Endometrioid Endometrial Carcinoma

Slide 1 · Endometrioid Endometrial

Carcinoma

Etiopathogenesis · precursor lesions · molecular alterations · morphology · clinical correlation

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

After this lecture, learners should be able to:

Explain the relationship among unopposed estrogen, atypical hyperplasia, and carcinoma.

Interpret major PI3K/AKT, genomic-instability, and molecular-subtype alterations.

Recognize glandular architecture, solid growth, and histologic grading.

Relate invasion, abnormal bleeding, specimen diagnosis, and outcome determinants.

Slide 3 · The disease in four linked dimensions

Clinical setting

Prolonged estrogenic drive

Precursor

Atypical hyperplasia / EIN

Transformation

Accumulating driver alterations

Phenotype

Invasive gland-forming carcinoma

The sequence is a teaching model; Not every tumor follows one obligatory linear trajectory.

Slide 4 · Dominant histologic subtype

Endometrioid carcinoma predominates among endometrial cancers.

Accounts for approximately 80%–85% of endometrial carcinomas.

Many tumors are well differentiated and resemble proliferative endometrial glands.

The name describes the endometrial gland-like architecture, not merely tumor location.

Endometrioid and serous carcinomas have distinct typical biology.

Slide 5 · Endometrioid versus serous carcinoma

Endometrioid subtype

Often in a hyperplasia-related setting

Frequently estrogen-associated

Gland-forming appearance is common

PI3K/AKT alterations prominent

Serous subtype

Typically arises in atrophic endometrium

Generally occurs at older ages

High-grade cytology regardless of growth pattern

Strongly associated with TP53 alterations

Slide 6 · What “endometrioid” signifies

Architecture supplies the defining morphological resemblance.

Well-formed tubular glands resemble those of proliferative endometrium.

Tumor may form packed, complex, confluent, or invasive glands.

Increasing solid epithelial growth corresponds to reduced glandular differentiation.

Grade, extent of spread, and molecular features are separate dimensions.

Slide 7 · Estrogen exposure and neoplastic progression

Hormonal drive

Persistent unopposed estrogenic stimulation

Proliferation

Increased gland-to-stroma ratio

Clonal selection

Atypical hyperplasia / EIN

Invasion

Endometrioid carcinoma

“Precursor” describes risk and clonal linkage; Morphology alone cannot establish that every hyperplasia will become malignant.

Slide 8 · Why obesity matters

Peripheral estrogen formation increases the trophic drive on endometrium.

Obesity as a major association with this carcinoma type.

Obesity is linked to peripheral conversion of androgens to estrogens.

Unopposed estrogen stimulation favors endometrial gland proliferation.

The association with obesity also explains frequent coexistence with metabolic disorders.

Slide 9 · Conditions associated with persistent estrogenic stimulation

Endogenous factors

Obesity: Peripheral estrogen synthesis

Anovulation and polycystic ovarian syndrome

Estrogen-producing ovarian processes

Menopausal hormonal imbalance

Exogenous / contextual factors

Prolonged estrogenic medication exposure

Unopposed estrogenic stimulation is the unifying mechanism

Individual factors are associations, not equivalent risk magnitude

Clinical risk assessment needs the full history

Slide 10 · Metabolic comorbidity

Do not confuse co-occurrence with histologic diagnostic criteria.

Hypertension and type 2 diabetes frequently coexist with endometrioid carcinoma.

Robbins relates this clustering substantially to obesity.

Neither hypertension nor diabetes identifies an endometrioid tumor histologically.

Pathologic diagnosis still rests on tissue architecture and cytology.

Slide 11 · Precursor-to-carcinoma model

Proliferative endometrium

Physiologic glands with stroma

Hyperplasia

Crowded glands relative to stroma

EIN / atypia

Clonal atypical glandular proliferation

Carcinoma

Invasive or unequivocally confluent malignant growth

The last distinction can be difficult in limited biopsies.

Slide 12 · Hyperplasia without atypia versus atypical hyperplasia

Without atypia

Increased gland-to-stroma ratio

Variable gland size; Cystic dilation possible

Intervening stroma is typically retained

Progression to cancer is uncommon

Atypical hyperplasia / EIN

Complex, crowded back-to-back glands

Nuclear rounding and vesicular chromatin

Conspicuous nucleoli may be present

Substantial morphologic overlap with carcinoma

Slide 13 · Atypical hyperplasia can coexist with carcinoma

Sampling limitations matter.

