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Cellular Signalling in Cell Fusion 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 November 2022) | Viewed by 3529

Special Issue Editor


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Guest Editor
Chair of Immunology, Witten/Herdecke University, 58448 Witten, Germany
Interests: cell fusion; breast cancer; stem cells; macrophages; inflammation; metastasis; drug resistance
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Special Issue Information

Dear Colleagues, 

The biological phenomenon of cell fusion remains a mystery. Even though it is mandatory for several physiological and pathophysiological processes, little is known about it. Cell fusion is a tightly regulated process since cells are not fusogenic per se. They first have to be converted to a pro-fusogenic state in order to be able to hybridize. Subsequently, they have to assume a non-fusogenic state once again.

Some questions remain. Which signals and signal pathways are necessary for cells to assume a pro-fusogenic state, and what does a pro-fusogenic state look like?

How do pro-fusogenic cells recognize their fusion partners and which proteins/mechanisms are involved? How is the cell fusion process ultimately terminated?

Which phenotype do hybrid cells adopt?

Do they remain at a multi-nuclear stage or does heterokaryon-to-synkaryon transition occur, which may be associated with aneuploidy?

These questions will be answered in this Special Issue.

Prof. Dr. Thomas Dittmar
Guest Editor

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Keywords

  • cell fusion
  • signal transduction
  • aneuploidy
  • cancer

Published Papers (1 paper)

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Review

26 pages, 1568 KiB  
Review
Generation of Cancer Stem/Initiating Cells by Cell–Cell Fusion
by Thomas Dittmar
Int. J. Mol. Sci. 2022, 23(9), 4514; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23094514 - 19 Apr 2022
Cited by 8 | Viewed by 3030
Abstract
CS/ICs have raised great expectations in cancer research and therapy, as eradication of this key cancer cell type is expected to lead to a complete cure. Unfortunately, the biology of CS/ICs is rather complex, since no common CS/IC marker has yet been identified. [...] Read more.
CS/ICs have raised great expectations in cancer research and therapy, as eradication of this key cancer cell type is expected to lead to a complete cure. Unfortunately, the biology of CS/ICs is rather complex, since no common CS/IC marker has yet been identified. Certain surface markers or ALDH1 expression can be used for detection, but some studies indicated that cancer cells exhibit a certain plasticity, so CS/ICs can also arise from non-CS/ICs. Another problem is intratumoral heterogeneity, from which it can be inferred that different CS/IC subclones must be present in the tumor. Cell–cell fusion between cancer cells and normal cells, such as macrophages and stem cells, has been associated with the generation of tumor hybrids that can exhibit novel properties, such as an enhanced metastatic capacity and even CS/IC properties. Moreover, cell–cell fusion is a complex process in which parental chromosomes are mixed and randomly distributed among daughter cells, resulting in multiple, unique tumor hybrids. These, if they have CS/IC properties, may contribute to the heterogeneity of the CS/IC pool. In this review, we will discuss whether cell–cell fusion could also lead to the origin of different CS/ICs that may expand the overall CS/IC pool in a primary tumor. Full article
(This article belongs to the Special Issue Cellular Signalling in Cell Fusion 2.0)
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