Your browser doesn't support javascript.
loading
Implications of cellular senescence in paediatric pituitary tumours.
Gonzalez-Meljem, Jose Mario; Martinez-Barbera, Juan Pedro.
Afiliação
  • Gonzalez-Meljem JM; Tecnologico de Monterrey, School of Engineering and Sciences, Mexico City, Mexico. Electronic address: jmgonzalezmeljem@tec.mx.
  • Martinez-Barbera JP; Developmental Biology and Cancer Programme, Birth Defects Research Centre, UCL Institute of Child Health, London, UK. Electronic address: j.martinez-barbera@ucl.ac.uk.
EBioMedicine ; 99: 104905, 2024 Jan.
Article em En | MEDLINE | ID: mdl-38043401
ABSTRACT
The long-standing view of senescent cells as passive and dysfunctional biological remnants has recently shifted into a new paradigm where they are main players in the development of many diseases, including cancer. The senescence programme represents a first line of defence that prevents tumour cell growth but also leads to the secretion of multiple pro-inflammatory and pro-tumourigenic factors that fuel tumour initiation, growth, and progression. Here, we review the main molecular features and biological functions of senescent cells in cancer, including the outcomes of inducing or targeting senescence. We discuss evidence on the role of cellular senescence in pituitary tumours, with an emphasis on adamantinomatous craniopharyngioma (ACP) and pituitary adenomas. Although senescence has been proposed to be a tumour-preventing mechanism in pituitary adenomas, research in ACP has shown that senescent cells are tumour-promoting in both murine models and human tumours. Future studies characterizing the impact of targeting senescent cells may result in novel therapies against pituitary tumours.
Assuntos
Palavras-chave

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Neoplasias Hipofisárias / Craniofaringioma Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Neoplasias Hipofisárias / Craniofaringioma Idioma: En Ano de publicação: 2024 Tipo de documento: Article