Carcinoma at hysterectomy in up to 40% of patients diagnosed with atypical hyperplasia.

The biopsy may sample an atypical precursor while missing a more advanced component.

Complex crowded glands with atypia warrant careful search for unequivocal carcinoma.

The estimate is from the source; It is not a universal predictive percentage.

Slide 14 · Shared driver mutations establish clonal continuity

Precursor and carcinoma may carry identical acquired mutations.

Matched atypical hyperplasia and carcinoma have shown shared PTEN, ARID1A, PIK3CA, and KRAS alterations.

This supports clonal progression rather than merely incidental coexistence.

Genetic alterations may precede overt invasive carcinoma.

Additional events contribute to tumor progression.

Slide 15 · Central growth-regulatory mechanism

PTEN loss

Decreased negative regulation

PI3K / AKT

Increased growth signaling

ER response

Amplified estrogen-responsive transcription

Growth advantage

Expansion of altered epithelial clones

Different molecular lesions can increase signaling through the same pathway.

Slide 16 · PTEN: Removal of a critical brake

PTEN normally restrains PI3K/AKT signaling.

PTEN encodes a lipid phosphatase and acts as a tumor suppressor.

Loss of PTEN increases PI3K/AKT pathway activity.

Mutations are found in roughly 30%–80% of endometrioid carcinomas.

The broad range reflects source-reported variation; It is not a single laboratory cutoff.

Slide 17 · PTEN loss does not equal inevitable cancer

PTEN alteration

Early genetic event

Affected gland

Altered growth control

Additional hits

Further selective advantage

Carcinoma

Malignant architectural phenotype

PTEN mutations in hyperplasia are not individually predictive of progression.

Slide 18 · PIK3CA: Activation of a signaling enzyme

A direct pathway accelerator.

PIK3CA encodes the catalytic subunit of phosphatidylinositol 3-kinase.

Activating PIK3CA mutations occur in approximately 40% of endometrioid carcinomas.

The change increases signaling along the PI3K/AKT axis.

It may coexist with other mutations that stimulate the same pathway.

Slide 19 · KRAS: An additional signaling input

Multiple upstream mutations can converge on a proliferative pathway.

Activating KRAS mutations occur in approximately one-quarter of cases.

KRAS activation can also stimulate PI3K/AKT signaling.

KRAS, PIK3CA, and PTEN changes should not be represented as mutually exclusive.

Concurrent pathway hits help explain progressive signal intensification.

Slide 20 · ARID1A: Chromatin-regulatory alteration

Disordered transcriptional regulation joins signaling activation.

ARID1A regulates chromatin structure and is inactivated in about one-third of tumors.

The source links ARID1A loss to oncogenic transcriptional changes associated with PI3K/AKT.

The precise mechanism is described as unclear.

ARID1A alterations are also observed in some endometriosis-associated ovarian carcinomas.

Slide 21 · Converging molecular drivers

PTEN

Tumor suppressor loss

Releases a signaling brake

PIK3CA

Oncogenic activation

Boosts PI3K signaling

KRAS

Upstream activation

Adds proliferative input

ARID1A

Chromatin dysregulation

Alters gene expression

These are not four exclusive genetic categories; Co-occurrence is possible.

Slide 22 · Why several mutations may coexist

The amount of pathway signaling can matter, not only its presence.

Individual endometrioid carcinomas may contain multiple PI3K/AKT–enhancing alterations.

Robbins suggests sequential increases in signal strength foster tumor evolution.

The observed combinations support a multistep process.

Do not infer a universal temporal order for PTEN, PIK3CA, KRAS, and ARID1A.

Slide 23 · Selected alterations: Textbook frequencies

Alteration

Approximate source frequency

Principal implication

PTEN

30%–80%

Loss of PI3K/AKT restraint

PIK3CA

~40%

Activating PI3K signaling

KRAS

~25%

Oncogenic signaling input

ARID1A

About one-third

Chromatin regulation / transcription

Percentages describe different alteration groups and can overlap; They must not be added.

Slide 24 · Estrogen receptor and PI3K/AKT cross-talk

Estrogen

Provides hormone-dependent trophic signal

PI3K/AKT activation

Augments ER-mediated target expression

Gene expression

Amplifies proliferation-associated output

The pathway is biologically linked to the hormonal environment.

