The role of HMGA2 in this differential diagnosis requires further research. Insufficient evidence is available to support the use of vimentin, Ki-67, HNF1B, WT1 and IMP2, and monoclonal carcinoembryonic antigen may be safely omitted from the antibody panel. Molecular classification of endometrial carcinomas has been shown to be superior to immunohistochemistry as an ancillary technique 29, but whether, and to what extent, it will replace immunohistochemistry remains to be seen, especially since it is more expensive, more time-consuming and not available in many pathology laboratories.
An endometrial carcinoma demonstrating a combination of papillary (small round papillae lacking overt stratification; Fig. 5A), tubulocystic (Fig. 5B) and/or solid (Fig. 5C) architectural patterns, with cuboidal or polygonal cells containing nuclei with a variable degree of pleomorphism (although usually lacking overt pleomorphism). Hobnail tumor cells and cytoplasmic clearing are often present but are not required for diagnosis.
Aberrant mutation-type p53 immunohistochemical expression is seen in up to one third of otherwise typical clear cell carcinomas 44,47,58,59 (Fig. 6C) and these cases are morphologically indistinguishable from p53-wild-type cases 47,58. Nevertheless, p53 immunohistochemistry can still provide useful information, as wild-type p53 staining minimizes the probability that the tumor is a true serous carcinoma 5, and mutation-type p53 expression is an adverse prognostic factor in histotypically ambiguous tumors 60. There is some evidence that p53-aberrant clear cell carcinomas show a more aggressive, “serous-like,” peritoneal pattern of spread 58,59. At the molecular level, ∼14% of morphologically and immunophenotypically characteristic clear cell carcinomas display a profile of mutations (mutations in TP53 and PPP2R1A; wild-type PTEN, CTNNB1, and ARID1A) typically seen in serous carcinoma 47,48. These findings suggest that a subset of tumors diagnosed as clear cell carcinomas might represent manifestations of extreme morphologic mimicry by serous carcinomas 48,61.
Between 12% and 30% of clear cell carcinomas reportedly contain an endometrioid component 38–41,83,89,100. The proportion of these tumors that represent true mixed carcinomas 103 (Fig. 7) rather than a single histotype displaying phenotypic diversity 61 is unclear and the wide range in incidence is likely indicative of interobserver variability in the classification of these tumors 1,4. It is likely that true mixed endometrioid and clear cell carcinoma is very uncommon. Areas of morphologic overlap between clear cell carcinoma and endometrioid carcinoma are largely attributable to the presence of clear cells in endometrioid carcinomas, which may occur for several reasons:
Immunohistochemistry may be of some value in such cases but there can be significant immunophenotypic overlap and markers are often not particularly useful. Negative staining with ER and PR would favor a diagnosis of clear cell carcinoma but these markers can be negative in clear cell areas in endometrioid carcinomas, especially when they exhibit squamous differentiation. While HNF1B and Napsin A are useful markers of clear cell carcinoma, they (especially HNF1B) may also be expressed in clear cells in endometrioid carcinomas.
A mixed endometrial carcinoma is defined in the latest World Health Organization (WHO) classification as a carcinoma composed of 2 or more histologic subtypes, in which the minor component constitutes 5% or more of the tumor, and in which the 2 components are recognizable on hematoxylin/eosin–stained sections 103. Each of the components must be spatially distinct from the other(s), and each must exhibit morphologic and immunophenotypic features that, viewed in isolation, is fully diagnostic of one histotype 61. Since evidence from molecular studies suggests that there is a high degree of morphologic mimicry in mixed carcinomas, it is imperative that each component is morphologically and immunophenotypically prototypical 61. As defined, true mixed serous-clear cell endometrial carcinomas are extremely uncommon (Fig. 8A).
