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MSI-High Endometrial Cancer

1. Disease Information

2026-04-05
Falcon MONDO:0011962 Model: Edison Scientific Literature 40 citations

1. Disease Information

1.1 Overview / definition

MSI-H endometrial cancer refers to endometrial tumors with microsatellite instability caused by defects in the DNA mismatch repair pathway (dMMR). MSI-H/dMMR tumors accumulate replication errors leading to a hypermutated state and increased neoantigen burden, which underlies heightened sensitivity to immune checkpoint blockade in many patients (omalley2022pembrolizumabinpatients pages 1-2, oaknin2023safetyefficacyand pages 1-2).

Key definitional quote (abstract-level): KEYNOTE-158 notes that dMMR may arise from Lynch syndrome germline variants in MMR genes or sporadic MLH1 promoter methylation, leading to MSI and high mutation/neoantigen burden (omalley2022pembrolizumabinpatients pages 1-2).

1.2 Synonyms / alternative names

1.3 Key identifiers (available from retrieved sources)

Note: ICD, MeSH, and Orphanet codes specific to “MSI-H endometrial cancer” were not directly retrievable from the provided corpus; MSI-H is typically represented as a biomarker-defined subtype rather than a separate coding entity in clinical classifications.

1.4 Evidence sources (patient-level vs aggregated)

Evidence in this report comes from: - Aggregated clinical trials and reviews (KEYNOTE-158; GARNET; RUBY; NRG-GY018) (omalley2022pembrolizumabinpatients pages 1-2, oaknin2023safetyefficacyand pages 1-2, mirza2023dostarlimabforprimary pages 1-3, liu2024ataleof pages 19-21) - Retrospective cohorts and real-world chart reviews (Europe ECHO-EU; single-institution molecular cohorts) (kelkar2024realworldprevalenceof pages 1-2, riedinger2023epigeneticmmrdefect pages 1-2, wang2023aretrospectivestudy pages 1-2)

2. Etiology

2.1 Disease causal factors (molecular causes)

MSI-H/dMMR in endometrial cancer arises primarily through: 1) Inherited (germline) pathogenic variants in MMR genes (Lynch syndrome) (omalley2022pembrolizumabinpatients pages 1-2) 2) Sporadic epigenetic silencing, most commonly MLH1 promoter hypermethylation, leading to MLH1/PMS2 protein loss and MSI (omalley2022pembrolizumabinpatients pages 1-2, riedinger2023epigeneticmmrdefect pages 1-2)

Quantitative mechanism distribution: In a cohort of 1,514 endometrioid EC, 25.9% were MMR-deficient and 80.4% of MMR defects were attributed to epigenetic MLH1 silencing (MLH1 promoter hypermethylation) (riedinger2023epigeneticmmrdefect pages 1-2).

2.2 Risk factors (general EC risk factors; not MSI-H specific)

A systematic review/meta-analysis on postmenopausal bleeding contextualizes major endometrial cancer risk factors such as obesity, anovulation/irregular menses, diabetes, and tamoxifen exposure (clarke2018associationofendometrial pages 1-2). These are general endometrial cancer risks and are not specific to MSI-H biology.

2.3 Protective factors / gene–environment interactions

Protective factors and formal gene–environment interaction evidence specific to MSI-H endometrial cancer were not directly available in the retrieved evidence set.

3. Phenotypes

3.1 Common presenting symptoms and clinical features

  • Postmenopausal bleeding (PMB): pooled prevalence among women with endometrial cancer 91% (95% CI 87–93%) (clarke2018associationofendometrial pages 1-2). (This statistic is not MSI-H-specific but is the dominant clinical presentation of endometrial cancer.)
  • MSI/dMMR status may correlate with tumor grade/histology: in a 333-patient cohort, MMR/MSI status correlated with high-grade endometrioid or non-endometrioid components (wang2023aretrospectivestudy pages 1-2).

3.2 Age distribution

In a 333-case cohort, the dMMR subgroup was significantly younger than pMMR, especially for patients <60 years (wang2023aretrospectivestudy pages 1-2).

In European recurrent/advanced endometrial cancer chart review cohorts, median age at recurrent/advanced diagnosis was 69 years (not MSI-H-specific) (kelkar2024realworldprevalenceof pages 1-2).