Slide 25 · Genomic instability can accelerate tumor evolution

Altered DNA maintenance produces a mutator phenotype.

Defects in DNA repair and replication fidelity increase the burden of somatic mutations.

This expands opportunities to acquire driver mutations.

Endometrioid carcinomas include mismatch-repair-deficient and polymerase-ε-altered subsets.

High mutation burden is a molecular characteristic, not synonymous with high histologic grade.

Slide 26 · Mismatch repair loss: Mechanism

MMR defect

Reduced correction of replication errors

Microsatellite instability

Accumulating sequence errors

Hypermutated tumor

Increased somatic mutation burden

Sporadic promoter methylation and inherited predisposition are distinct etiologic routes.

Slide 27 · Sporadic mismatch repair defects

Epigenetic silencing may disable a repair protein.

Mismatch repair defects in approximately 20% of sporadic endometrioid carcinomas.

Loss of MLH1 expression commonly results from promoter hypermethylation in sporadic tumors.

Mismatch repair defects can also arise in Lynch syndrome.

A tumor MMR abnormality alone does not prove a germline pathogenic variant.

Slide 28 · Lynch syndrome association

Syndromic risk deserves separate recognition.

Endometrial carcinoma can develop in patients with inherited mismatch repair predisposition.

Lynch syndrome in approximately 3%–5% of females with endometrial cancer.

The syndrome also confers important risk of colorectal carcinoma.

Tumor mismatch repair assessment supports identification of potentially affected patients.

Slide 29 · MMR assessment at diagnosis

Pathology connects tumor phenotype with hereditary risk.

Robbins recommends examining endometrioid carcinoma for DNA mismatch repair defects.

An abnormal tumor result requires appropriate subsequent clinical interpretation.

Sporadic MLH1 promoter methylation is a relevant alternative to hereditary MMR loss.

The source does not supply a complete reflex-testing algorithm; None is invented here.

Slide 30 · POLE proofreading alteration

POLE exonuclease defect

Impaired polymerase proofreading

DNA replication errors

Many somatic point mutations

Ultramutated phenotype

Exceptionally high mutation burden

The key distinction is altered replication fidelity, not just greater proliferation.

Slide 31 · Polymerase ε–altered tumors

A small subset with exceptional point mutation burden.

Proofreading-disrupting POLE mutations in fewer than 10% of endometrial carcinomas.

These tumors can carry extremely high somatic point mutation burdens.

The POLE-defined molecular category is termed ultramutated.

Molecular class should not be guessed from microscopic grade alone.

Slide 32 · TP53 in progression of high-grade endometrioid tumors

Timing differs from typical serous carcinoma.

TP53 loss-of-function mutations in about half of poorly differentiated endometrioid carcinomas.

TP53 mutations are absent from most well-differentiated endometrioid tumors.

This pattern suggests later involvement in progression of some tumors.

By contrast, TP53 mutations are frequent early events in serous carcinoma.

Slide 33 · Four molecular patterns in endometrial carcinoma

POLE

Ultramutated

Proofreading error

MMR-deficient / MSI

Hypermutated

Repair deficiency

Copy-number low / NSMP

Often endometrioid

PI3K/AKT drivers

Copy-number high / p53

Often aggressive

TP53 alteration

Histologic subtype and molecular classification are related but not interchangeable.

Slide 34 · POLE molecular class

Defining event: Pathogenic proofreading-associated POLE alteration.

The central biological effect is an exceptionally high burden of mutations.

Tumors may still show endometrioid glandular or solid histology.

Diagnosis of this molecular class requires appropriate molecular evidence.

Textbook description is not a substitute for a current validated testing specification.

Slide 35 · Mismatch-repair-deficient molecular class

Defining biological mechanism: Defective DNA repair.

Microsatellite instability is linked to a hypermutated phenotype.

The cause may be sporadic or hereditary.

These tumors with prominent infiltrating T cells in some cases.

The presence of T cells is a clue, not a molecular diagnostic assay.

Slide 36 · Copy-number-low / NSMP pattern

A frequent pattern with endometrioid morphology.

This group is associated with mutations upregulating PI3K/AKT signaling.

The name refers to a molecular category, not an independent architectural grade.

Absence of a defining POLE, MMR, or p53 result cannot be asserted without testing.

Morphologic gland formation and molecular class are distinct observations.

