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EZH2 in Bladder Cancer, a Promising Therapeutic Target. [revisión]

Por: Martínez Fernández, Mónica [Instituto de Investigación i+12] | Rubio, Carolina [Instituto de Investigación imas12] | Segovia, Cristina [Instituto de Investigación imas12] | López Calderón, Fernando F [Instituto de Investigación imas12] | Dueñas, Marta [Instituto de Investigación i+12] | Paramio, Jesús M [Instituto de Investigación i+12].
Colaborador(es): Instituto de Investigación imas12.
Tipo de material: materialTypeLabelArtículoEditor: International journal of molecular sciences, 2015Descripción: 16(11):27107-32.Recursos en línea: Acceso libre Resumen: Bladder Cancer (BC) represents a current clinical and social challenge. The recent studies aimed to describe the genomic landscape of BC have underscored the relevance of epigenetic alterations in the pathogenesis of these tumors. Among the epigenetic alterations, histone modifications occupied a central role not only in cancer, but also in normal organism homeostasis and development. EZH2 (Enhancer of Zeste Homolog 2) belongs to the Polycomb repressive complex 2 as its catalytic subunit, which through the trimethylation of H3 (Histone 3) on K27 (Lysine 27), produces gene silencing. EZH2 is frequently overexpressed in multiple tumor types, including BC, and plays multiple roles besides the well-recognized histone mark generation. In this review, we summarize the present knowledge on the oncogenic roles of EZH2 and its potential use as a therapeutic target, with special emphasis on BC pathogenesis and management.
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Formato Vancouver:
Martínez Fernández M, Rubio C, Segovia C, López Calderón FF, Dueñas M, Paramio JM. EZH2 in Bladder Cancer, a Promising Therapeutic Target. Int J Mol Sci. 2015 Nov 13;16(11):27107-32.

PMID: 26580594
PMC4661858

Contiene 208 referencias

Bladder Cancer (BC) represents a current clinical and social challenge. The recent studies aimed to describe the genomic landscape of BC have underscored the relevance of epigenetic alterations in the pathogenesis of these tumors. Among the epigenetic alterations, histone modifications occupied a central role not only in cancer, but also in normal organism homeostasis and development. EZH2 (Enhancer of Zeste Homolog 2) belongs to the Polycomb repressive complex 2 as its catalytic subunit, which through the trimethylation of H3 (Histone 3) on K27 (Lysine 27), produces gene silencing. EZH2 is frequently overexpressed in multiple tumor types, including BC, and plays multiple roles besides the well-recognized histone mark generation. In this review, we summarize the present knowledge on the oncogenic roles of EZH2 and its potential use as a therapeutic target, with special emphasis on BC pathogenesis and management.

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