3.3 HPO term suggestions (symptom-oriented)

(ontology suggestions; frequencies are not always available per MSI-H subtype) - Abnormal uterine bleeding / postmenopausal bleeding: HP:0000858 (Abnormal uterine bleeding) and/or HP:0000141 (Postmenopausal bleeding; term availability may vary by HPO release) - Anemia from chronic bleeding: HP:0001903 - Pelvic pain: HP:0000233

3.4 Quality-of-life impact

Direct QoL instruments (e.g., EQ-5D, PROMIS) specific to MSI-H endometrial cancer were not extracted from the available texts.

4. Genetic / Molecular Information

4.1 Causal genes and pathways

Core mismatch repair genes implicated in MSI-H/dMMR endometrial cancer include MLH1, PMS2, MSH2, MSH6, with heterodimer pairing (MLH1–PMS2; MSH2–MSH6) and loss patterns detectable by IHC (oaknin2023safetyefficacyand pages 1-2, carvalho2024unravelingtheheterogeneity pages 5-7).

4.2 Somatic vs germline contributions

KEYNOTE-158 explicitly frames dMMR etiology as either inherited mutations (Lynch syndrome) or sporadic MLH1 promoter methylation (omalley2022pembrolizumabinpatients pages 1-2).

4.3 Frequent MMR IHC loss patterns (tumor phenotype)

In a 333-case study: - Overall dMMR: 25.2% - Overall MSI-H: 24.0% - Among dMMR: MLH1/PMS2 loss 59.5%, MSH2/MSH6 loss 22.6%, isolated PMS2 loss 8.3%, isolated MSH6 loss 9.5% (wang2023aretrospectivestudy pages 1-2).

4.4 Epigenetics

MLH1 promoter hypermethylation is repeatedly supported as a major driver of sporadic dMMR/MSI-H EC (riedinger2023epigeneticmmrdefect pages 1-2, omalley2022pembrolizumabinpatients pages 1-2).

5. Environmental Information

No specific environmental toxicant, occupational, or infectious cause unique to MSI-H endometrial cancer was identified in the retrieved evidence. General endometrial cancer risk factors are summarized in Section 2.2 (clarke2018associationofendometrial pages 1-2).

6. Mechanism / Pathophysiology

6.1 Causal chain (from molecular defect to phenotype and treatment sensitivity)

1) MMR deficiency → replication mismatches not corrected → genome-wide mutation accumulation, including at microsatellites (MSI) (oaknin2023safetyefficacyand pages 1-2) 2) Hypermutated state → increased neoantigens and immune infiltration/immune checkpoint engagement → potential susceptibility to PD-1 blockade (omalley2022pembrolizumabinpatients pages 1-2, mirza2023dostarlimabforprimary pages 1-3) 3) Clinical phenotype: MSI-H/dMMR subset constitutes ~25–31% of EC and is clinically actionable for immunotherapy selection (omalley2022pembrolizumabinpatients pages 1-2, mirza2023dostarlimabforprimary pages 1-3)

6.2 Mechanistic heterogeneity: epigenetic vs mutational MMRd

A major contemporary concept is that mechanism of MMR loss (e.g., MLH1 hypermethylation vs MMR gene mutations) may shape immune microenvironment and response heterogeneity, motivating more nuanced biomarker strategies (liu2024ataleof pages 19-21, riedinger2023epigeneticmmrdefect pages 1-2).

6.3 GO / CL / UBERON term suggestions

  • UBERON: Endometrium UBERON:0001295; Uterus UBERON:0000995 (anatomy suggestions)
  • GO biological processes: DNA mismatch repair GO:0006298; DNA replication GO:0006260; somatic hypermutation-like mutation accumulation (conceptual)
  • CL cell types: Endometrial epithelial cell CL:0000066 (epithelial cell; more specific endometrial epithelial subtypes may be available depending on CL version); CD8-positive T cell CL:0000625 (immune infiltration relevance from MSI biology)

7. Anatomical Structures Affected

7.1 Primary site

  • Endometrium (uterine lining) and uterine corpus are primary tissues affected (UBERON suggestions above).

7.2 Metastatic/advanced disease patterns

In advanced settings, a European recurrent/advanced cohort had >75% Stage IIIB–IV at initial diagnosis, reflecting frequent extrauterine spread in the real-world advanced population (kelkar2024realworldprevalenceof pages 1-2).