Slide 37 · Copy-number-high / p53-abnormal pattern

Aggressive biology can cross histologic boundaries.

Classically associated with serous carcinoma and some high-grade endometrioid tumors.

TP53 alterations coexist with many chromosomal copy-number changes.

High-grade morphology alone is not proof of the category.

The category helps illustrate why a purely gland-based classification is incomplete.

Slide 38 · Histology and molecular type answer different questions

Histologic assessment

Molecular assessment

Architecture: Gland-forming versus solid

POLE proofreading status

Cytologic atypia / differentiation

DNA mismatch repair or MSI status

Squamous elements and invasion

P53 / copy-number-associated pattern

Tumor grade and local extent

Biological classification independent of grade

Slide 39 · Tumor-infiltrating lymphocytes

Genomic instability can alter tumor immunogenicity.

POLE-mutant and mismatch-repair-deficient tumors with numerous infiltrating T lymphocytes.

High mutation burden may produce proteins with novel antigenic sequences.

The described inflammatory infiltrate is interpreted as an ineffective host response in the text.

Lymphocyte density alone should not be used to assign a POLE or MMR category.

Slide 40 · Gross growth patterns

Localized / polypoid lesion

Focal exophytic mass into uterine cavity

May have a broad-based or protruding configuration

An example is a fundal fungating mass

Gross distribution does not define grade

Diffuse endometrial involvement

Tumor may involve much of the endometrial lining

Subsequent myometrial invasion changes stage

Architectural tumor type must be confirmed microscopically

Gross mapping assists extent assessment

Slide 41 · Anatomic progression of invasion

Endometrium

Malignant glands originate at the mucosal surface

Myometrium

Infiltration beyond endometrial compartment

Adjacent tissues

Direct extension may involve structures beyond uterus

Distant sites

Nodal, then late systemic dissemination

This summarizes the spread sequence and is not an individual-patient prediction.

Slide 42 · Myometrial invasion changes the disease extent

The same histologic tumor can occupy very different anatomic compartments.

Endometrioid carcinoma can invade into the underlying myometrium.

Beyond the uterine wall, extension may involve neighboring structures or organs.

Broad-ligament involvement can produce a palpable mass.

Anatomic extent should be reported independently from histologic grade.

Slide 43 · Routes and destinations of spread

Location of tumor cells matters for staging and prognosis.

Direct contiguous invasion can precede involvement of adjacent structures.

Regional lymph-node dissemination can occur.

Late distant metastatic sites include lung, liver, and bone.

This description gives a typical sequence, not a deterministic pathway.

Slide 44 · Architecture under the microscope

Gland formation

Well-formed malignant glands

Complexity

Back-to-back or confluent structures

Solid growth

Loss of recognizably glandular architecture

The proportion of solid epithelial tumor determines the histologic grade in the source scheme.

Slide 45 · Grade 1: Predominantly gland-forming

Simplified architectural schematic — not a photomicrograph

Predominantly well-formed glands

Very little solid epithelial growth

Preserved glandular differentiation

Slide 46 · Grade 1: What supports the interpretation

Look for malignant architecture even when cells appear deceptively bland.

The majority of the tumor consists of well-formed glands.

Intervening stromal boundaries may be lost within confluent malignant glands.

Desmoplastic stromal reaction favors carcinoma over hyperplasia where demonstrable.

The schematic is architectural only: Real H&E remains necessary for diagnosis.

Slide 47 · Grade 2: Glands mixed with solid areas

Simplified architectural schematic — not a photomicrograph

Glands coexist with solid tumor

Intermediate reduction in gland formation

Architectural heterogeneity is central

Slide 48 · Grade 2: Architectural heterogeneity

Both glandular and solid components should be evaluated.

Well-formed glands coexist with sheets of solid tumor cells.

Solid growth accounts for no more than half of the tumor in grade 2.

Grade 2 retains appreciable glandular differentiation.

Only the tumor epithelial architecture—not squamous areas—should control grading.

Slide 49 · Grade 3: Predominantly solid tumor

Simplified architectural schematic — not a photomicrograph

Solid growth dominates

More than 50% solid architecture

Glandular differentiation may be limited

Slide 50 · Grade 3: Reduced glandular differentiation

Solid growth predominates by definition scheme.

More than 50% of the tumor shows a solid growth pattern.

Limited glandular elements may remain, requiring careful tumor typing.