Serous carcinomas that contain cells with clear cytoplasm are much more likely to represent pure serous carcinomas than mixed serous-clear cell carcinomas. The evidence in favor of this interpretation includes: (1) the frequent presence of “clear cells” in endometrial carcinomas of various histotypes minimizes the importance of cytoplasmic clearing as a stand-alone indicator for clear cell carcinoma. (2) Data from ovarian carcinomas, in which histotyping is more reproducible 30–32, indicate that serous carcinomas with clear cells have a morphologic, immunophenotypic and molecular profile that is more consistent with serous carcinoma than clear cell carcinoma 108–110. (3) One seminal study found that in serous carcinomas with clear cells, none of the cases had a tubulocystic pattern, and serous endometrial intraepithelial carcinoma was present in a high proportion of the cases 111.
These are the most challenging tumors to classify. The existence of truly ambiguous tumors in the clear cell carcinoma/serous carcinoma spectrum is one likely contributing factor to the interobserver variability that exists in the histotyping of high-grade endometrial carcinomas 1,2,4. These tumors have hybrid morphologic features overlapping those of serous carcinoma and clear cell carcinoma (Fig. 8B). The frequency of aberrant mutation-type p53 staining in these cases (36%) 112 is comparable with that reported in conventional clear cell carcinoma (33%–38%) 44,47,58,59, and substantially less than that expected in serous carcinoma. Immunohistochemistry, in our experience, has not proven to be very useful in the categorization of this group of cases. The true nature of these cases is unclear, and since they are not prototypical clear cell carcinoma or serous carcinoma, we recommend their provisional categorization in the “ambiguous” category, with descriptive diagnoses such as “High-grade carcinoma with clear cell and serous features” until they can be better categorized by novel modalities in the future. However, such a diagnosis should be made sparingly and only in those cases that defy classification after thorough morphologic and immunohistochemical evaluation.
In summary, otherwise typical serous carcinomas with clear cells should be categorized as serous carcinomas, and serous carcinomas with spatially distinct areas of clear cell carcinoma should be categorized as mixed serous carcinoma-clear cell carcinomas. Cases that are not morphologically typical of either histotype should be reported descriptively (Box 2).
Undifferentiated and dedifferentiated carcinomas are clinically aggressive malignancies that are probably under-recognized 115,117,118. They have been widely recognized only in the past decade, and data pertaining to them is based upon a limited number of relatively small studies 115,117–126. In our experience, undifferentiated carcinomas and dedifferentiated carcinomas together represent ∼10% of high-grade endometrial carcinomas and hence about 2% of endometrial carcinomas overall 127. Silva et al. 124 reported that undifferentiated carcinomas accounted for 9% of all endometrial carcinomas; however, this report was from a major tertiary cancer center and it is unclear whether the frequency was inflated due to inclusion of referral and consultation cases.
Approximately 40% of undifferentiated carcinomas are associated with a component of FIGO grade 1 or 2 endometrioid carcinoma; these cases are termed “dedifferentiated carcinoma” (Fig. 9B). It is possible that in some cases of undifferentiated carcinoma, an antecedent low-grade component was overgrown by the undifferentiated element. When present, the differentiated low-grade endometrioid component is typically found lining the endometrial cavity, with the undifferentiated component present deep to it. This may account for a diagnosis of low-grade endometrioid carcinoma in a biopsy specimen and dedifferentiated carcinoma at hysterectomy. In rare cases, low-grade endometrioid carcinoma is present in the uterus and the undifferentiated component is only seen in the metastases, which may be identified synchronously or subsequently 117,118,121,124. Rare cases contain foci of FIGO grade 3 endometrioid carcinoma juxtaposed with undifferentiated carcinoma 118.
