Pattern of SMARCB1 (INI1) and SMARCA4 (BRG1) in poorly differentiated endometrioid adenocarcinoma of the uterus: analysis of a series with emphasis on a novel SMARCA4-deficient dedifferentiated rhabdoid variant

Strehl, Johanna; Wachter, David; Fiedler, Jutta; Heimerl, Engelbert; Beckmann, Matthias W.; Hartmann, Arndt; Agaimy, Abbas

doi:10.1016/j.anndiagpath.2015.04.001

Cited by 102 publications

(90 citation statements)

References 28 publications

(39 reference statements)

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“…Strehl et al (2015), reported involvement of SWI/SNF complex in the pathogenesis of dedifferentiation of EEC in a subset of cases and highlighted correlation of SWI/SNF alterations with the aggressive rhabdoid phenotype.…”

Section: Cell Signaling Pathwaysmentioning

confidence: 99%

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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Section: Cell Signaling Pathwaysmentioning

confidence: 99%

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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“…The extent of the differentiated component was highly variable ranging from extensive to minor, being just represented by a mere minute focus of intraepithelial neoplasia. Very recently, a case of SMARCA4-deficient undifferentiated carcinoma with rhabdoid features was reported to originate from differentiated SMARCA4-intact endometrioid adenocarcinoma of the endometrium [17]. In light of these recent observations, it is conceivable that at least a subset of SCCOHT might have originated from a very early epithelial neoplasm (intraepithelial lesion) by a specific pathway of dedifferentiation, in which inactivation of SMARCA4 is the central or even the only molecular alteration.…”

Section: Discussionmentioning

confidence: 97%

“…Assessment of SMARCB1 and SMARCA4 was done the same way, that is, only unequivocal clean absent staining in the tumor cell nuclei was considered "deficient." As a control, the presence of homogeneous strong nuclear staining of stromal fibroblasts, inflammatory cells, and vascular endothelial cells in the background was a prerequisite for assessable staining in the tumor as described recently [17].…”

Section: Methodsmentioning

confidence: 99%

SMARCA4-deficient undifferentiated carcinoma of the ovary (small cell carcinoma, hypercalcemic type): clinicopathologic and immunohistochemical study of 3 cases

Agaimy¹,

Thiel²,

Hartmann³

et al. 2015

Annals of Diagnostic Pathology

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“…In addition, variable staining can be seen with CK5, p63, p40, p16, E-cadherin, and synaptophysin. Original tumor diagnosis often includes poorly differentiated non-keratinizing (basaloid) squamous cell carcinoma, SNUC, As observed in a recent study [4], assessment of SMARCB1 expression on tissue microarrays should be interpreted with caution. Tumor areas with suboptimal tissue preservation and areas closely associated with tumor cell necrosis may show variable reduction in the SMARCB1 reactivity.…”

Section: Ancillary Studies and Initial Tumor Classificationmentioning

confidence: 95%

“…This is an important illustration for tumor heterogeneity and the drawbacks associated with utilization of tissue microarrays (Fig. 4) [4].…”

Section: Ancillary Studies and Initial Tumor Classificationmentioning

confidence: 99%

Reappraisal of sinonasal undifferentiated carcinoma: SMARCB1 (INI1)-deficient sinonasal carcinoma: a single-institution experience

et al. 2015

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Sinonasal carcinomas are rare and of diverse histology, often involve critical anatomic structures, and are associated with an aggressive clinical course and poor prognosis. Differentiating these tumor types may have clinical impact as advances in entity-specific therapeutic intervention could increase survival and quality of life and occasionally result in a cure. Recently, a unique subset of sinonasal carcinomas characterized by basaloid/rhabdoid tumor morphology and loss of expression of SMARCB1 (INI1) was identified. We tested a total of 256 tumors including head and neck (n = 241) and thoracic (n = 15) tumors with basaloid/rhabdoid morphology for loss of expression of SMARCB1 (INI1) using full tissue sections and tissue microarrays. Among these, four tumors of the sinonasal tract were found to be SMARCB1 (INI1) deficient and were reclassified as SMARCB1 (INI1)-deficient sinonasal carcinomas. These tumors appear to be restricted to the sinonasal tract, and their unique clinical, morphological, and immunohistochemical features seem to warrant inclusion as a separate new entity among the existing high-grade sinonasal neoplasms. Separation from the other types of sinonasal malignancies is important as the identification of SMARCB1 (INI1) deficiency may provide a new target for novel treatment approaches and may ultimately lead to improved patient survival.

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Pattern of SMARCB1 (INI1) and SMARCA4 (BRG1) in poorly differentiated endometrioid adenocarcinoma of the uterus: analysis of a series with emphasis on a novel SMARCA4-deficient dedifferentiated rhabdoid variant

Cited by 102 publications

References 28 publications

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

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

SMARCA4-deficient undifferentiated carcinoma of the ovary (small cell carcinoma, hypercalcemic type): clinicopathologic and immunohistochemical study of 3 cases

Reappraisal of sinonasal undifferentiated carcinoma: SMARCB1 (INI1)-deficient sinonasal carcinoma: a single-institution experience

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