High-grade endometrioid carcinoma can contain TP53 alterations.

Morphology must be integrated with other evidence rather than assuming serous histology.

Slide 51 · Morphologic grades: The source-based distinction

Grade

Architectural pattern

Essential observation

1 — well differentiated

Nearly entirely well-formed glands

Predominantly glandular

2 — moderately differentiated

Glands admixed with solid growth

Solid component ≤50%

3 — poorly differentiated

Predominantly solid epithelial growth

Solid component >50%

This reproduces the simplified Robbins description, not a comprehensive current grading protocol.

Slide 52 · Binary grade concept

Why some reporting frameworks group grades.

Advocacy for a two-tier interpretation.

Grades 1 and 2 may be combined as low-grade endometrioid carcinoma.

Grade 3 is treated as high-grade disease in this binary approach.

Histologic grading and molecular classification should still be reported as different attributes.

Slide 53 · Atypical hyperplasia versus well-differentiated carcinoma

Atypical hyperplasia / EIN

Crowded and complex glands with nuclear atypia

Back-to-back growth can occur

Limited samples may be ambiguous

No unequivocal stromal invasion shown

Well-differentiated carcinoma

Confluent or complex malignant glandular growth

Desmoplastic stroma favors invasion

Complex papillary arrangements may support carcinoma

Examination of a larger specimen can clarify extent

Slide 54 · The carcinoma–EIN interface is a sampling problem

A biopsy is a sample, not a complete architectural map.

Some EIN foci closely resemble well-differentiated carcinoma.

Textbook emphasizes complexity of reliably distinguishing the two in limited material.

Findings supporting invasion must be evaluated in the actual tissue.

A hysterectomy specimen may reveal carcinoma missed at initial biopsy.

Slide 55 · Squamous differentiation in endometrioid carcinoma

A separate morphologic element can appear within the tumor.

Up to approximately 20% contain squamous foci.

Squamous areas can appear cytologically bland in low-grade tumors.

Squamous elements may look overtly malignant in poorly differentiated tumors.

Squamous differentiation does not by itself define an additional molecular subtype.

Slide 56 · Do not grade the squamous component

Gland-forming tumor architecture remains the basis of grade.

The source explicitly states that areas of squamous differentiation are ignored for grading.

Grade 1–3 is based on non-squamous glandular versus solid growth.

Failure to exclude squamous nests can falsely increase apparent solid fraction.

Quantitative grading must use the specified tumor component.

Slide 57 · Clinical presentation

Abnormal uterine bleeding is the central warning symptom.

Carcinoma may be initially asymptomatic.

Irregular bleeding and postmenopausal vaginal bleeding are characteristic presentations.

Bleeding often prompts early evaluation while disease is confined to the uterus.

Symptoms establish an indication for investigation, not a histologic diagnosis.

Slide 58 · Age and clinical context

Epidemiology guides suspicion but is not diagnostic.

A peak among postmenopausal females approximately 55–65 years old.

Endometrial carcinoma can also occur in younger females.

Increasing incidence in younger patients.

Risk factors and age should guide evaluation of bleeding without substituting for biopsy.

Slide 59 · There is no established general screening test in the source

Symptom-triggered assessment is therefore central.

No screening test is available for endometrial carcinoma.

Patients may experience bleeding before spread becomes extensive.

Clinical suspicion should lead to appropriate tissue investigation.

Hereditary-risk management protocols are separate from population screening statements.

Slide 60 · From bleeding to tissue diagnosis

Presentation

Abnormal uterine bleeding

Sampling

Biopsy or curettage

Histology

Classify glands, cytology and invasion

Integration

Consider tumor molecular features

This educational sequence is not a comprehensive clinical management algorithm.

Slide 61 · Why histology is essential

The diagnosis must be established in sampled tissue.

Endometrial biopsy or curettage provides tissue for microscopic evaluation.

Architecture distinguishes glandular crowding, EIN, and overt carcinoma.

Limited fragments can constrain assessment of invasion.

Biopsy-based morphology may be complemented by surgical resection findings.

Slide 62 · Three axes of outcome assessment

Stage

Extent of disease in and beyond the uterus

Histologic grade

Relative glandular differentiation versus solid growth

Histologic / molecular type

Biologic pattern of the tumor

These dimensions should be integrated, not substituted for one another.