Additional morphologic features that are present in some undifferentiated and dedifferentiated carcinomas include focal alveolar, nested and vaguely corded or trabecular growth patterns, rhabdoid/plasmacytoid morphology (vesicular nucleus containing a large nucleolus and abundant pink cytoplasm; Fig. 9C), focal marked nuclear pleomorphism (Fig. 9D), multinucleation, spindling, and “abrupt” keratinization 118,124,128,129. Some tumors also show prominent tumor-infiltrating lymphocytes and myxoid stroma. The morphologic criteria have continued to evolve and vary to some extent between studies. For example, the degree of permissible neuroendocrine differentiation (as judged immunohistochemically) was initially restricted to <10% of tumor cells 115, but in one subsequent study of undifferentiated carcinoma, “diffuse staining” was recorded in 9% of cases; we recommend that neuroendocrine marker positivity in undifferentiated carcinoma should be limited to <10% of the tumor cells 129.
The majority of undifferentiated carcinomas (and the undifferentiated component of dedifferentiated carcinoma) lack expression of PAX8, ER, and PR but up to 20% of tumors may show focal staining with these markers 121,130. P53 expression is usually wild-type but is aberrant (mutation-type) in a minority of cases. More than 80% of undifferentiated carcinomas display evidence of epithelial differentiation in the form of intense EMA and cytokeratin (especially cytokeratin 18) staining of a small proportion of tumor cells (Fig. 10A); diffuse expression of EMA and cytokeratins is not typically found but can occur. Tumor cells typically express vimentin and a substantial number express CD138. E-cadherin labeling is absent or minimal 121,130–132. CD34 expression, which is otherwise very uncommon in epithelial neoplasms, is sometimes seen 133. Chromogranin and/or synaptophysin staining can be present, but only in a minority of tumor cells (<10%) 130. Loss of BRG-1 (the protein product of SMARCA4) expression can be seen (Fig. 10B), particularly in examples that have DNA MMR protein deficiency and some cases show loss of INI-1 (the protein product of SMARCB1) or ARID1A 125,134. BRG-1, INI-1, and ARID1A are involved in chromatin remodeling through SWI/SNF complexes 125,134. Loss of expression of MLH1 and PMS2, mostly due to hMLH1 promoter methylation is seen in ∼50% to 60% of cases. Rare cases with germline DNA MMR gene mutations diagnostic of Lynch syndrome have been reported 135. Occasional cases may also harbor a hotspot POLE mutation affecting the exonuclease domain. Possible mechanisms underlying the transition from differentiated to undifferentiated carcinoma include the acquisition of mutations in SMARCA4, ARID1B, CTNNB1, PPP2R1A or TP53 136.
Accurate diagnosis is important in view of the poor prognosis of undifferentiated/dedifferentiated carcinoma, and this is likely to become even more important as tumor subtype-specific targeted therapies are developed.
In contrast to grade 3 endometrioid carcinomas, undifferentiated carcinomas are dyscohesive and do not exhibit epithelial formations, such as glands, although occasional nests and trabeculae are allowed. Undifferentiated carcinoma forms diffuse monotonous sheets, sometimes in a myxoid stroma. Most grade 3 endometrioid carcinomas, on the other hand, are composed of cohesive cells with at least focal glandular formation and squamous differentiation, which may be abortive. While gland formation excludes a diagnosis of undifferentiated carcinoma, the distinction of “true” glands from lacunar-type spaces occurring secondary to apoptosis/necrosis or artifact can be problematic and subjective. The distinction between undifferentiated carcinoma and grade 3 endometrioid carcinoma may be particularly problematic in poorly fixed specimens and sometimes cannot be resolved, even with immunohistochemistry; such cases are probably best diagnosed as “high-grade endometrial carcinoma” with an explanatory note.
