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This chapter should be cited as follows:
Ching SOH, Ip PPC, Glob Libr Women's Med
ISSN: 1756-2228; DOI 10.3843/GLOWM.421963

The Continuous Textbook of Women’s Medicine Series – Gynecology Module

Volume 13

Gynecological cancer

Volume Editors: Professor Hextan Ngan, Department of Obstetrics and Gynaecology, The University of Hong Kong, Hong Kong
Professor Karen Chan, Department of Obstetrics and Gynaecology, The University of Hong Kong, Hong Kong

Chapter

Endometrial Cancer Pathology

First published: May 2026

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INTRODUCTION

Endometrial carcinoma is one of the commonest gynecologic cancers in high-income countries,1,2,3,4 with the highest incidence being in North America.5 Traditionally, it has been classified into histological subtypes based on morphology, as reflected in the World Health Organization (WHO) Classification of Tumours.6 In a landmark paper published in 2013 in Nature, The Cancer Genome Atlas (TCGA) proposed a new molecular classification with prognostic significance,7 which has gradually been incorporated into clinical practice.

EPIDEMIOLOGY

The peak incidence of endometrial carcinoma occurs in the 7th to 8th decades.2 The worldwide incidence has increased by over 130% in the past 30 years,5 with largest increase observed in South Africa and several countries in Asia.3 The disease-associated mortality in the USA is rising by an average of 2.5% annually.4,8

The major risk factors for endometrial carcinoma include conditions associated with estrogen excess, such as obesity, endogenous estrogen exposure from early menarche and polycystic ovarian syndrome, chronic anovulation, late menopause, exogenous estrogen replacement therapy and tamoxifen therapy.2,5 Patients with genetic syndromes, including Lynch syndrome and Cowden syndrome, also have increased risk for endometrial carcinomas.5 High-grade carcinomas are associated with lower body mass index (BMI), parity, African ethnicity and a personal history of breast cancer.2

CLINICAL FEATURES

The commonest presentation is abnormal uterine bleeding, including postmenopausal bleeding. The prevalence of post-menopausal bleeding among patients with endometrial cancer is around 90%.9 Most patients are diagnosed at an early stage when disease is confined to the uterus. Advanced disease may present with pelvic or abdominal symptoms resembling those of ovarian carcinoma, including pelvic or abdominal pain and a mass lesion,2,10 and they may present with distant metastases.10

CLASSIFICATION OF ENDOMETRIAL CARCINOMAS

Historically, endometrial carcinoma was classified into two distinct types. Type I was estrogen-related, occurred in obese or metabolically disturbed women and was histologically low-grade, with a favorable prognosis. In contrast, Type II was usually not associated with estrogen, occurred in non-obese women with atrophic endometrium and included high-grade histologies such as serous and clear cell carcinomas, with a poorer prognosis.10 However, these categories show significant overlap in clinical, pathological and molecular features, and the histological diagnosis of high-grade carcinomas shows considerable interobserver variability.11,12 As such, classification of endometrial carcinomas according to these two subtypes is no longer recommended as a formal classification system. In the ensuing decades, endometrial carcinomas were classified primarily according to microscopic architecture and cellular features,13,14 which formed the basis of the first four editions of the World Health Organization (WHO) Blue Books published in 1973,15 1994,16 200317 and 2014.18 Diagnostic entities in the current, 5th edition of the WHO Classification of Female Genital Tumours are primarily histology-based, with incorporation of biomarker expression, and include:10

  • Endometrioid carcinoma
  • Serous carcinoma
  • Clear cell carcinoma
  • Undifferentiated and dedifferentiated carcinomas
  • Mixed carcinoma
  • Other endometrial carcinomas (mesonephric-like adenocarcinoma, squamous cell carcinoma and mucinous carcinoma (gastrointestinal type))
  • Carcinosarcoma

In the forthcoming 6th edition of the WHO Classification of Female Genital Tumours, in the chapter on epithelial tumors of the uterine corpus, mesonephric-like adenocarcinoma will be recognized as a standalone entity.

The histology-based diagnostic entities often share overlapping microscopic features and may result in considerable interobserver diagnostic variability. More importantly, they do not provide information on biological behavior or precise prognosis, which is essential to treatment. These will be explained in detail in the following sections.

HISTOPATHOLOGICAL GRADING

Grading is prognostically significant for endometrioid carcinomas and is conducted according to the International Federation of Gynecology and Obstetrics (FIGO) system. A grade is assigned by determining the percentage of non-squamous and non-morular solid glandular components.19 The presence of severe cytological atypia in more than 50% of tumor cells raises the grade by one level.

