Endometrioid endometrial carcinoma
- Lesion
The common endometrial cancer: it grows from estrogen-driven hyperplasia, looks like endometrium gone crowded, and is usually caught early by bleeding.
What it is
Endometrioid carcinoma is the commonest endometrial cancer. It follows the estrogen-driven path from atypical hyperplasia, with early loss of PTEN and later mutations in PIK3CA, ARID1A, KRAS, CTNNB1 or the mismatch repair system. It forms glands that resemble normal endometrium, is graded by how much of it grows as solid sheets, and spreads by invading the myometrium and cervix before reaching lymph nodes. Stage, grade and depth of invasion decide the prognosis.
Structure
- Gross: a polypoid or diffuse friable tumour filling the cavity, with depth of invasion seen on the cut wall.
- Microscopy: back-to-back or cribriform glands lined by columnar cells resembling proliferative endometrium, with little intervening stroma.
- Squamous morules, mucinous or secretory change may be present.
- Higher grades show solid sheets of cells and greater nuclear atypia.
Step by step
- Unopposed estrogen drives endometrial proliferation.
- A clone with PTEN loss forms atypical hyperplasia.
- Mutations in PIK3CA, KRAS, ARID1A or CTNNB1, or mismatch-repair failure, accumulate.
- The clone invades the endometrial stroma, then the myometrium.
- Deep invasion and lymphovascular invasion raise the risk of nodal spread.
Markers
- ER and PR positive
- PTEN loss
- MLH1, PMS2, MSH2, MSH6 (mismatch repair)
- p53 wild-type pattern (usually)
- Beta-catenin nuclear (CTNNB1 mutation)
Clinical notes
- Presents with postmenopausal or irregular bleeding; most are diagnosed at an early stage.
- Risk factors are those of estrogen excess and metabolic disease: obesity, diabetes, hypertension, nulliparity, polycystic ovary syndrome, tamoxifen.
- Treatment is hysterectomy with salpingo-oophorectomy and nodal assessment; selected young patients with low-grade disease may receive progestins first.
Test yourself
Think of the answer, then tap the question to see it.
Which tumour suppressor is most often lost early in endometrioid carcinoma?
PTEN, which normally brakes the PI3K-AKT pathway.
How is endometrioid carcinoma graded?
By the proportion of solid, non-squamous, non-morular growth (FIGO grades 1 to 3), raised by one grade for marked nuclear atypia.
What is the main route of local spread?
Invasion into the myometrium, then the cervical stroma, serosa and adnexa, with lymphatic spread to pelvic and para-aortic nodes.
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Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Endometrial Cancer (StatPearls (NCBI Bookshelf), 2026); Endometrial Cancer Treatment (PDQ®)–Health Professional Version (National Cancer Institute, 2026).
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Representative model, for educational purposes only.