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Residual Disease in Glioma Recurrence: A Dangerous Liaison with Senescence
Diana A Putavet1, Peter L J de Keizer1
1Center for Molecular Medicine, Division LAB, University Medical Center Utrecht, 3584CG Utrecht, The Netherlands.
Abstract:
With a dismally low median survival of less than two years after diagnosis, Glioblastoma (GBM) is the most lethal type of brain cancer. The standard-of-care of surgical resection, followed by DNA-damaging chemo-/radiotherapy, is often non-curative. In part, this is because individual cells close to the resection border remain alive and eventually undergo renewed proliferation. These residual, therapy-resistant cells lead to rapid recurrence, against which no effective treatment exists to date. Thus, new experimental approaches need to be developed against residual disease to prevent GBM survival and recurrence. Cellular senescence is an attractive area for the development of such new approaches. Senescence can occur in healthy cells when they are irreparably damaged. Senescent cells develop a chronic secretory phenotype that is generally considered pro-tumorigenic and pro-migratory. Age is a negative prognostic factor for GBM stage, and, with age, senescence steadily increases. Moreover, chemo-/radiotherapy can provide an additional increase in senescence close to the tumor. In light of this, we will review the importance of senescence in the tumor-supportive brain parenchyma, focusing on the invasion and growth of GBM in residual disease. We will propose a future direction on the application of anti-senescence therapies against recurrent GBM.
Insights
Glioblastoma (GBM) recurrence is driven by therapy-resistant cells. Targeting cellular senescence, a state of irreversible cell damage, offers a promising new strategy to prevent GBM survival and recurrence.
Area of Science:
- Oncology
- Cellular Biology
- Neuroscience
Background:
- Glioblastoma (GBM) has a poor prognosis with a median survival under two years.
- Standard treatments (surgery, chemotherapy, radiotherapy) are often curative, leaving residual, therapy-resistant cells.
- These residual cells drive rapid GBM recurrence, necessitating novel therapeutic strategies.
Purpose of the Study:
- To review the role of cellular senescence in Glioblastoma (GBM) residual disease.
- To explore how senescence contributes to GBM invasion and growth in the brain parenchyma.
- To propose anti-senescence therapies as a future direction for treating recurrent GBM.
Main Methods:
- Literature review focusing on cellular senescence and Glioblastoma (GBM).
- Analysis of the impact of aging and chemo-/radiotherapy on senescence in the brain.
- Discussion of the pro-tumorigenic secretory phenotype of senescent cells.
Main Results:
- Cellular senescence, increased by age and therapy, plays a critical role in GBM residual disease.
- Senescent cells in the brain parenchyma promote GBM invasion and growth.
- The secretory phenotype of senescent cells contributes to a pro-tumorigenic microenvironment.
Conclusions:
- Cellular senescence is a key factor in Glioblastoma (GBM) recurrence.
- Targeting senescent cells presents a viable therapeutic avenue to combat residual GBM.
- Anti-senescence therapies hold potential for improving outcomes in recurrent Glioblastoma.
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