Historically, the system has been three-tiered:20,21

  • Grade 1: tumors with ≤ 5% solid growth
  • Grade 2: tumors with 6–50% solid growth
  • Grade 3: tumors with > 50% solid growth

A binary grading system has now been adopted, in which Grade 1 and 2 tumors are classified as low-grade, and Grade 3 as high-grade.19 This updated system has demonstrated similar or improved prognostic performance and interobserver reproducibility.19,21 A three-tier grading system remains relevant in the setting of endometrial biopsies from women who wish to remain fertile. Non-endometrioid carcinomas, including serous, clear cell, undifferentiated and dedifferentiated carcinoma, carcinosarcoma, mesonephric-like carcinoma, neuroendocrine carcinoma, endometrial carcinoma with somatically derived germ cell components, gastric (gastrointestinal)-type endometrial carcinoma, and pilomatrix-like high-grade endometrioid carcinoma are considered high-grade tumors, by definition.

MOLECULAR CLASSIFICATION

Based on genomic characterization, endometrial cancers are classified into four groups: POLE ultramutated (good prognosis), mismatch repair (MMR) deficient (microsatellite instability hypermutated, intermediate prognosis), no specific molecular profile (low–copy-number alterations, intermediate prognosis) and p53 abnormal (high–copy-number alterations, poor prognosis)7,10 (Figure 1). This approach enables better prognostication22 (Figure 2), especially in high-grade (Grade 3) endometrial carcinomas,23 and has been endorsed by the International Society of Gynecological Pathologists21,24 (Table 1) (Figure 3).

1

Histological features of endometrial carcinoma according to molecular subtypes. (A) Low-grade endometrioid carcinoma, no specific molecular profile (NSMP). The columnar tumor cells form back-to-back crowded glands with wide-open lumens and a smooth luminal border. (B) p53 abnormal endometrial serous carcinoma. Complex papillary structures covered by highly stratified tumor cells and forming slit-like spaces between them. (C) POLE-ultramutated low-grade endometrioid carcinoma. This tumor is histologically indistinguishable from other low-grade endometrioid carcinomas of other molecular subtypes. (D) POLE-ultramutated high-grade endometrioid carcinoma. Solid sheets of tumor cells with severe nuclear pleomorphism. (E) Mismatch repair-deficient low-grade endometrioid carcinoma. There is a striking lymphocytic infiltrate at the tumor infiltrating front. (F) Endometrioid carcinoma, NSMP, with extensive lymphovascular space invasion. Tumor glands admixed with fibrin and red blood cells are found inside clear spaces lined by endothelial cells. Scale bar represents 100 μm.

2

Kaplan–Meier survival curves of four molecular subtypes of endometrial carcinoma. POLE-ultramutated endometrial carcinoma (POLE EC) has excellent prognosis, in contrast to p53 abnormal endometrial carcinoma (CNH EC), which has the worse outcome. Mismatch repair-deficient endometrial carcinoma (MSI EC) and endometrial carcinoma of no specific molecular profile (CNL EC) have intermediate prognosis. Data generated from publicly available data of 373 endometrial cancer samples from TCGA Program.25

1

Molecular classification according to The Cancer Genome Atlas (TCGA).

Subtype

Prevalence

Molecular features

Histological features

Prognosis

POLE ultramutated

5–10% of endometrioid carcinomas7

  • POLE gene encodes DNA polymerase epsilon, which is responsible for DNA proofreading and replication26
  • Mutation in exonuclease domain causes defect in proofreading, leading to increased mutations (ultramutated)27
  • Architectural, cytological and immunohistochemical heterogeneity
  • Eosinophilic cytoplasmic change, scattered bizarre nuclei and increased tumor-infiltrating lymphocytes or peritumoral lymphocytes28,29

Associated with good prognosis7

Mismatch repair (MMR) deficient

Around 1/3 of endometrioid carcinomas,7 associated with Lynch syndrome in 3% of cases30

  • Mutations or epigenetic changes of DNA mismatch repair genes (more commonly related to MLH1 hypermethylation, less frequently to MSH2, MSH6 or PMS2 silencing)
  • Deficiency in DNA mismatch pathway leads to high level of genetic mutations (hypermutated)31
  • Subclonal loss of MMR protein expression (loss in discrete areas with retained expression among adjacent tumor cells) may be associated with POLE mutation, MLH1 promoter hypermethylation32,33
  • Also associated with increased tumor-infiltrating lymphocytes or peritumoral lymphocytes,34 but the features tend to be less well developed
  • Associated with high-risk features including advanced stage and larger tumor size
  • Intermediate prognosis, worse survival rate for MLH1 methylated carcinomas

p53 abnormal

Around 10% of endometrioid carcinomas7

  • Alterations of TP53 gene (tumor suppressor gene)
  • Abnormal patterns on p53 immunohistochemistry include overexpression (> 90% of tumor cells), absence of cytoplasmic and nuclear staining, or cytoplasmic staining only35
  • Associated with increase in copy number alterations (copy number-high)7
  • High-grade cytological features with marked pleomorphism, non-serous carcinoma cases may resemble serous carcinoma (histologic ambiguity)12,36
  • A minority show mild cytologic atypia only37

Poor prognosis7

No specific molecular profile (NSMP)

