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An overview of current therapeutic strategies for glioblastoma and the role of CD73 as an alternative curative approach
Arab, S; Hasannejad, Farkhonde.
Afiliación
  • Arab, S; Semnan University of Medical Sciences. Semnan. Iran
  • Hasannejad, Farkhonde; Semnan University of Medical Sciences. Semnan. Iran
Clin. transl. oncol. (Print) ; 24(5): 742-756, mayo 2022.
Article en En | IBECS | ID: ibc-203778
Biblioteca responsable: ES1.1
Ubicación: ES15.1 - BNCS
ABSTRACT
Glioblastoma multiforme (GBM) is a complicated and heterogeneous brain tumor with short-term survival outcomes. Commercial therapies are not practical due to cell infiltration capacity, high proliferative rate, and blood–brain barrier. In this context, recognition of the molecular mechanism of tumor progression might help the development of new cancer therapeutics. Recently, more evidence has supported CD73 and downstream adenosine A2A/A2B receptor signaling playing a crucial role in glioblastoma pathogenesis; therefore, targeting CD73 in murine tumor models can reduce tumor development. CD73 is an ecto-enzyme inducing tumor metastasis, angiogenesis, and immune escape via the production of extracellular adenosine in the tumor microenvironment. In this review, we provided information about clinical characteristics as well as the therapeutic management of glioblastoma. Then, we focused on newly available experimental evidence distinguishing between the essential role of CD73 on this tumor growth and a new method for the treatment of GBM patients.
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Texto completo: 1 Colección: 06-national / ES Base de datos: IBECS Asunto principal: Neoplasias Encefálicas / 5'-Nucleotidasa / Línea Celular Tumoral / Microambiente Tumoral Límite: Animals / Humans Idioma: En Revista: Clin. transl. oncol. (Print) Año: 2022 Tipo del documento: Article

Texto completo: 1 Colección: 06-national / ES Base de datos: IBECS Asunto principal: Neoplasias Encefálicas / 5'-Nucleotidasa / Línea Celular Tumoral / Microambiente Tumoral Límite: Animals / Humans Idioma: En Revista: Clin. transl. oncol. (Print) Año: 2022 Tipo del documento: Article