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Transdifferentiation, also known as lineage reprogramming, was first discovered by Selman and Kafatos in 1974 in silkmoths. They observed that the moths’ cuticle-producing cells transformed into salt-producing cells. Many such cases of natural transdifferentiation occur in organisms. In humans, pancreatic alpha cells can become beta cells. In newts, the loss of the eye’s lens causes the pigmented epithelial cells to transdifferentiate into the lens cells.
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The ability of induced pluripotent stem cells or iPSCs to differentiate into most body cell types has stimulated repair and regenerative medicine research over the past few decades. iPSC-derived blood cells, hepatocytes, beta islet cells, cardiomyocytes, neurons, and other cell types can repair injuries or regenerate damaged tissue in diseases such as diabetes and neurodegenerative disorders.
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Related Experiment Video

Updated: Feb 27, 2026

Generation of CAR T Cells for Adoptive Therapy in the Context of Glioblastoma Standard of Care
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GSCs in the Transdifferentiation Phenomenon: Focus on CAR-T-Based Therapy.

Martina Di Marco1, Alessandro Lo Giudice1, Francesca Chiara Cecala1

  • 1Institute of Human Anatomy and Histology, Department of Biomedicine, Neurosciences and Advanced Diagnostics (BiND), University of Palermo, 90133 Palermo, Italy.

Cells
|February 26, 2026
PubMed
Summary

Glioblastoma stem cells (GSCs) drive lethal brain tumors through transdifferentiation. Chimeric antigen receptor (CAR)-T therapies show promise for targeting these resilient cells and improving glioblastoma treatment outcomes.

Keywords:
CAR-T therapyGBMGSCstransdifferentiation

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Area of Science:

  • Oncology
  • Immunotherapy
  • Cancer Biology

Background:

  • Glioblastoma (GBM) is a lethal brain tumor driven by resilient glioblastoma stem cells (GSCs).
  • GSCs promote tumor growth, recurrence, and therapy resistance via transdifferentiation into endothelial- and pericyte-like cells.
  • This transdifferentiation supports tumor neovascularization and immune suppression, contributing to GBM's malignancy.

Purpose of the Study:

  • To review the molecular mechanisms of GSC transdifferentiation.
  • To summarize current chimeric antigen receptor (CAR)-T cell therapies targeting GSCs.
  • To highlight the potential of CAR-T immunotherapy for overcoming GBM treatment resistance.

Main Methods:

  • Literature review of GSC transdifferentiation mechanisms.
  • Survey of existing CAR-T cell therapy strategies for glioblastoma.
  • Integration of GSC biology and CAR-T therapy advancements.

Main Results:

  • GSC transdifferentiation is a key mechanism for GBM aggressiveness and therapeutic resistance.
  • CAR-T therapies offer a targeted approach to eliminate GSCs and their pro-tumorigenic functions.
  • CAR-T interventions can potentially disrupt GSC-mediated vascularization and immune evasion.

Conclusions:

  • Understanding GSC transdifferentiation is crucial for developing effective GBM treatments.
  • CAR-T cell therapy represents a promising next-generation immunotherapy for glioblastoma.
  • Targeting GSCs with CAR-T cells may overcome therapeutic resistance and improve patient outcomes.