50–70% of endometrioid carcinomas7

  • Diffuse and strong expression of estrogen receptor (ER) found in 90% of carcinomas38
  • Mainly low-grade (Grade 1–2) cancers,39 showing mixed glandular and solid architecture, morules are more commonly seen

Intermediate prognosis7

3

International Society of Gynecological Pathologists’ recommendation for molecular classification of endometrial carcinoma achieved through molecular analysis for POLE hotspot mutations, mismatch repair deficient immunohistochemistry or microsatellite instability testing, and p53 immunohistochemistry.24

Approximately 5% of tumors possess more than one molecular feature (e.g. POLE ultramutated and p53 abnormal, or MMR deficient and p53 abnormal) and are considered multiple classifiers, and these generally retain the expected prognosis associated with POLE or MMR deficiency, respectively.40


HISTOPATHOLOGICAL TYPES OF ENDOMETRIAL CARCINOMA

Endometrioid carcinoma of the uterine corpus

Endometrioid carcinoma is the most common type, accounting for approximately 80% of cases.41 It is typically preceded by endometrial atypical hyperplasia, which shares similar molecular alterations, and is associated with prolonged exposure to unopposed estrogen.10 Macroscopically, tumors may be exophytic or diffusely infiltrative, with areas of necrosis and hemorrhage.

Histologically, common architectural patterns include confluent glandular, cribriform and complex papillary structures. The neoplastic glands tend to have smooth luminal contours lined by columnar cells.42 Most tumors typically have mild to moderate nuclear atypia, enlarged and round nuclei, coarse chromatin and prominent nucleoli (Figures 1A, C and D). When a tumor is architecturally low grade, but the tumor cells have severe nuclear atypia, further investigations are crucial to exclude an aggressive endometrial carcinoma.37 Presence of mitotic figures is not a diagnostic feature of malignancy. Similar to non-neoplastic endometrium, a variety of metaplastic changes are observed in endometrioid carcinoma. They include syncytial papillary change, secretory change, hobnail, eosinophilic, ciliated cell, tubal, mucinous, morular and squamous metaplasias.10

Serous carcinoma of the uterine corpus

Serous carcinomas constitute about 10% of endometrial carcinomas but account for 40% of recurrent cases and deaths.43 Most patients present with postmenopausal vaginal bleeding, and approximately 40–50% of patients develop extrauterine metastases in surgically staged cases.43,44 They are associated with personal history of breast cancer, tamoxifen use45 and pelvic irradiation,46 with possible association with germline BRAC1/2 mutations.47 The hallmark molecular feature is TP53 mutations,7 leading to inactivation of the tumor suppressor gene.48 It is important to note that not all endometrial carcinomas with TP53 mutations are classified as serous carcinomas. Histologically, endometrioid carcinoma, including low-grade endometrioid carcinoma, clear cell carcinoma and carcinosarcoma may also harbor TP53 mutations.37,49,50,51

Serous carcinomas often arise in atrophic endometrium or endometrial polyps of postmenopausal women.44 Tumor cells form complex papillary or glandular structures, with irregular, elongated glands and slit-like luminal spaces. Cytological atypia and nuclear pleomorphism is usually significant (Figure 1B). Multinucleation and calcifications are identified in some serous carcinomas.52

Localized disease has a relatively better prognosis, but cases with extrauterine metastases (including those with coexistent serous endometrial intraepithelial carcinoma and minimally invasive disease) have poorer outcomes with increased risk of death.44 HER2 overexpression/gene amplification occurs in 25–30% of cases,53 and the addition of trastuzumab (anti-HER2 antibody) in combination with conventional chemotherapy regimen has been shown to improve survival in HER2-positive serous carcinoma of the uterine corpus.54

Clear cell carcinoma of the uterine corpus

Accounting for < 10% of endometrial carcinomas,55 clear cell carcinomas have no distinct specific molecular profile but show considerable overlap with endometrioid and serous carcinomas.56,57

Clear cell carcinomas are characterized histologically by tubulocystic, papillary and solid architectures, with short, rounded papillae often associated with hyalinized stroma.49,58,59 The neoplastic cells commonly display cuboidal, flat, polygonal or hobnail morphology with clear to eosinophilic cytoplasm. They show variable nuclear pleomorphism, typically with at least focal areas with moderate to severe nuclear atypia. Frequent nuclear stratification, cellular tufting and detached budding are absent or, at most, focally found.58,59 Mitotic activity is variable (Figure 4A). As other types of high-grade endometrial carcinoma may contain clear cells, strict adherence to architectural and cytological criteria for diagnosis is important for accurate diagnosis.59,60 On immunohistochemistry, the tumor cells are positive for Napsin A (56–93%) and AMACR (75–88%),49 and ER and PR are negative or only focally expressed.59 The four markers should be used as a panel as non-specific staining may occur with Napsin A.