8. Temporal Development

8.1 Onset and course

Endometrial cancer typically presents in mid-to-late adulthood; dMMR cases may be younger than pMMR (wang2023aretrospectivestudy pages 1-2). MSI-H endometrial cancer can be diagnosed at early stages but also occurs in advanced/recurrent settings where systemic therapy selection is biomarker-driven (kelkar2024realworldprevalenceof pages 1-2, mirza2023dostarlimabforprimary pages 1-3).

8.2 Staging system updates (FIGO 2023)

FIGO 2023 explicitly promotes integrating molecular subtype (including MMRd) into reporting by appending molecular information to FIGO stage (“m” with subscript) and notes that molecular testing can change stage assignment for some tumors (especially POLEmut/p53abn examples) (berek2023figostagingof pages 1-4, berek2023figostagingof pages 4-5).

9. Inheritance and Population

9.1 MSI-H/dMMR prevalence within endometrial cancer

Multiple sources converge on MSI-H/dMMR comprising roughly ~25–31% of endometrial cancers: - KEYNOTE-158 cites ~25–31% MSI-H in endometrial cancers (omalley2022pembrolizumabinpatients pages 1-2) - RUBY notes dMMR/MSI-H tumors account for ~25–30% of endometrial cancers; trial population had 23.9% dMMR/MSI-H (118/494) (mirza2023dostarlimabforprimary pages 1-3) - A 333-case cohort found 25.2% dMMR and 24.0% MSI-H (wang2023aretrospectivestudy pages 1-2)

9.2 Real-world testing patterns (implementation statistic)

Before biomarker-directed therapy became widely available in Europe, MSI/MMR testing rates in recurrent/advanced endometrial cancer were ~one-third: - 36.4% tested in 1L and 34.9% tested in 2L cohorts; among those tested, ~15% were MSI-H/dMMR (kelkar2024realworldprevalenceof pages 1-2).

10. Diagnostics

10.1 Clinical tumor testing (core diagnostic definition)

MMR immunohistochemistry (IHC) is commonly used to define dMMR status based on loss of MMR protein expression. - Presence of all four proteins (MLH1, MSH2, MSH6, PMS2) indicates MMR proficiency; loss of one or more indicates dMMR (oaknin2023safetyefficacyand pages 1-2).

PCR-based MSI testing classifies MSI-H and can be defined by instability in ≥2 loci using standard panels (carvalho2024unravelingtheheterogeneity pages 5-7).

10.2 Test concordance / discordance (statistics)

10.3 MLH1 promoter methylation testing (reflex testing)

MLH1 promoter hypermethylation is a key discriminator of sporadic vs hereditary pathways, and methylation was used as an independent measure (“truth set”) in discordance resolution; an amplicon-sequencing MSI assay achieved 90% concordance with MLH1 methylation among discordant samples (62/69) (sowter2024detectionofmismatch pages 1-2).

10.4 Germline testing and Lynch syndrome screening workflow

A practical workflow described in a 2024 review includes parallel assessment of MMR IHC and MSI with MLH1 promoter methylation testing as appropriate, and triage to genetic referral based on results and family history (liu2024ataleof pages 19-21).

Guideline-level source retrieved: NCCN Genetic/Familial High-Risk Assessment: Colorectal, Endometrial, and Gastric Version 3.2024 is available as a peer-reviewed guideline summary article (JNCCN, Dec 2024; DOI: https://doi.org/10.6004/jnccn.2024.0061) but detailed surveillance schedules were not extracted from full text in the present evidence set.

11. Outcome / Prognosis

11.1 Response and survival outcomes with immunotherapy (biomarker-selected)

MSI-H/dMMR endometrial cancer has high response rates to PD-1 blockade, with durable responses in a substantial subset.

