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Cancer stem cells in glioblastoma – an update

Sengupta, S and Mukherjee, A and Somasundaram, K (2023) Cancer stem cells in glioblastoma – an update. [Book Chapter]

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Official URL: https://doi.org/10.1016/B978-0-323-99873-4.00001-3


Cancer arises due to genetic alterations, which allow cells to proliferate uncontrollably and acquire other features to become an invasive tumor. The rationale behind the traditional therapies is that they target rapidly proliferating tumor cells. However, these therapies have failed due to genetic and cellular heterogeneity, which allows a subpopulation of cancer cells to escape treatment resulting in cancer recurrence. Considerable evidence points to the existence of cancer stem-like cells (CSCs) that form a varying yet a minority fraction within tumors. The CSCs alone can initiate tumors in vivo and are responsible for therapy resistance, thus warranting more attention on their origin and biology. The process of tumor initiation by CSCs presumably involves, besides their self-renewal, differentiation into bulk cells (non-CSCs), which forms the basis of plasticity that arises due to epigenetic programming. Evidence indicates that non-CSCs reprogram to create CSCs, thus making the proportions of CSCs and non-CSCs highly dynamic in a given tumor. Transdifferentiation is another type of plasticity wherein, tumor cells or CSCs acquire features of different cell lineage like endothelial cells resulting in a more aggressive tumor. Understanding the mechanisms behind various forms of cellular plasticity may help develop novel strategies for treating cancer. © 2023 Elsevier Inc. All rights reserved.

Item Type: Book Chapter
Publication: New Insights into Glioblastoma: Diagnosis, Therapeutics and Theranostics
Publisher: Elsevier
Additional Information: The copyright for this article belongs to the Elsevier
Department/Centre: Division of Biological Sciences > Microbiology & Cell Biology
Date Deposited: 04 Nov 2023 03:02
Last Modified: 04 Nov 2023 03:02
URI: https://eprints.iisc.ac.in/id/eprint/83142

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