4

Histological features of clear cell carcinoma, dedifferentiated carcinoma and carcinosarcoma. (A) Clear cell carcinoma of the uterus is identical to its ovarian counterpart. In the tubulocystic pattern, the lining epithelium is an admixture of hobnail and clear cells. (B) Dedifferentiated endometrial carcinoma contains a component of well-formed glands juxtaposed to discohesive sheets of epithelioid carcinoma cells (seen in left part of image). (C) Carcinosarcoma is composed of a high-grade adenocarcinoma and malignant spindle cells (seen in right part of image). Scale bar represents 100 μm.

The 5-year survival rate for clear cell carcinomas ranges from 55% to 79%.49 All four molecular subgroups are represented in clear cell carcinoma, with NSMP and p53-abnormal subgroups being more common.50,57 Older age and advanced stage correlate with poorer prognosis,58 and patients with MMR-deficient tumors tend to have better survival rate.61

Mesonephric-like carcinoma of the uterine corpus

A rare type of tumor, there is a paucity of epidemiological data for mesonephric-like carcinoma of the uterine corpus. Most patients are postmenopausal, and > 50% of cases are diagnosed at advanced stage (FIGO Stage II–IV).62,63 They share histological and immunohistochemical similarities with mesonephric and mesonephric-like carcinomas located elsewhere in the female genital tract.64,65 Mesonephric ducts are embryonic tubes that develop into the male reproductive organs; they regress in females during embryonic development, and remnants of these ducts may be located along the lateral walls of the vagina, cervix and adnexal structures.66 Despite their name, they are mostly likely of Müllerian origin and acquired mesonephric-like phenotype subsequently.67

Common architectural growth of mesonephric-like carcinomas include tubular, ductal, papillary, retiform, spindled and solid patterns, commonly with an admixture of different patterns in the same tumor.65 Eosinophilic colloid-like material may be identified in the luminal spaces. The tumor cells may display nuclear features resembling papillary thyroid carcinoma, including open chromatin and nuclear grooves.68 On immunohistochemistry, these tumors are positive for GATA3, TTF1 and CD10, with apical luminal staining in tubules.66 The extent of staining of these three markers is variable and morphology remains important. Mesonephric-like carcinoma usually shows minimal or absent expression of ER and PR, and wild-type expression of p53.64,68 They also demonstrate mismatch repair proficiency.69 Compared with other endometrial carcinomas, mesonephric-like carcinomas are more aggressive, with shorter progression-free survival (18.2 months vs 183 months for low-grade endometrioid carcinoma and 67.1 months for uterine serous carcinoma) and a higher risk of distant metastasis, including lung metastasis.68

Undifferentiated and dedifferentiated carcinomas of the uterine corpus

Undifferentiated carcinoma is defined as malignant epithelial neoplasm lacking overt lineage differentiation. Dedifferentiated carcinoma features both undifferentiated carcinoma and differentiated components.70 They account for 2% of endometrial carcinomas.70 More than half of patients with carcinomas containing undifferentiated components present at an advanced stage (Stage III–IV).71 A possible association with mismatch repair deficiency and Lynch syndrome has been suggested.72 Inactivating mutations involving chromatin remodeling genes (SMARCA4, SMARCB1, ARID1A and ARID1B) are found in two-thirds of dedifferentiated carcinomas and in half of undifferentiated carcinomas.73,74

The common histological features of undifferentiated carcinoma include solid growth with no nesting, glandular or trabecular architecture.75 The tumor cells are typically arranged in discohesive sheets with high mitotic activity. Rhabdoid morphology and focal myxoid matrix may be present.70 Dedifferentiated carcinoma consists of undifferentiated carcinoma and a differentiated component, most commonly low-grade endometrioid carcinoma (Figure 4B), though some cases are associated with high-grade endometrioid or serous carcinoma.76,77 A key differential diagnosis is high-grade endometrioid carcinoma, which may also show solid growth.70 Immunohistochemically, the undifferentiated carcinoma component in > 80% of tumors shows loss of epithelial and Müllerian differentiations, and is characterized by loss of or reduced expression in one or more cytokeratins and PAX-8;75 there is usually loss of E-cadherin staining, and mismatch repair proteins are lost in > 50% of cases.75,76 Abnormal overexpression of p53 is seen in 15–31% of cases.75,77 Loss of expression of SMARCA4 (BRG1), SMARCB1 (INI1), ARID1A or ARID1B occurs in approximately two-thirds of cases.77,78

Undifferentiated and dedifferentiated carcinomas are generally highly aggressive, with 55–95% of cases developing recurrence or resulting in death.70 Tumors with POLE hotspot mutations tend to have a more favorable prognosis, while those with mismatch repair deficiency have an intermediate outcome.78,79

Mixed carcinoma of the uterine corpus

Mixed carcinoma refers to endometrial carcinomas composed of two or more histological types, with at least one component being serous, clear cell or mesonephric-like.80 It is an uncommon tumor81 and large-scale epidemiological data are lacking. These tumors typically arise from progression or divergence from low-grade endometrioid carcinoma with a shared clonal origin.82,83 They often show mismatch repair protein deficiency84 and POLE hotspot mutations.85,86

Histologically, the different types must be spatially distinct, and variants of other endometrial carcinoma types or carcinosarcoma should be excluded before diagnosing mixed carcinoma.51,80 The most common combination is endometrioid and serous carcinoma, followed by endometrioid and clear cell carcinoma.80 A small proportion of serous or clear cell carcinoma within a mixed carcinoma may indicate an adverse prognosis.87,88 Any percentage of high-grade carcinoma that fits the histological and immunohistochemical features, admixed with low-grade endometrioid carcinoma, should be reported; such tumors are classified as mixed endometrial carcinoma.