KEYNOTE-158 (pembrolizumab; previously treated advanced MSI-H/dMMR EC): - ORR 48% (95% CI 37–60) - Median PFS 13.1 months - Median OS not reached (omalley2022pembrolizumabinpatients pages 1-2)

GARNET (dostarlimab; recurrent/advanced dMMR/MSI-H EC): - ORR 45.5% in dMMR/MSI-H - Median DOR not reached at ~27.6 months follow-up (oaknin2023safetyefficacyand pages 1-2)

RUBY (first-line dostarlimab + carboplatin/paclitaxel): - dMMR/MSI-H subgroup: 24-month PFS 61.4% vs 15.7% with placebo-chemo; HR 0.28 (mirza2023dostarlimabforprimary pages 1-3)

NRG-GY018 (first-line pembrolizumab + carboplatin/paclitaxel): - dMMR cohort: 12-month PFS 74% vs 38%; HR 0.30 (liu2024ataleof pages 19-21)

11.2 Prognostic implications of epigenetic MMR defects

In a large endometrioid EC cohort, epigenetic MLH1-associated MMR defects were associated with higher LN metastasis risk and worse DFS compared with MMR-proficient tumors, supporting the idea that not all MMRd mechanisms are equivalent in clinical behavior (riedinger2023epigeneticmmrdefect pages 1-2).

12. Treatment

12.1 Current applications / real-world implementations

In 2023–2024, MSI-H/dMMR status is routinely used as a predictive biomarker to select PD-1–based therapies in advanced/recurrent disease and increasingly in first-line advanced/recurrent disease (mirza2023dostarlimabforprimary pages 1-3, liu2024ataleof pages 19-21).

A key implementation gap is testing uptake: in pre-approval European cohorts, only ~35–36% of recurrent/advanced patients were tested for MSI/MMR (kelkar2024realworldprevalenceof pages 1-2).

12.2 Key therapies (with MAXO suggestions)

  • Pembrolizumab (anti–PD-1) monotherapy in previously treated MSI-H/dMMR advanced EC (KEYNOTE-158 outcomes above) (omalley2022pembrolizumabinpatients pages 1-2)
  • MAXO suggestions: immune checkpoint inhibitor therapy; anti–PD-1 therapy
  • Dostarlimab (anti–PD-1) monotherapy for recurrent/advanced dMMR/MSI-H EC (GARNET outcomes above) (oaknin2023safetyefficacyand pages 1-2)
  • MAXO suggestions: immune checkpoint inhibitor therapy; anti–PD-1 therapy
  • Chemo-immunotherapy (frontline advanced/recurrent):
  • Dostarlimab + carboplatin/paclitaxel (RUBY) (mirza2023dostarlimabforprimary pages 1-3)
  • Pembrolizumab + carboplatin/paclitaxel (NRG-GY018) (liu2024ataleof pages 19-21)
  • MAXO suggestions: combination antineoplastic therapy; platinum-based chemotherapy; taxane therapy; immune checkpoint inhibitor therapy

13. Prevention

13.1 Secondary prevention: universal tumor screening to identify Lynch syndrome

Universal MMR testing (IHC ± MSI) is used for Lynch syndrome screening and also informs immunotherapy eligibility (wang2023aretrospectivestudy pages 1-2, liu2024ataleof pages 19-21).

13.2 Cascade testing impact

A Lancet review reports that cascade testing can identify “an average three family members with Lynch syndrome per index case” (crosbie2022endometrialcancer pages 5-6).

Note: Specific chemoprevention and gynecologic surveillance intervals for Lynch syndrome (e.g., aspirin; endometrial biopsy schedules) were not extracted from full guideline text in the current evidence set.

14. Other Species / Natural Disease

No naturally occurring veterinary MSI-H endometrial cancer evidence was retrieved.

15. Model Organisms

15.1 Endometrial-specific organoid models (Lynch syndrome–related)

A 2023 thesis reports CRISPR-Cas9 generation of MLH1- and PMS2-deficient endometrial organoids from benign hysterectomy tissues of Lynch syndrome patients and single-cell RNA-seq, concluding that MMR deficiency alone may not immediately alter transcriptomic state or differentiation of benign endometrial glands (degrood2023investigationintothe pages 1-7).

15.2 Mouse genetic models relevant to gynecologic malignancies

The same thesis reviews murine models with constitutive/conditional loss of Mlh1, Msh2, Msh6, Pms2 and highlights models with increased gynecologic relevance (e.g., Msh6−/− showing higher gynecologic rates among knockouts; Mlh1−/−/Pten+/− increasing endometrial cancer incidence) (degrood2023investigationintothe pages 25-28).

15.3 Cross-cancer MMRd models informing immunogenicity constraints

A Nature Genetics study developed autochthonous mouse models with engineered MMR deficiency (targeting Msh2/Mlh1/Msh3/Msh6) and found that despite hypermutation, tumors “did not display increased T cell infiltration or ICB response,” emphasizing the importance of clonal architecture and intratumor heterogeneity for immunogenicity (westcott2023mismatchrepairdeficiency pages 1-2).

