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Corrigendum to: "The cell cycle inhibitor p21<sup>CIP1</sup> is essential for irinotecan-induced senescence and plays a decisive role in re-sensitization of temozolomide-resistant glioblastoma cells to irinotecan" [Biomed. Pharmacother. 181 (2024) 117634].

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Senotherapeutics in Malignant Brain Cancer Therapy.

Bernd Kaina1, Markus Christmann2

  • 1Institute of Toxicology, University Medical Center, Obere Zahlbacher Str. 67, Mainz, D-55131, Germany. kaina@uni-mainz.de.

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Summary

Glioblastoma (GBM) treatment with temozolomide induces cellular senescence, a key factor in tumor recurrence. New senotherapeutic strategies targeting senescent GBM cells are crucial for improving treatment outcomes.

Keywords:
ApoptosisGlioblastomaSenescenceSenolyticsSenomorphicsSenopreventicsSenotherapeuticsTemozolomide

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Area of Science:

  • Neuro-oncology
  • Cancer Biology
  • Cellular Senescence

Background:

  • Glioblastoma (GBM) is an aggressive brain cancer with poor prognosis despite standard radio-chemotherapy.
  • Temozolomide (TMZ), a first-line alkylating agent, induces apoptosis and cellular senescence in GBM cells.
  • Senescent GBM cells alter the tumor microenvironment, promote inflammation, and can reactivate, leading to recurrence.

Purpose of the Study:

  • To elucidate pathways of therapy-induced cellular senescence in GBM cells.
  • To review senotherapeutic agents (senolytics, senomorphics, senopreventics) for GBM treatment.
  • To discuss novel treatment strategies targeting senescent GBM cells.

Main Methods:

  • Review of current literature on GBM cellular senescence.
  • Analysis of mechanisms underlying temozolomide-induced senescence in GBM.
  • Identification and categorization of senotherapeutic drugs and natural compounds.

Main Results:

  • Temozolomide and radiation induce cellular senescence as a primary response in GBM cells.
  • Senescent GBM cells exhibit incomplete G2 arrest and endoreduplication, potentially due to CDKN2A inactivation.
  • These unique cellular responses contribute to GBM's resistance to conventional therapies.

Conclusions:

  • Cellular senescence is a critical, non-lethal response of GBM cells to radio-chemotherapy.
  • Complete elimination of GBM cells by current therapies is unlikely due to senescence.
  • Senotherapeutics (senolytics, senomorphics, senopreventics) represent promising supportive strategies for GBM treatment.