, fibronectin, laminin vs normal myometrium; TGF-β and activin-A are principal ECM-deposition drivers; antifibrotic strategies distinct from antiproliferative approaches proposed · archive: pending ↩
doi:10.1056/NEJMoa2008283 · Al-Hendy A, Lukes AS, Poindexter AN et al. · “Treatment of Uterine Fibroid Symptoms with Relugolix Combination Therapy” · New England Journal of Medicine 384(7):630–642 · 2021 · n=388 randomized in LIBERTY 1 (L1) + 382 in LIBERTY 2 (L2); two replicate 24-week international double-blind phase 3 RCTs · randomized, placebo-controlled, phase 3 · key finding: relugolix combination therapy (40 mg relugolix + 1 mg estradiol + 0.5 mg norethindrone acetate once daily) achieved ≥50% menstrual blood loss reduction to <80 ml in 73% (L1) and 71% (L2) vs 19% and 15% placebo (P<0.001 both); bone mineral density was similar with combination therapy and placebo but decreased with relugolix monotherapy · archive: downloaded ↩
doi:10.1016/s0960-0760(03)00360-1 · Simpson ER · “Sources of estrogen and their importance” · Journal of Steroid Biochemistry and Molecular Biology 86(3–5):225–230 · 2003 · review · key finding: in postmenopausal women estradiol is produced at multiple extragonadal sites (adipose, bone, brain, vascular endothelium); local adipose tissue concentrations can exceed circulating levels by an order of magnitude due to high local aromatase activity · archive: not_oa ↩
doi:10.1016/j.jsbmb.2015.07.008 · Wang X, Simpson ER, Brown KA · “Aromatase overexpression in dysfunctional adipose tissue links obesity to postmenopausal breast cancer” · Journal of Steroid Biochemistry and Molecular Biology 153:35–44 · 2015 · review · key finding: obesity-driven adipose inflammation (via IL-6, TNF-α, PGE2) upregulates CYP19A1 expression, increasing local estrogen synthesis; mechanistic link between adipose dysfunction and estrogen-dependent malignancy · archive: not_oa ↩
doi:10.1158/1055-9965.EPI-16-0225 · Brinton LA, Trabert B, Anderson GL et al. · “Serum Estrogens and Estrogen Metabolites and Endometrial Cancer Risk among Postmenopausal Women” · Cancer Epidemiology, Biomarkers & Prevention 25(7):1081–1089 · 2016 · n=313 endometrial cancer cases (271 type I, 42 type II) + 354 matched controls (WHI-OS nested case-control) · observational · key finding: serum unconjugated estradiol shows strongest association with endometrial cancer (OR 6.19, 95% CI 2.95–13.03, fifth vs first quintile, p=0.0001); nearly all estrogen metabolites elevated risk; stronger associations for Type I than Type II tumors (Phet=0.01) · archive: downloaded ↩
doi:10.1002/cam4.4434 · Dashti SG, Simpson JA, Viallon V et al. · “Adiposity and breast, endometrial, and colorectal cancer risk in postmenopausal women: Quantification of the mediating effects of leptin, C-reactive protein, fasting insulin, and estradiol” · Cancer Medicine 11(7):1914–1926 · 2022 · n=~24,000 postmenopausal women (EPIC cohort) · observational (causal mediation analysis) · key finding: adiposity increases endometrial cancer risk (RR 2.12); effects mediated through estradiol, leptin, CRP, and insulin in proportions that vary by cancer type; estradiol strongest mediator for endometrial cancer · archive: pending ↩
doi:10.3390/ijms24076192 · Wilson RB, Lathigara D, Kaushal D · “Systematic Review and Meta-Analysis of the Impact of Bariatric Surgery on Future Cancer Risk” · International Journal of Molecular Sciences 24(7):6192 · 2023 · meta-analysis (32 studies overall; 8 studies in the endometrial cancer subgroup: n=346,430 bariatric surgery vs 1,075,024 controls) · key finding: bariatric surgery associated with RR 0.38 (95% CI 0.26–0.55, p<0.00001) for endometrial cancer; significant heterogeneity across endometrial studies (I²=94%) · archive: downloaded ↩
doi:10.14735/amko20163S7 · Weinberger V, Zikán M · “Breast Cancer — Specifics of Gynecological Care and Counseling” · Klinická Onkologie 29(Suppl 3):S7–S15 · 2016 · review · key finding: postmenopausal tamoxifen users show 2–3-fold elevated endometrial cancer risk vs non-users after ≥5 years; risk not elevated in premenopausal users; polyps and hyperplasia are additional tamoxifen-associated endometrial findings · archive: pending ↩

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