Expert opinions / analysis (authoritative sources, 2023–2024 emphasis)

  • A 2024 Cancer review emphasizes that endometrial cancers require comprehensive assessment using IHC and sequencing-based techniques and that heterogeneity (e.g., MLH1 hypermethylation vs germline/somatic MMR mutation) may affect response to immune checkpoint inhibitors (liu2024ataleof pages 19-21).
  • A 2024 Cancers review highlights that dMMR status alone is not always sufficient to predict immunotherapy response and that better predictive biomarkers are needed (carvalho2024unravelingtheheterogeneity pages 4-5).

Key recent statistics (quick reference)

Evidence Table: Practice-changing trials and implementation data

Table (click to expand)
Setting Study/Trial Agent(s) Biomarker population Key outcomes (ORR, PFS/OS with timepoints/HR) Publication (journal, month year) URL/DOI
Previously treated advanced/recurrent KEYNOTE-158 Pembrolizumab monotherapy Advanced MSI-H/dMMR endometrial cancer ORR 48% (95% CI 37–60); median DOR not reached; median PFS 13.1 months (95% CI 4.3–34.4); median OS not reached; treatment-related AEs in 76%, grade 3–4 in 12% (omalley2022pembrolizumabinpatients pages 1-2) J Clin Oncol, Mar 2022 https://doi.org/10.1200/JCO.21.01874
Previously treated advanced/recurrent GARNET Dostarlimab monotherapy Recurrent/advanced dMMR/MSI-H endometrial cancer ORR 45.5% (65/143); median DOR not reached at median follow-up 27.6 months; ORR 54.9% in CPS≥1 subgroup; high TMB subgroup ORR 47.8% (oaknin2023safetyefficacyand pages 1-2) Clin Cancer Res, Jun 2023 https://doi.org/10.1158/1078-0432.CCR-22-3915
First-line primary advanced or first recurrent RUBY Dostarlimab + carboplatin/paclitaxel, then dostarlimab maintenance dMMR/MSI-H subgroup within stage III/IV or first recurrent EC dMMR/MSI-H tumors in 118/494 (23.9%); 24-month PFS 61.4% vs 15.7% with placebo-chemo; HR for progression/death 0.28 (95% CI 0.16–0.50; P<0.001). Overall population: 24-month PFS 36.1% vs 18.1%; HR 0.64; 24-month OS 71.3% vs 56.0%; HR for death 0.64 (95% CI 0.46–0.87) (mirza2023dostarlimabforprimary pages 1-3) N Engl J Med, Jun 2023 https://doi.org/10.1056/NEJMoa2216334
First-line advanced/recurrent NRG-GY018 Pembrolizumab + carboplatin/paclitaxel dMMR cohort and pMMR cohort in measurable stage III/IVA, stage IVB, or recurrent EC In dMMR cohort, 12-month PFS 74% with pembrolizumab-chemo vs 38% with placebo-chemo; HR for progression/death 0.30 (95% CI 0.19–0.48; P<0.001). In pMMR cohort, median PFS 13.1 vs 8.7 months; HR 0.54 (95% CI 0.41–0.71) (liu2024ataleof pages 19-21) N Engl J Med, Jun 2023 https://doi.org/10.1056/NEJMoa2302312
Real-world implementation in advanced/recurrent care ECHO-EU-1L / ECHO-EU-2L MSI/MMR testing in practice (not therapeutic trial) Recurrent/advanced EC in UK, Germany, Italy, France, Spain Testing prevalence: 36.4% in first-line cohort and 34.9% in second-line cohort. Among tested patients, ~15% had MSI-H/MMRd in both cohorts; most were non-MSI-high/MMR-proficient (80.7% first-line; 74.7% second-line); discordant results in 3.4% and 10.8%, respectively (kelkar2024realworldprevalenceof pages 1-2) Arch Gynecol Obstet, Apr 2024 https://doi.org/10.1007/s00404-024-07504-3

Table: This table summarizes pivotal therapeutic trial results and real-world biomarker testing implementation for MSI-H/dMMR endometrial cancer. It is useful for quickly comparing response and survival outcomes across approved PD-1–based strategies and understanding how often MSI/MMR testing was being performed in practice.

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