The prognosis of mixed carcinoma is poorer than that of pure low-grade tumors, regardless of the percentage of high-grade component.88,89 They are graded as high-grade endometrial carcinomas. It remains uncertain whether mixed carcinomas confer a better prognosis than pure high-grade carcinomas.90,91 Cases with mismatch repair deficiency or POLE hotspot mutations are potentially associated with better prognosis.86

Other endometrial carcinomas

Primary endometrial squamous cell carcinoma

Primary endometrial squamous cell carcinoma is defined as endometrial carcinoma with exclusive squamous differentiation and no endometrioid component.65 It comprises < 1% of endometrial carcinomas and commonly occurs in postmenopausal women (average age, 67 years).92,93,94 It may be associated with chronic pyometra, nulliparity and ichthyosis uteri (keratinizing squamous metaplasia of endometrium), which may occur in the setting of uterine prolapse, pelvic radiotherapy or cervical stenosis.91 Most cases are not related to human papillomavirus.92,93,94 TP53 alterations may be identified. The histological features include infiltrating nests of squamous cells with keratinization; extensive sampling is required to exclude an underlying endometrioid carcinoma component.93 The prognosis is reported to be poor based on limited data.93,95

Gastric (gastrointestinal)-type endometrial carcinoma

Gastric (gastrointestinal)-type endometrial carcinoma exhibits gastric/gastrointestinal differentiation without a definite endometrioid component.65 Most cases occur in postmenopausal women (median age, 69 years),96,97 and > 60% are classified as p53-abnormal molecular subgroup.97 Clinical presentation may include mucoid vaginal discharge.96 The tumor typically shows gastrointestinal differentiation by histology (e.g. goblet cells, mucin pools and signet ring cells), and typical endometrioid glands should be absent.96,97,98 The background endometrium may display gastric-type mucinous metaplasia, which is a postulated precursor lesion.96,97,98 Diagnosis may be made when there is expression of neutral mucin as demonstrated by combined alcian blue-PAS stain, and immunohistochemistry including expression of HIK-1083, claudin 18.2, and loss of both ER and PR. This type of carcinoma is reported to behave aggressively, even at early stages with low-grade morphology, although no direct comparison with other types of endometrial carcinoma are available.96,97,98

Endometrial carcinoma with features resembling yolk sac tumors or choriocarcinomas

Endometrial carcinoma with features resembling yolk sac tumors or choriocarcinomas (or other germ cell/trophoblastic tumors) are classified as 'endometrial carcinoma with somatically derived germ cell/trophoblastic component'.65 These are rare (≤ 1%) and typically occur in postmenopausal women.99,100,101,102 Elevated serum alpha-fetoprotein (AFP) or human chorionic gonadotropin (hCG) may be seen.99,102 The germ cell or trophoblastic component share similar genetic mutations with Müllerian-type carcinomas, indicating a somatic origin.99,100 Histologically, the yolk sac component is commonly glandular or papillary, solid, reticular, microcystic or hepatoid, and commonly associated with extracellular basement membrane-like material. The cells lining glands and papillae are tall and columnar, and contain subnuclear and/or supranuclear cytoplasmic vacuoles (resembling primitive endoderm), irregular and enlarged nuclei with vesicular chromatin and prominent nucleoli. Cells in the reticular and solid patterns and those forming Schiller-Duval bodies, have a blastemal appearance and are characterized by a high nuclear/cytoplasmic ratio, with small, dark and hyperchromatic nuclei. The choriocarcinoma component is recognized by a bilaminar growth pattern of cytotrophoblasts and syncytiotrophoblastic giant cells. The background Müllerian type endometrial carcinoma may be endometrioid, serous, clear cell, dedifferentiated carcinomas or carcinosarcoma. Rare cases of pure germ cell or trophoblastic tumors may represent overgrowth of their pre-existing Müllerian type carcinoma.100,101,102 These tend to be aggressive and respond poorly to treatment.100 Recently, endometrial carcinoma with somatically derived yolk sac components have been shown to belong primarily to p53 abnormal molecular subgroup (> 70%), with smaller numbers as mismatch repair deficient and NSMP subgroups.102 Demonstration of HER2 overexpression in these tumors may provide an additional therapeutic option.102