Slide 63 · Source-based anatomic stage concepts

Stage I

Confined to corpus uteri

Stage II

Involves cervical stroma

Stage III

Outside uterus, within true pelvis

Stage IV

Extrapelvic or bladder/rectal mucosal extension

Simplified anatomic schema as printed; Not presented as the current comprehensive FIGO 2023 staging system.

Slide 64 · Why early recognition affects outcome

Localized disease is generally more amenable to curative management.

Bleeding can lead to histologic diagnosis before extensive spread.

Outcome strongly with stage at diagnosis.

Grade and tumor subtype also affect outcome.

This lecture does not substitute historical survival estimates for individualized prediction.

Slide 65 · Therapeutic implications: Principles only

Pathology informs the treatment pathway, but treatment is stage-dependent.

Surgery as a major treatment modality for endometrioid carcinoma.

Radiation may be used to reduce local recurrence in selected cases.

Systemic therapy is considered when disease extends beyond the uterus.

Current regimen selection and molecular treatment criteria require guideline verification.

Slide 66 · Application case: Bleeding and obesity

Illustrative teaching vignette

A 61-year-old postmenopausal patient with obesity has intermittent vaginal bleeding. Endometrial sampling is planned.

What sequence of mechanisms links this clinical setting to endometrioid carcinoma?

Slide 67 · Case analysis: Estrogen and clonal selection

The case establishes a mechanism of risk, not a final diagnosis.

Adipose-associated estrogen production can produce persistent stimulation of endometrial glands.

Hyperplasia, particularly atypical hyperplasia / EIN, is an important precursor setting.

PTEN and related signaling alterations may be acquired before overt carcinoma.

Histologic sampling is needed to identify the actual lesion.

Slide 68 · Application case: Grade from architecture

Illustrative teaching vignette

An endometrial malignancy shows many abnormal glands and a substantial, but nonpredominant, solid epithelial component. Separate squamous nests are also present.

Which elements determine its grade, and what must be excluded from the estimate?

Slide 69 · Case analysis: Grade versus squamous component

Architectural assessment is intentionally selective.

Grade is determined by the non-squamous glandular/solid component.

A solid fraction at or below one-half is compatible with grade 2 if a substantial solid component is present.

Squamous foci are excluded from grading.

Exact grading may require evaluation of the full sampled tumor.

Slide 70 · Application case: Mismatch repair result

Illustrative teaching vignette

An endometrioid carcinoma is found to lack expression of a mismatch repair protein on tumor testing. The clinical team asks whether Lynch syndrome is established.

Why is a tumor MMR abnormality not automatically a hereditary diagnosis?

Slide 71 · Case analysis: Sporadic versus inherited MMR loss

A shared tumor phenotype can have distinct causes.

Abnormal MMR testing indicates a repair-deficient tumor phenotype.

MLH1 silencing through promoter methylation is a common sporadic cause.

Lynch syndrome is a separate inherited predisposition involving MMR genes.

Appropriate downstream evaluation is needed; Tumor results alone do not specify inheritance.

Slide 72 · Integrated morphology-to-mechanism recap

Observed feature

Mechanistic or interpretive link

Atypical gland crowding

Clonal precursor lesion may precede carcinoma

Confluent glands / desmoplasia

Supports carcinoma rather than simple atypical hyperplasia

Progressively solid architecture

Reduced glandular differentiation and increased grade

Many infiltrating T cells

May accompany MMR-deficient or POLE-altered tumors

Myometrial invasion

Greater anatomic disease extent

Slide 73 · Five conclusions to retain

Integrate the precursor, molecular, and morphologic narratives.

Most endometrial carcinomas are endometrioid and often related to hyperplasia.

Unopposed estrogen and convergent PI3K/AKT alterations provide mechanistic context.

MMR, POLE, and p53 alterations distinguish biologically important molecular patterns.

Histologic grade reflects glandular versus solid growth; Squamous areas do not count.

Stage, grade, and subtype influence prognosis; Biopsy establishes diagnosis.

Slide 74 · Selected reading and source scope

Primary textbook

Robbins, Cotran & Kumar: Pathologic Basis of Disease. 11th edition (2026). Chapter 22, The Female Genital Tract.

Read in context

Endometrial hyperplasia; carcinoma of the endometrium; endometrioid and serous carcinoma; grading and clinical features in adjacent text.

Scope of this lecture

Textbook-based histopathology and pathogenesis; not an updated FIGO staging or treatment guideline.