Mechanisms of apoptosis in central nervous system tumors: application to theory

Joachim P Steinbach1, Michael Weller

  • 1Laboratory of Molecular Neuro-Oncology, Department of Neurology, University of Tübingen, Medical School, Hoppe-Seyler-Strasse 3, 72076 Tübingen, Germany.

Insights

Apoptosis, programmed cell death, is crucial for brain tumor therapy. This review covers glioma apoptosis mechanisms, assessment methods, and novel strategies to induce cell death for improved treatment outcomes.

Area of Science:

  • Neuro-oncology
  • Cellular Biology
  • Molecular Medicine

Background:

  • Apoptosis is essential for effective brain tumor treatment.
  • Malignant gliomas exhibit spontaneous apoptosis.
  • Understanding apoptosis is key to developing new therapies.

Purpose of the Study:

  • To review spontaneous apoptosis mechanisms in malignant gliomas.
  • To discuss methods for assessing apoptosis in vitro and in vivo.
  • To explore novel strategies for inducing apoptosis in glioma cells.

Main Methods:

  • Literature review of apoptosis mechanisms and assessment techniques.
  • Analysis of experimental therapies targeting glioma apoptosis.
  • Evaluation of gene therapy and targeted gene expression approaches.

Main Results:

  • Apoptosis pathways in gliomas are complex.
  • Various methods exist to quantify apoptosis in tumor samples.
  • Novel strategies show promise for inducing glioma cell death.

Conclusions:

  • Quantifying apoptosis in biopsies aids diagnosis and prognosis.
  • Targeting apoptosis pathways offers therapeutic potential for malignant gliomas.
  • Future research should focus on refining these novel strategies.

Related Concept Videos

Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

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The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
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