Neuroendocrine carcinoma of the endometrium

Neuroendocrine carcinoma of the endometrium is characterized by features of small cell carcinoma.65 It accounts for < 1% of endometrial carcinomas,103 in women with a median age of 57 years.104 It may present with paraneoplastic syndrome such as retinopathy105 and Cushing syndrome due to ectopic ACTH secretion.106 The molecular profile is similar to that of conventional endometrial carcinomas, supporting a non-neuroendocrine origin.103,107 Histologically, these tumors resemble small cell neuroendocrine carcinomas of other organs, and often with a component of conventional endometrial carcinoma.103,104,107 Neuroendocrine markers (e.g. synaptophysin and chromogranin) should be present in at least 10% of tumor cells.65 This histotype is associated with a poor prognosis, with median survival around 17 months and 5-year survival of approximately 38%.108 Pure neuroendocrine carcinoma has a worse prognosis than that of mixed cases.109

Pilomatrix-like high-grade endometrioid carcinoma (PiMHEC)

Pilomatrix-like high-grade endometrioid carcinoma (PiMHEC) is a recently described, aggressive subtype of endometrial carcinoma. It affects postmenopausal women and is often at advanced FIGO stage at presentation. Histologically, the high-grade carcinoma comprises solid sheets or nests of basaloid to squamoid cells with severe pleomorphism, frequent mitoses and striking tumor necrosis. The defining feature is the presence of abundant ghost or shadow cells with keratinization closely mimicking cutaneous pilomatrix carcinoma. This tumor is often admixed with a low-grade endometrioid carcinoma. These tumors show reduced or loss of ER, PR and PAX8, and diffuse nuclear b-catenin expression. Most PiMHEC harbor CTNNB1 exon 3 mutations.110,111,112

Carcinosarcoma of the uterine corpus

Carcinosarcomas are defined as biphasic tumors with components of both high-grade carcinoma and sarcoma.51 They comprise approximately 5% of endometrial cancers, and most cases occur in postmenopausal women.113 Tamoxifen-related carcinosarcomas account for approximately 8% of uterine carcinosarcomas.114,115 Carcinosarcomas have also been reported as a potential long-term complication (> 5 years) following pelvic irradiation.116 The carcinomatous and sarcomatous components share similar genetic mutations, indicating a common cell of origin,117,118 with epithelial-mesenchymal transition playing a role;119 TP53 alterations are identified in 90% of cases117,118 and most cases are classified as p53-abnormal molecular subtype.

An admixture of malignant epithelial and mesenchymal components is characteristic of carcinosarcomas (Figure 4C). The carcinomatous component typically features endometrioid or serous differentiation, while the mesenchymal component is usually a high-grade sarcoma, with occasional heterologous differentiation (including rhabdomyosarcoma, chondrosarcoma and, rarely, osteosarcoma).51,118 Most (> 90%) metastases consist of carcinoma or carcinosarcoma, rather than pure sarcoma.118

The diagnosis of carcinosarcomas confers a poorer prognosis, as these tumors account for 30% of uterine cancer deaths.120 Early-stage disease (FIGO Stage I–II) shows a disease-specific survival rate of about 60% at 5 years, which decreases to less than 25% and 10% for Stages III and IV, respectively.121 The p53-abnormal and NSMP molecular subtypes are associated with worse prognosis, while POLE-ultramutated carcinomas tend to have excellent prognosis.122,123

BIOMARKER TESTING

Biomarker testing in endometrial carcinoma plays an important role in classification and determination of prognosis and treatment response7 The principal biomarkers and current recommendations for their use are detailed in Table 2. Figure 5 provides examples of immunohistochemical staining of these biomarkers.

2

Biomarkers for endometrial cancers.

Biomarker

Clinical implication

Current recommendation

Hormone receptor: ER and PR 

Expression predicts better prognosis in endometrioid carcinomas124,125,126

Current NCCN guidelines recommend testing for ER and PR status in cases of advanced stage (Stage III–IV) or recurrent endometrioid endometrial carcinomas127

HER2 (human epidermal growth factor receptor 2)

HER2 protein overexpression is identified in approximately 35% of p53-abnormal endometrial carcinomas;128 to identify patients who may benefit from anti-HER2 agents

HER2 testing recommended by NCCN guidelines in cases with p53-abnormal endometrial carcinomas127

MMR (mismatch repair) proteins: MLH1, MSH2, MSH6, PMS2

MMR-deficient tumors are more responsive to immune checkpoint inhibitor (dostarlimab or pembrolizumab) combined with standard chemotherapy129

MMR immunohistochemistry testing is included in the diagnostic algorithm for molecular classification, as recommended by WHO,130 FIGO,19 CAP35and ESGO/ESTRO/ESP131 guidelines; MLH1 promotor methylation status may be performed in case of MLH1/PMS2 deficiency, and Lynch syndrome screening should be performed if no hypermethylation of MLH1 is found or in case of strong family history131

p53 protein (encoded by TP53)

