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dc.contributor.authorLeskelä, Susanna
dc.contributor.authorPérez-Mies, Belén
dc.contributor.authorRosa-Rosa, Juan Manuel
dc.contributor.authorCristobal, Eva
dc.contributor.authorBiscuola, Michele
dc.contributor.authorPalacios-Berraquero, María L.
dc.contributor.authorOng, SuFey
dc.contributor.authorMatias-Guiu, Xavier
dc.contributor.authorPalacios, José
dc.date.accessioned2020-03-12T11:42:41Z
dc.date.available2020-03-12T11:42:41Z
dc.date.issued2019
dc.identifier.issn2072-6694
dc.identifier.urihttp://hdl.handle.net/10459.1/68211
dc.description.abstractEndometrial carcinosarcoma (ECS) represents one of the most extreme examples of tumor heterogeneity among human cancers. ECS is a clinically aggressive, high-grade, metaplastic carcinoma. At the morphological level, intratumor heterogeneity in ECS is due to an admixture of epithelial (carcinoma) and mesenchymal (sarcoma) components that can include heterologous tissues, such as skeletal muscle, cartilage, or bone. Most ECSs belong to the copy-number high serous-like molecular subtype of endometrial carcinoma, characterized by the TP53 mutation and the frequently accompanied by a large number of gene copy-number alterations, including the amplification of important oncogenes, such as CCNE1 and c-MYC. However, a proportion of cases (20%) probably represent the progression of tumors initially belonging to the copy-number low endometrioid-like molecular subtype (characterized by mutations in genes such as PTEN, PI3KCA, or ARID1A), after the acquisition of the TP53 mutations. Only a few ECS belong to the microsatellite-unstable hypermutated molecular type and the POLE-mutated, ultramutated molecular type. A common characteristic of all ECSs is the modulation of genes involved in the epithelial to mesenchymal process. Thus, the acquisition of a mesenchymal phenotype is associated with a switch from E- to N-cadherin, the up-regulation of transcriptional repressors of E-cadherin, such as Snail Family Transcriptional Repressor 1 and 2 (SNAI1 and SNAI2), Zinc Finger E-Box Binding Homeobox 1 and 2 (ZEB1 and ZEB2), and the down-regulation, among others, of members of the miR-200 family involved in the maintenance of an epithelial phenotype. Subsequent differentiation to different types of mesenchymal tissues increases tumor heterogeneity and probably modulates clinical behavior and therapy response.ca_ES
dc.description.sponsorshipThis review was funded by grants from the Instituto de Salud Carlos III (ISCIII) (PIE15/00050 and PI16/00887) and CIBERONC (CB16/12/00316 and CB16/12/00231, CB16/12/00361), co-financed by the European Development Regional Fund. ‘A way to achieve Europe’ (FEDER), and by the Spanish Association Against Cancer Scientific Foundation (grants: AIO-aecc 2016 and Grupos Coordinados Traslacionales aecc 2018).ca_ES
dc.language.isoengca_ES
dc.publisherMDPIca_ES
dc.relation.isformatofReproducció del document publicat a https://doi.org/10.3390/cancers11070964ca_ES
dc.relation.ispartofCancers, 2019, vol. 11, núm. 7, article number 964ca_ES
dc.rightscc-by, (c) Leskela et al., 2019ca_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectUterine carcinosarcomaca_ES
dc.subjectEndometrial carcinomaca_ES
dc.subjectMetaplastic carcinomaca_ES
dc.subjectEpithelial-tomesenchymal transitionca_ES
dc.titleMolecular Basis of Tumor Heterogeneity in Endometrial Carcinosarcomaca_ES
dc.typeinfo:eu-repo/semantics/articleca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessca_ES
dc.identifier.doihttps://doi.org/10.3390/cancers11070964


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cc-by, (c) Leskela et al., 2019
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