TY - JOUR
T1 - Cellular Senescence in Diffuse Gliomas
T2 - From Physiopathology to Possible Treatments
AU - Ordónez-Rubiano, Edgar G.
AU - Cómbita, Alba
AU - Baldoncini, Matías
AU - Payán-Gómez, César
AU - Gómez-Amarillo, Diego F.
AU - Hakim, Fernando
AU - Camargo, Julián
AU - Zorro-Sepúlveda, Valentina
AU - Luzzi, Sabino
AU - Zorro, Oscar
AU - Parra-Medina, Rafael
N1 - Publisher Copyright:
© 2024 Elsevier Inc.
PY - 2024/11
Y1 - 2024/11
N2 - Cellular senescence in gliomas is a complex process that is induced by aging and replication, ionizing radiation, oncogenic stress, and the use of temozolomide. However, the escape routes that gliomas must evade senescence and achieve cellular immortality are much more complex, in which the expression of telomerase and the alternative lengthening of telomeres, as well as the mutation of some proto-oncogenes or tumor suppressor genes, are involved. In gliomas, these molecular mechanisms related to cellular senescence can have a tumor-suppressing or promoting effect and are directly involved in tumor recurrence and progression. From these cellular mechanisms related to cellular senescence, it is possible to generate targeted senostatic and senolytic therapies that improve the response to currently available treatments and improve survival rates. This review aims to summarize the mechanisms of induction and evasion of cellular senescence in gliomas, as well as review possible treatments with therapies targeting pathways related to cellular senescence.
AB - Cellular senescence in gliomas is a complex process that is induced by aging and replication, ionizing radiation, oncogenic stress, and the use of temozolomide. However, the escape routes that gliomas must evade senescence and achieve cellular immortality are much more complex, in which the expression of telomerase and the alternative lengthening of telomeres, as well as the mutation of some proto-oncogenes or tumor suppressor genes, are involved. In gliomas, these molecular mechanisms related to cellular senescence can have a tumor-suppressing or promoting effect and are directly involved in tumor recurrence and progression. From these cellular mechanisms related to cellular senescence, it is possible to generate targeted senostatic and senolytic therapies that improve the response to currently available treatments and improve survival rates. This review aims to summarize the mechanisms of induction and evasion of cellular senescence in gliomas, as well as review possible treatments with therapies targeting pathways related to cellular senescence.
KW - Cellular senescence
KW - Diffuse glioma
KW - Glioblastoma
KW - Glioma
KW - Molecular pathology
KW - Senescence
UR - http://www.scopus.com/inward/record.url?scp=85203280665&partnerID=8YFLogxK
U2 - 10.1016/j.wneu.2024.08.060
DO - 10.1016/j.wneu.2024.08.060
M3 - Review article
C2 - 39233309
AN - SCOPUS:85203280665
SN - 1878-8750
VL - 191
SP - 138
EP - 148
JO - World Neurosurgery
JF - World Neurosurgery
ER -