Mutations are associated with the copy number–high molecular subtype, which has a poor prognosis;7 combined adjuvant chemotherapy and radiotherapy are recommended132

p53 testing is part of molecular classification, suggested by WHO, FIGO and ESGO/ESTRO/ESP19,130,131

PD-L1

Expression predicts better response to immune checkpoint inhibitors133

PD-L1 may be considered in cases with normal MMR status35

CAP, College of American Pathologists; ER, estrogen receptor; FIGO, International Federation of Gynecology and Obstetrics; ESGO, European Society of Gynaecological Oncology; ESP, European Society of Pathologists; ESTRO, European Society of Radiotherapy and Oncology; NCCN, National Comprehensive Cancer Network; PR, progesterone receptor; WHO, World Health Organization.

5

Immunohistochemistry of endometrial carcinoma biomarkers. (A) Loss of MLH1 nuclear staining in the tumor cells with intact expression in background stromal cells. (B) Intact nuclear expression of MSH2 in tumor cells. (C) Heterogeneous weak-to-moderate nuclear staining consistent with wild-type p53 expression. (D) Abnormal diffuse p53 overexpression in > 90% of tumor cell nuclei. (E) Abnormal null pattern of p53 with absence of nuclear staining in tumor cells and retained staining in background stromal cells. (F) Basolateral and circumferential membranous staining for HER2 (score 3+). Scale bar represents 100 μm.

STAGING

Endometrial carcinomas are staged according to the Union for International Cancer Control (UICC) TNM Classification (published in 2017) or FIGO staging.10 The latter was updated in 2023 (Appendix 1),19 replacing the staging system proposed in 2009 (Appendix 2).134

Stage-I and -II tumors represent tumors confined to the uterus and cervical stroma (except Stage IA3). Stage-III tumors show locoregional spread, while Stage-IV tumors involve spread to mucosa of non-gynecological organs and/or distant metastases.19 Changes from the 2009 FIGO staging system include the integration of molecular classification; notably, the status of POLE and p53 mutations influences prognosis for tumors confined to the uterine corpus. Tumors with POLE mutation are classified as Stage IAmPOLEmut, while those with abnormal p53 status are assigned a high stage (Stage IICmp53abn).19

Pathological parameters essential for staging, applicable to all endometrial carcinomas include:

  • Histological type: tumors are classified into non-aggressive types (Grade 1 and 2 endometrioid endometrial carcinomas) and aggressive types (serous, clear cell, undifferentiated and dedifferentiated carcinoma, carcinosarcoma, mesonephric-like carcinoma, neuroendocrine carcinoma, endometrial carcinoma with somatically derived germ cell components, gastric/gastrointestinal-type endometrial carcinoma, high-grade endometrioid carcinoma and pilomatrix-like high-grade endometrioid carcinoma)
  • FIGO histological grade: low (FIGO Grades 1 and 2) and high (FIGO Grade 3)
  • Myometrial invasion: ≥ 50% myometrial invasion is a prognostic risk factor135
  • Lymphovascular space invasion (LVSI): should be assessed at the invasive front;19,136,137 substantial LVSI (defined by ≥ 5 LVSI) and cervical/endocervical LVSI are associated with worse survival compared to focal LVSI (< 5 LVSI)137
  • Lower uterine segment involvement: linked to higher risk of distant metastasis or death;136,138 patients with Lynch syndrome more frequently have involvement of this segment139
  • Cervical stromal invasion: defined as tumor destruction of endocervical fibrous stroma 
  • Adnexal involvement: synchronous low-grade tumors of the endometrium and ovary are associated with good prognosis;10,140 Stage IA3 is reserved for low-grade synchronous endometrioid carcinoma composed of unilateral ovarian tumor without capsular extension, and endometrial tumor without deep (≥ 50%) myometrial invasion, substantial LVSI or additional metastases19
  • Uterine serosal involvement (a Stage IIIA2 disease)
  • Lymph node status: sentinel lymph node ultrastaging (sectioning of lymph node in 2 mm intervals) is recommended
  • Molecular subtypes

CONCLUSION

Endometrial cancer is a common malignancy with rising incidence, particularly among postmenopausal women. Advances in histological and molecular classification have improved prognostic stratification, aiding therapeutic decision-making.141 Ongoing research aims to discover new, clinically significant biomarkers, and refining staging systems that are globally applicable.