Dedifferentiated carcinomas with a significant low-grade glandular component may be misclassified as grade 2 endometrioid carcinoma, significantly underestimating their aggressive behavior 116,124. Dedifferentiated carcinomas may also be confused with grade 3 endometrioid carcinomas but the former is a more overtly “biphasic” neoplasm in view of its distinct low-grade endometrioid and undifferentiated components. However, extensive sampling may be required to identify the differentiated component of dedifferentiated carcinoma. Although by definition grade 3 endometrioid carcinoma shows a predominant solid growth pattern, up to 49% of the tumor can show glandular differentiation and there is often an intimate admixture of the solid and glandular components within the same nests. The cells within the solid areas and those forming glands usually have similar cytologic appearances. In contrast, the glandular and diffuse elements in dedifferentiated carcinoma are typically separate, and the diffuse component shows greater cytologic atypia than the low-grade glandular component. A solid cohesive growth pattern is characteristic of grade 3 endometrioid carcinomas whereas cellular dyscohesion and rhabdoid morphology are more characteristic of the undifferentiated component of dedifferentiated carcinoma. The distinction between dedifferentiated carcinoma and carcinosarcoma is discussed in the section on carcinosarcoma.
Immunohistochemically, undifferentiated carcinomas and the undifferentiated component of dedifferentiated carcinomas often show loss of PAX8, E-cadherin, ER, and PR immunoreactivity 121,130. In contrast, grade 3 endometrioid carcinomas usually retain PAX8 expression while hormone receptor expression is variable 8. Loss of BRG1 and/or INI1 expression has been reported in undifferentiated carcinoma and the undifferentiated component of dedifferentiated carcinomas 125,134; loss of another subunit of the SWI/SNF complex, BAF250a (the protein product of ARID1A) is common in both low-grade and high-grade endometrial carcinomas 137,138. Overall, therefore a cytokeratin/EMA-focal and PAX8/ER/E-cadherin-negative immunoprofile, along with loss of BRG-1 or INI-1 expression would favor undifferentiated or dedifferentiated carcinoma over grade 3 endometrioid carcinoma (Box 3).
The presence of even minimal amounts of carcinomatous epithelium has traditionally been used to qualify a predominantly sarcomatous tumor as a carcinosarcoma 139. The literature is inconsistent on the volume of sarcomatous differentiation required to label a tumor as a carcinosarcoma, which has ranged from as little as 2% 140 to 25% 141. The authors recommend that the sarcomatous component should measure at least 1 mm in one dimension; while this is an arbitrary figure that is not evidence-based, it reflects the authors’ view that a minimal sarcomatous component should not result in a diagnosis of carcinosarcoma. The clinical significance, if any, of minimal volume sarcoma in a predominantly carcinomatous tumor has not been systematically studied. In contrast, high volume sarcomatous differentiation may portend more aggressive behavior and poor prognosis 139,140,142–144. Some studies also suggest that such largely sarcomatous tumors tend to be associated with pure sarcomatous metastases, which spread preferentially via lymphohematogenous routes to lymph nodes and distant sites, without peritoneal spread 139,140,142,143. This is in contrast to most carcinosarcomas in which the epithelial component preferentially metastasizes to peritoneal sites.
Carcinosarcomas are divided into homologous and heterologous types, according to whether the mesenchymal component exhibits differentiation that is intrinsic (endometrial stromal sarcoma or leiomyosarcoma; Figs. 11A, B) or extrinsic (chondrosarcoma, Fig. 11C; rhabdomyosarcoma, Fig. 11D; etc.) to the uterus. Accurate subclassification of the sarcomatous component is a useful exercise but is not currently relevant to management. This separation was based on reports suggesting a more ominous prognosis for heterologous tumors 145,146 but this remains controversial. One follow-up study concluded that the prognosis for both homologous and heterologous carcinosarcomas was equally poor 139. However, a more recent report found significantly poorer 3-yr survival in patients with stage I heterologous tumors (45%) than in those with homologous tumors (93%) 147. The authors concluded that heterologous carcinosarcomas exhibited true sarcomatous differentiation and that homologous tumors were best classified as metaplastic carcinomas based on their behavioral similarity to high-grade endometrial carcinomas.
