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Intratumor Heterogeneity and Therapy Resistance of Solid Tumors: Treacherous Apoptosis, Reversible Senescence, Genome Chaos, and More

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

Deadline for manuscript submissions: 20 January 2025 | Viewed by 2854

Special Issue Editor

Prof. Dr. Razmik Mirzayans

E-Mail Website
Guest Editor
Department of Oncology, Cross Cancer Institute, University of Alberta, Edmonton, AB T6G 1Z2, Canada
Interests: DNA damage response; p53 signaling; senescence; polyploidy; multinucleation; radioresistance; chemoresistance
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Single-cell biology has revealed that acquired resistance of cancer cells to therapeutic agents is multifactorial, with several unrelated mechanisms employed simultaneously by different subsets of cancer cells within the same tumor (intratumor heterogeneity). These include therapy-induced dormancy (durable proliferation arrest through polyploidy, multinucleation, and other manifestations of genome chaos), oncogenic caspase-3 activation (treacherous apoptosis), anastasis (a cell recovery phenomenon that rescues cancer cells from the brink of apoptotic and other modes of cell death), and cell fusion. The wild-type p53 and its downstream effector p21WAF1 also contribute to intratumor heterogeneity by activating transient cell cycle checkpoints to promote DNA repair, downregulating apoptotic cell death, and triggering a reversible proliferation arrest through premature senescence.

The purpose of this Special Issue is to provide a comprehensive update on the growing complexity of molecular and cellular responses to anticancer agents. Reviews and original research articles that utilize single cell biology to study the long-term fate of solid tumors/tumor-derived cell lines following treatment with anticancer agents are particularly welcomed.

Prof. Dr. Razmik Mirzayans
Guest Editor

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • intratumor heterogeneity
  • p53 signaling
  • cell fusion
  • reversible senescence
  • anastasis
  • oncogenic caspse-3
  • chromothripsis (genome chaos)
  • polyploid giant cancer cells (PGCCS)
  • atavistic basis of therapy resistance
  • cancer cell dormancy

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Published Papers (1 paper)

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Research

24 pages, 1138 KiB  
Article
The Spiral Model of Evolution: Stable Life Forms of Organisms and Unstable Life Forms of Cancers
by Andrzej Kasperski and Henry H. Heng
Int. J. Mol. Sci. 2024, 25(17), 9163; https://doi.org/10.3390/ijms25179163 - 23 Aug 2024
Cited by 1 | Viewed by 2385
Abstract
If one must prioritize among the vast array of contributing factors to cancer evolution, environmental-stress-mediated chromosome instability (CIN) should easily surpass individual gene mutations. CIN leads to the emergence of genomically unstable life forms, enabling them to grow dominantly within the stable life [...] Read more.
If one must prioritize among the vast array of contributing factors to cancer evolution, environmental-stress-mediated chromosome instability (CIN) should easily surpass individual gene mutations. CIN leads to the emergence of genomically unstable life forms, enabling them to grow dominantly within the stable life form of the host. In contrast, stochastic gene mutations play a role in aiding the growth of the cancer population, with their importance depending on the initial emergence of the new system. Furthermore, many specific gene mutations among the many available can perform this function, decreasing the clinical value of any specific gene mutation. Since these unstable life forms can respond to treatment differently than stable ones, cancer often escapes from drug treatment by forming new systems, which leads to problems during the treatment for patients. To understand how diverse factors impact CIN-mediated macroevolution and genome integrity–ensured microevolution, the concept of two-phased cancer evolution is used to reconcile some major characteristics of cancer, such as bioenergetic, unicellular, and multicellular evolution. Specifically, the spiral of life function model is proposed, which integrates major historical evolutionary innovations and conservation with information management. Unlike normal organismal evolution in the microevolutionary phase, where a given species occupies a specific location within the spiral, cancer populations are highly heterogenous at multiple levels, including epigenetic levels. Individual cells occupy different levels and positions within the spiral, leading to supersystems of mixed cellular populations that exhibit both macro and microevolution. This analysis, utilizing karyotype to define the genetic networks of the cellular system and CIN to determine the instability of the system, as well as considering gene mutation and epigenetics as modifiers of the system for information amplification and usage, explores the high evolutionary potential of cancer. It provides a new, unified understanding of cancer as a supersystem, encouraging efforts to leverage the dynamics of CIN to develop improved treatment options. Moreover, it offers a historically contingent model for organismal evolution that reconciles the roles of both evolutionary innovation and conservation through macroevolution and microevolution, respectively. Full article
(This article belongs to the Special Issue Intratumor Heterogeneity and Therapy Resistance of Solid Tumors: Treacherous Apoptosis, Reversible Senescence, Genome Chaos, and More)
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