Endometrial carcinoma: molecular alterations involved in tumor development and progression

In the western world, endometrial carcinoma (EC) is the most common cancer of the female genital tract. The annual incidence has been estimated at 10-20 per 100 000 women. Two clinicopathological variants are recognized: the estrogen related (type I, endometrioid) and the non-estrogen related (type...

Descripción completa

Detalles Bibliográficos
Autores: Yeramian, A, Moreno-Bueno, G, Dolcet, X, Catasus, L, Abal Posada, Miguel, Colas, E, Reventos, J, Palacios, J, Prat, J, Matias-Guiu, X
Tipo de recurso: artículo
Fecha de publicación:2013
País:España
Institución:Servizo Galego de Saúde (SERGAS)
Repositorio:RUNA. Repositorio da Consellería de Sanidade e Sergas
OAI Identifier:oai:runa.sergas.gal:20.500.11940/4073
Acceso en línea:http://hdl.handle.net/20.500.11940/4073
Access Level:acceso abierto
Palabra clave:Animals
Cell Transformation, Neoplastic
Disease Progression
Endometrial Neoplasms
Female
Humans
id ES_730b3765e98f1267c56e275b6dfd6416
oai_identifier_str oai:runa.sergas.gal:20.500.11940/4073
network_acronym_str ES
network_name_str España
repository_id_str
spelling Endometrial carcinoma: molecular alterations involved in tumor development and progressionYeramian, AMoreno-Bueno, GDolcet, XCatasus, LAbal Posada, MiguelColas, EReventos, JPalacios, JPrat, JMatias-Guiu, XAnimalsCell Transformation, NeoplasticDisease ProgressionEndometrial NeoplasmsFemaleHumansIn the western world, endometrial carcinoma (EC) is the most common cancer of the female genital tract. The annual incidence has been estimated at 10-20 per 100 000 women. Two clinicopathological variants are recognized: the estrogen related (type I, endometrioid) and the non-estrogen related (type II, non-endometrioid).The clinicopathological differences are paralleled by specific genetic alterations, with type I showing microsatellite instability and mutations in phosphatase and tensin homologue deleted on chromosome 70, PIK3CA, K-RAS and CTNNB1 (beta-catenin), and type II exhibiting TP53 mutations and chromosomal instability. Some non-endometrioid carcinomas probably arise from pre-existing endometrioid carcinomas as a result of tumor progression and, not surprisingly, some tumors exhibit combined or mixed features at the clinical, pathological and molecular levels. In EC, apoptosis resistance may have a role in tumor progression. Understanding pathogenesis at the molecular level is essential in identifying biomarkers for successful targeted therapies. In this review, the genetic changes of endometrial carcinogenesis are discussed in the light of the morphological features of the tumors and their precursors.2013info:eu-repo/semantics/articlehttp://hdl.handle.net/20.500.11940/4073reponame:RUNA. Repositorio da Consellería de Sanidade e Sergasinstname:Servizo Galego de Saúde (SERGAS)Inglésinfo:eu-repo/semantics/openAccessoai:runa.sergas.gal:20.500.11940/40732026-06-12T08:40:47Z
dc.title.none.fl_str_mv Endometrial carcinoma: molecular alterations involved in tumor development and progression
title Endometrial carcinoma: molecular alterations involved in tumor development and progression
spellingShingle Endometrial carcinoma: molecular alterations involved in tumor development and progression
Yeramian, A
Animals
Cell Transformation, Neoplastic
Disease Progression
Endometrial Neoplasms
Female
Humans
title_short Endometrial carcinoma: molecular alterations involved in tumor development and progression
title_full Endometrial carcinoma: molecular alterations involved in tumor development and progression
title_fullStr Endometrial carcinoma: molecular alterations involved in tumor development and progression
title_full_unstemmed Endometrial carcinoma: molecular alterations involved in tumor development and progression
title_sort Endometrial carcinoma: molecular alterations involved in tumor development and progression
dc.creator.none.fl_str_mv Yeramian, A
Moreno-Bueno, G
Dolcet, X
Catasus, L
Abal Posada, Miguel
Colas, E
Reventos, J
Palacios, J
Prat, J
Matias-Guiu, X
author Yeramian, A
author_facet Yeramian, A
Moreno-Bueno, G
Dolcet, X
Catasus, L
Abal Posada, Miguel
Colas, E
Reventos, J
Palacios, J
Prat, J
Matias-Guiu, X
author_role author
author2 Moreno-Bueno, G
Dolcet, X
Catasus, L
Abal Posada, Miguel
Colas, E
Reventos, J
Palacios, J
Prat, J
Matias-Guiu, X
author2_role author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Animals
Cell Transformation, Neoplastic
Disease Progression
Endometrial Neoplasms
Female
Humans
topic Animals
Cell Transformation, Neoplastic
Disease Progression
Endometrial Neoplasms
Female
Humans
description In the western world, endometrial carcinoma (EC) is the most common cancer of the female genital tract. The annual incidence has been estimated at 10-20 per 100 000 women. Two clinicopathological variants are recognized: the estrogen related (type I, endometrioid) and the non-estrogen related (type II, non-endometrioid).The clinicopathological differences are paralleled by specific genetic alterations, with type I showing microsatellite instability and mutations in phosphatase and tensin homologue deleted on chromosome 70, PIK3CA, K-RAS and CTNNB1 (beta-catenin), and type II exhibiting TP53 mutations and chromosomal instability. Some non-endometrioid carcinomas probably arise from pre-existing endometrioid carcinomas as a result of tumor progression and, not surprisingly, some tumors exhibit combined or mixed features at the clinical, pathological and molecular levels. In EC, apoptosis resistance may have a role in tumor progression. Understanding pathogenesis at the molecular level is essential in identifying biomarkers for successful targeted therapies. In this review, the genetic changes of endometrial carcinogenesis are discussed in the light of the morphological features of the tumors and their precursors.
publishDate 2013
dc.date.none.fl_str_mv 2013
dc.type.none.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv http://hdl.handle.net/20.500.11940/4073
url http://hdl.handle.net/20.500.11940/4073
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.source.none.fl_str_mv reponame:RUNA. Repositorio da Consellería de Sanidade e Sergas
instname:Servizo Galego de Saúde (SERGAS)
instname_str Servizo Galego de Saúde (SERGAS)
reponame_str RUNA. Repositorio da Consellería de Sanidade e Sergas
collection RUNA. Repositorio da Consellería de Sanidade e Sergas
repository.name.fl_str_mv
repository.mail.fl_str_mv
_version_ 1869410780345008128
score 15,300724

Similares en LA Referencia