The morphology of metastases from carcinosarcomas is variable but the majority contain an epithelial component. One study 142 evaluated the cellular composition of 62 metastases, 51 of which were diagnosed at the time of surgery. Carcinoma or carcinosarcoma accounted for over 90% of metastatic tumors, with only a few comprising pure sarcoma. The characteristics of the stromal component, including grade, mitotic index, and the presence and types of heterologous elements, has not been associated with outcome in most studies. In contrast, an epithelial component consisting of serous carcinoma correlates with a higher frequency of metastases. Features associated with poor outcome in carcinomas, such as deep myometrial invasion, lymphovascular space invasion, and cervical involvement, are also associated with adverse prognosis in carcinosarcomas 139,142.
A recent large-scale molecular genetic analysis of uterine carcinosarcomas by the Cancer Genome Atlas 148 revealed extensive copy-number alterations and highly recurrent somatic mutations, most frequently in TP53, PTEN, PIK3CA, PPP2R1A, FBXW7, and KRAS. The similarity in mutational profile to uterine endometrioid and serous carcinomas provides genomic support for the categorization of carcinosarcomas as a subset of uterine carcinomas. A proportion of carcinosarcomas was also characterized by an epithelial-to-mesenchymal transition (EMT) gene signature 148.
In practice, tumors with malignant epithelial and mesenchymal differentiation are reported as carcinosarcomas, with additional comments clarifying the cell type and grade of the epithelial component (although typing of the epithelial component may be particularly difficult in carcinosarcomas), and other parameters that are associated with prognosis in epithelial tumors. The presence of heterologous elements and their differentiation should also be noted.
Dedifferentiated carcinomas and carcinosarcomas show a low-power biphasic appearance but in the case of carcinosarcoma, the more diffuse tumor component comprises cytologically malignant mesenchymal elements that are typically spindled and pleomorphic and may exhibit heterologous differentiation 149. This contrasts with the monotonous round cells of the undifferentiated component of most dedifferentiated carcinomas. While dedifferentiated carcinoma can rarely contain a population of somewhat spindled cells, this is usually a minor feature in contrast to the more overtly sarcomatous appearances of carcinosarcoma. Many carcinosarcomas exhibit heterologous mesenchymal differentiation, most commonly in the form of chondrosarcoma, rhadomyosarcoma or osteosarcoma, but this is not a feature of dedifferentiated carcinoma. The epithelial elements of these tumors also differ in that the glandular component of dedifferentiated carcinoma is most often a low-grade endometrioid carcinoma, whereas in most carcinosarcomas, the epithelial element is a high-grade carcinoma (serous, clear cell, grade 3 endometrioid carcinoma or difficult-to-classify high-grade adenocarcinoma). However, the carcinomatous component of a carcinosarcoma can have undifferentiated appearances, at least in some areas, and the distinction from undifferentiated carcinoma or dedifferentiated carcinoma may be very difficult, particularly in biopsy specimens.
Immunohistochemistry has limited utility in this differential diagnosis. Typically, cytokeratins are diffusely expressed by the epithelial component of carcinosarcomas and there is sometimes focal staining of the mesenchymal elements 150. The latter may also express more specific mesenchymal markers if heterologous differentiation is present (eg, myogenin in rhabdomyosarcoma). Vimentin and p16 staining are of limited value since many dedifferentiated carcinomas are positive 130,132. Similarly, PAX8 is not useful in this differential diagnosis since the mesenchymal component of carcinosarcoma, like the undifferentiated component of dedifferentiated carcinoma, is usually PAX8-negative 151. As noted above, loss of MMR protein expression is relatively common (∼50%–60% of cases) in dedifferentiated carcinoma 118,125,130, and some tumors arise in patients with Lynch syndrome 152. In contrast, abnormal MMR protein expression is much less common in carcinosarcoma; the Cancer Genome Atlas analysis found microsatellite instability in 2 of 57 (4%) cases 148, although other studies have reported frequencies of MMR-deficient cases ranging between 6% and 33% 153,154.
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