Fascin expression in undifferentiated and dedifferentiated endometrial carcinoma

Stewart, Colin J.R.; Crook, Maxine L.

doi:10.1016/j.humpath.2015.06.011

Cited by 20 publications

(21 citation statements)

References 32 publications

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“…A recent publication of Stewart and Crook [11] suggested that fascin expression may contribute to the aggressive behavior of UCE/DCEs. In our study, fascin immunoexpression was higher in UCE/DCEs than other high-grade endometrial carcinomas except for SC, which supported its role in the poorer clinical outcomes of UCE/DCE and SC.…”

Section: Discussionmentioning

confidence: 99%

“…[11–13] Epithelial-mesenchymal transition (EMT)-related proteins, for example, E-cadherin and β-catenin are also subjects of interest in the field of endometrial carcinomas; loss of E-cadherin expression in endometrial carcinomas has been correlated with advanced stage and worse prognosis in some studies. [14–16] None of the aforementioned immunohistochemical markers, namely fascin, E-cadherin, β-catenin, and SALL4, is specific to any type of tumor and used for various reasons.…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, it can be used for predicting the aggressive clinical course of a malignant tumor, as well as differentiating neoplastic cells of classic Hodgkin lymphoma from other types of lymphomas with anaplastic large cells. [11,12] Similarly, SALL4 can be used to detect tumor stem cells, as well as being a malignant germ cell tumor marker. [13,17] E-cadherin and β-catenin can be used in the differential diagnosis of subtypes of breast carcinomas and malignant soft tissue tumors, as well as to show tumor aggression.…”

Section: Introductionmentioning

confidence: 99%

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High expression of SALL4 and fascin, and loss of E-cadherin expression in undifferentiated/dedifferentiated carcinomas of the endometrium

et al. 2017

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Undifferentiated/dedifferentiated endometrial carcinomas (UCE/DCEs) of the endometrium are rare tumors with poor prognosis. There are few clinicopathologic studies with detailed immunohistochemical analysis regarding UCE/DCEs.We evaluated the diagnostic value of a selected tumor stem-cell marker and epithelial-mesenchymal transition (EMT) markers, in addition to previously studied markers in identifying UCE/DCEs from other types of high-grade endometrial carcinomas.Eleven cases of UCE/DCEs with complete clinical follow-up that were diagnosed between 2006 and 2015 were included in the study. For immunohistochemical comparison, 11 clinically matched cases for each type of other high-grade endometrial carcinomas (high-grade endometrioid (F3-EC), serous [SC], and clear cell carcinoma [CCC]) were used as a control group. An immunohistochemical analysis including fascin, SALL4, E-cadherin, and β-catenin, in addition to epithelial and neuroendocrine markers was performed in each case.The majority of UCE/DCEs displayed diffuse expression of fascin (81.9%) and loss of E-cadherin expression (54.5%). SALL4 expression was detected in 36.3% of the UCE/DCE cases. SALL4 expression was significantly more frequent in UCE/DCEs than all other high-grade carcinomas (P < 0.001). Loss of E-cadherin and fascin expression was significantly more frequent in UCE/DCEs than high-grade endometrioid and clear cell adenocarcinomas (P = 0.012, 0.014 and P = 0.01, 0.003, respectively).We suggest that loss of E-cadherin expression together with fascin and SALL4 immunopositivity in addition to morphologic features have an impact in differential diagnosis of UCE/DCEs from other high-grade endometrial carcinomas.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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High expression of SALL4 and fascin, and loss of E-cadherin expression in undifferentiated/dedifferentiated carcinomas of the endometrium

et al. 2017

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“…ZEB1 overexpression and downregulation of miR-200s in these tumors was associated with absent or downregulated E-cadherin expression (Romero-Perez et al 2013). Upregulation of fascin, an actin binding protein, was recently suggested to represent an EMT like process in UECs and also contribute toward the invasive character of this aggressive EC subtype (Stewart & Crook 2015a).…”

Section: Emt Effectors and Core Regulators In Eec Progression And Metmentioning

confidence: 91%

Tumor progression, metastasis, and modulators of epithelial–mesenchymal transition in endometrioid endometrial carcinoma: an update

Makker

Goel

2015

Endocrine-Related Cancer

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Endometrioid endometrial carcinoma (EEC), also known as type 1 endometrial cancer (EC), accounts for over 70-80% of all cases that are usually associated with estrogen stimulation and often develops in a background of atypical endometrial hyperplasia. The increased incidence of EC is mainly confined to this type of cancer. Most EEC patients present at an early stage and generally have a favorable prognosis; however, up to 30% of EEC present as high risk tumors, which have invaded deep into the myometrium at diagnosis and progressively lead to local or extra pelvic metastasis. The poor survival of advanced EC is related to the lack of effective therapies, which can be attributed to poor understanding of the molecular mechanisms underlying the progression of disease toward invasion and metastasis. Multiple lines of evidence illustrate that epithelial-mesenchymal transition (EMT)-like events are central to tumor progression and malignant transformation, endowing the incipient cancer cell with invasive and metastatic properties. The aim of this review is to summarize the current knowledge on molecular events associated with EMT in progression, invasion, and metastasis of EEC. Further, the role of epigenetic modifications and microRNA regulation, tumor microenvironment, and microcystic elongated and fragmented glands like invasion pattern have been discussed. We believe this article may perhaps stimulate further research in this field that may aid in identifying high risk patients within this clinically challenging patient group and also lead to the recognition of novel targets for the prevention of metastasis -the most fatal consequence of endometrial carcinogenesis.

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“…They found this well before dedifferentiated endometrial carcinoma was identified as a separate entity. Stewart et al [19] found diffuse fascin expression in the undifferentiated component of 94% of cases of dedifferentiated endometrial carcinomas. Onder et al [20] found diffuse expression of fascin in 82% of cases and loss of E-cadherin expression in 55% of cases.…”

Section: Discussionmentioning

confidence: 98%

Dedifferentiated endometrial carcinoma: an ongoing diagnostic dilemma

Hamza¹,

Khawar²,

Ibrar³

et al. 2018

pjp

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Tumours of uterine corpus are the most common gynaecological malignancies. The clinicopathological features of most of these tumours are well understood; however, dedifferentiated endometrial carcinoma still requires a lot of research to establish adequate management guidelines. The entity was first described in 2006 and is an aggressive tumour with poor prognosis. We present two cases of this tumour with a literature review, emphasising morphologic and immunohistochemical features that may help in the differential diagnosis.

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Fascin expression in undifferentiated and dedifferentiated endometrial carcinoma

Cited by 20 publications

References 32 publications

High expression of SALL4 and fascin, and loss of E-cadherin expression in undifferentiated/dedifferentiated carcinomas of the endometrium

High expression of SALL4 and fascin, and loss of E-cadherin expression in undifferentiated/dedifferentiated carcinomas of the endometrium

Tumor progression, metastasis, and modulators of epithelial–mesenchymal transition in endometrioid endometrial carcinoma: an update

Dedifferentiated endometrial carcinoma: an ongoing diagnostic dilemma

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