PRACTICE RECOMMENDATIONS

  • Incorporating histological and molecular features into endometrial carcinoma classification improves diagnostic accuracy and prognosis prediction in regions with available resources.10
  • Molecular classification can alter the management of endometrial carcinomas.21
  • A binary grading system is recommended for biopsy and curettage specimens when surgical staging is planned; distinguishing Grades 1 and 2 remains important for fertility-sparing therapeutic approaches.21
  • Patients diagnosed with mismatch repair-deficient endometrial carcinoma should proceed to MLH1 promoter methylation if there is MLH1 and PMS2 loss on immunohistochemistry. In the absence of MLH1 promoter hypermethylation, patients should be referred to counseling for Lynch syndrome screening.24,138
  • Biomarker testing should include ER, PR, p53, MLH1, MSH2, MSH6, and PMS2. HER2 should be added to p53-abnormal endometrial carcinoma, and scoring should be done according to the most recent College of American Pathologists guidelines.35


CONFLICTS OF INTEREST

The author(s) of this chapter declare that they have no interests that conflict with the contents of the chapter.

APPENDIX 1

2023 FIGO staging of cancer of the endometrium19

Stage

Description

Stage I

Confined to the uterine corpus and ovary


IA

Disease limited to the endometrium OR non-aggressive histological type, i.e. low-grade endometrioid, with invasion of less than half of myometrium with no or focal lymphovascular space involvement (LVSI) OR good prognosis disease



IA1

Non-aggressive histological type limited to an endometrial polyp OR confined to the endometrium



IA2

Non-aggressive histological types involving less than half of the myometrium with no or focal LVSI



IA3

Low-grade endometrioid carcinomas limited to the uterus and ovarya


IB

Non-aggressive histological types with invasion of half or more of the myometrium, and with no or focal LVSI


IC

Aggressive histological types limited to a polyp or confined to the endometrium

Stage II

Invasion of cervical stroma without extrauterine extension OR with substantial LVSI OR aggressive histological types with myometrial invasion


IIA

Invasion of the cervical stroma of non-aggressive histological types


IIB

Substantial LVSI of non-aggressive histological types


IIC

Aggressive histological types with any myometrial involvement

Stage III

Local and/or regional spread of the tumor of any histological subtype


IIIA

Invasion of uterine serosa, adnexa or both by direct extension or metastasis



IIIA1

Spread to ovary or Fallopian tube (except when meeting Stage IA3 criteria)a



IIIA2

Involvement of uterine subserosa or spread through the uterine serosa


IIIB

Metastasis or direct spread to the vagina and/or to the parametrium or pelvic peritoneum



IIIB1

Metastasis or direct spread to the vagina and/or the parametrium



IIIB2

Metastasis to the pelvic peritoneum


IIIC

Metastasis to the pelvic or para-aortic lymph nodes or bothb



IIIC1

Metastasis to the pelvic lymph nodes




IIIC1i

Micrometastasis




IIIC1ii

Macrometastasis



IIIC2

Metastasis to para-aortic lymph nodes up to the renal vessels, with or without metastasis to the pelvic lymph nodes




IIIC2i

Micrometastasis




IIIC2i

Macrometastasis

Stage IV

Spread to the bladder mucosa and/or intestinal mucosa and/or distant metastasis


IVA

Invasion of the bladder mucosa and/or the intestinal/bowel mucosa


IVB

Abdominal peritoneal metastasis beyond the pelvis


IVC

Distant metastasis, including metastasis to any extra- or intra-abdominal lymph nodes above the renal vessels, lungs, liver, brain, or bone

  • Disease limited to low-grade endometrioid carcinomas involving the endometrium and ovaries (Stage IA3) should fulfill the following criteria:
    • no more than superficial myometrial invasion (< 50%)
    • absence of extensive/substantial LVSI
    • absence of additional metastases
    • the ovarian tumor is unilateral, limited to the ovary, without capsule invasion/rupture (equivalent to pT1a).
  • Micrometastasis: > 2 mm in size; macrometastasis (0.2–2 mm and/or > 200 cells)

FIGO endometrial cancer stage with molecular classification19

Stage 

Molecular findings in patients with early endometrial cancer (Stages I and II after surgical staging)

Stage IAmPOLEmut

POLEmut endometrial carcinoma, confined to the uterine corpus or with cervical extension, regardless of the degree of LVSI or histological type

Stage IICmp53abn

p53abn endometrial carcinoma confined to the uterine corpus with any myometrial invasion, with or without cervical invasion, and regardless of the degree of LVSI or histological type

APPENDIX 2

Revised FIGO 2009 staging system134

Stage

Description

Stage I

Tumor confined to the uterine corpus 


IA

No or less than half myometrial invasion


IB

Invasion to or more than half of the myometrium

Stage II

Tumor invades cervical stroma, but does not extend beyond the uterus

Stage III

Local and/or regional spread of the tumor


IIIA

Tumor invades the serosa and/or adnexa


IIIB

Vaginal and/or parametrial involvement


IIIC

Metastases to the pelvic and/or para-aortic lymph nodes

IIIC1

Positive pelvic nodes

IIIC2

Positive para-aortic lymph nodes with or without positive pelvic lymph nodes

Stage IV

Tumor invades bladder and/or bowel mucosa, and/or distant metastases


IVA

Tumor invades bladder and/or bowel mucosa


IVB

Distant metastases, including intra-abdominal metastases and/or inguinal lymph nodes

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