Cancer Stem Cells and Radiation Therapy

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Biophysics".

Deadline for manuscript submissions: closed (25 March 2022) | Viewed by 4275

Special Issue Editor


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Guest Editor
Department of Radiation Oncology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA
Interests: cancer stem cells; radiation; glioma; breast cancer; stem cells

Special Issue Information

Dear Colleagues,

Growing evidence supports the hierarchical organization of solid cancer with a small population of cancer stem cells/cancer-initiating cells at the apex of this hierarchy, able to regrow a tumor after sublethal treatment and to produce more differentiated progeny. The heterogeneity of cancers and the cancer stem cell hypothesis are a century-old concept in oncology that has been taken into consideration in radiation biology and radiotherapy for decades. Radiotherapy is and will remain a main pillar of clinical cancer treatment in the foreseeable future, and radiation is the most precisely administered ‘drug’ against cancer, and the one we continue to know the most about. Nevertheless, the radiobiology of cancer stem cells/cancer-initiating cells is less developed. In recent years, novel marker systems and culturing techniques that enrich cancer cells have taken radiobiology research on tumor-initiating cells to the next level.

It is becoming increasingly clear that the heterogeneity of cancer cells is not restricted to differences in tumorgenicity but also extends to their response to genotoxic stress, interaction with the tumor microenvironment, and targeted therapies in combined modality regimens. The purpose of this Special Issue is to summarize our current state of knowledge on the radiation biology of cancer stem/cancer-initiating cells in solid cancers, experimental methods, and gold standards to assess cancer stem cell/tumor-initiating cell traits at the functional level in vitro and in vivo and to highlight recent developments in the field to improve the efficacy of radiotherapy against cancer stem/cancer-initiating cells.   

Prof. Dr. Frank Pajonk
Guest Editor

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Published Papers (1 paper)

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23 pages, 2352 KiB  
Perspective
Role of the Circadian Clock “Death-Loop” in the DNA Damage Response Underpinning Cancer Treatment Resistance
by Ninel Miriam Vainshelbaum, Kristine Salmina, Bogdan I. Gerashchenko, Marija Lazovska, Pawel Zayakin, Mark Steven Cragg, Dace Pjanova and Jekaterina Erenpreisa
Cells 2022, 11(5), 880; https://doi.org/10.3390/cells11050880 - 3 Mar 2022
Cited by 12 | Viewed by 3654
Abstract
Here, we review the role of the circadian clock (CC) in the resistance of cancer cells to genotoxic treatments in relation to whole-genome duplication (WGD) and telomere-length regulation. The CC drives the normal cell cycle, tissue differentiation, and reciprocally regulates telomere elongation. However, [...] Read more.
Here, we review the role of the circadian clock (CC) in the resistance of cancer cells to genotoxic treatments in relation to whole-genome duplication (WGD) and telomere-length regulation. The CC drives the normal cell cycle, tissue differentiation, and reciprocally regulates telomere elongation. However, it is deregulated in embryonic stem cells (ESCs), the early embryo, and cancer. Here, we review the DNA damage response of cancer cells and a similar impact on the cell cycle to that found in ESCs—overcoming G1/S, adapting DNA damage checkpoints, tolerating DNA damage, coupling telomere erosion to accelerated cell senescence, and favouring transition by mitotic slippage into the ploidy cycle (reversible polyploidy). Polyploidy decelerates the CC. We report an intriguing positive correlation between cancer WGD and the deregulation of the CC assessed by bioinformatics on 11 primary cancer datasets (rho = 0.83; p < 0.01). As previously shown, the cancer cells undergoing mitotic slippage cast off telomere fragments with TERT, restore the telomeres by ALT-recombination, and return their depolyploidised offspring to telomerase-dependent regulation. By reversing this polyploidy and the CC “death loop”, the mitotic cycle and Hayflick limit count are thus again renewed. Our review and proposed mechanism support a life-cycle concept of cancer and highlight the perspective of cancer treatment by differentiation. Full article
(This article belongs to the Special Issue Cancer Stem Cells and Radiation Therapy)
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