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Cancers
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The Role of Chromosomal Instability in Cancer
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The Role of Chromosomal Instability in Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: closed (30 September 2024) | Viewed by 5828

Special Issue Editor

Prof. Dr. Henry H. Heng

E-Mail Website
Guest Editor
Center for Molecular Medicine and Genomics, and Pathology Department, Wayne State University School of Medicine, Detroit, MI 48201, USA
Interests: cancer evolution; chromosomal coding; karyotype mediated-drug resistance; fuzzy inheritance; genome instability and chaos; genome theory; mechanism of heterogeneity; system inheritance
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The current Cancer Genome Project has unexpectedly thrown chromosomal instability (CIN) into the spotlight. While it is hard to identify the common recurrent gene mutation pattern for the majority of cancer types, the phenomenon of elevated CIN is overwhelming across all. Furthermore, landscapes of chromosomal or genome-level changes have better clinical prediction power than gene mutation profiles. Such facts challenge the somatic gene mutation theory of cancer and call for a search for new conceptual frameworks and technological platforms. 

In recent years, our understanding of cancer evolution mechanisms has undergone significant progress. Two-phased evolution, comprising a chromosomal alteration-mediated punctuated macroevolutionary phase and gene mutation-mediated gradual microevolutionary phase, has been identified; the Genome Architecture Theory of evolution has been proposed to explain how the karyotype (comprised of chromosomal sets) codes a “system inheritance” that organizes gene interaction; and genome chaos, rapid genome reorganization (including chromothripsis and polyploid giant cancer cells), has been identified as powerful source of new genomic information.

The role of CIN in cancer is highly significant and deserves further, timely research. Thus, this issue may include the following topics:

  1. A case study that links CIN to any hallmark of cancer (via specific molecular mechanisms).
  2. The mechanistic study of CIN.
  3. The study of the relationship between different types of chromosomal variations (e.g., aneuploidy, polyploidy, chromosome translocations, chromothripsis, and other subtypes of genome chaos).
  4. Studies measuring CIN (e.g., single-cell data, high-C data, converting sequence data into cytogenetic data, and 3D image analysis).
  5. Studies using CIN as a biomarker for prognosis and diagnosis.
  6. Studies on the relationship between CIN and major phase transitions such as transformation, metastasis, and drug resistance.

Prof. Dr. Henry H. Heng
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • aneuploidy
  • cancer evolution
  • chromothripsis
  • chromosomal translocation
  • genome chaos
  • genome instability
  • heterogeneity
  • karyotype coding
  • polyploid giant cancer cells

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Published Papers (3 papers)

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16 pages, 3855 KiB  
Article
Polyploid Giant Cancer Cells Generated from Human Cytomegalovirus-Infected Prostate Epithelial Cells
by Fidaa Bouezzedine, Ranim El Baba, Sandy Haidar Ahmad and Georges Herbein
Cancers 2023, 15(20), 4994; https://doi.org/10.3390/cancers15204994 - 15 Oct 2023
Cited by 9 | Viewed by 1835
Abstract
Background: Prostate cancer is the most commonly diagnosed malignancy and the sixth leading cause of cancer death in men worldwide. Chromosomal instability (CIN) and polyploid giant cancer cells (PGCCs) have been considered predominant hallmarks of cancer. Recent clinical studies have proven the association [...] Read more.
Background: Prostate cancer is the most commonly diagnosed malignancy and the sixth leading cause of cancer death in men worldwide. Chromosomal instability (CIN) and polyploid giant cancer cells (PGCCs) have been considered predominant hallmarks of cancer. Recent clinical studies have proven the association of CIN, aneuploidy, and PGCCs with poor prognosis of prostate cancer (PCa). Evidence of HCMV transforming potential might indicate that HCMV may be involved in PCa. Methods: Herein, we underline the role of the high-risk HCMV-DB and -BL clinical strains in transforming prostate epithelial cells and assess the molecular and cellular oncogenic processes associated with PCa. Results: Oncogenesis parallels a sustained growth of “CMV-Transformed Prostate epithelial cells” or CTP cells that highly express Myc and EZH2, forming soft agar colonies and displaying stemness as well as mesenchymal features, hence promoting EMT as well as PGCCs and a spheroid appearance. Conclusions: HCMV-induced Myc and EZH2 upregulation coupled with stemness and EMT traits in IE1-expressing CTP might highlight the potential role of HCMV in PCa development and encourage the use of anti-EZH2 and anti-HCMV in PCa treatment. Full article
(This article belongs to the Special Issue The Role of Chromosomal Instability in Cancer)
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13 pages, 1365 KiB  
Commentary
Amitotic Cell Division, Malignancy, and Resistance to Anticancer Agents: A Tribute to Drs. Walen and Rajaraman
by Razmik Mirzayans and David Murray
Cancers 2024, 16(17), 3106; https://doi.org/10.3390/cancers16173106 - 8 Sep 2024
Viewed by 1651
Abstract
Cell division is crucial for the survival of living organisms. Human cells undergo three types of cell division: mitosis, meiosis, and amitosis. The former two types occur in somatic cells and germ cells, respectively. Amitosis involves nuclear budding and occurs in cells that [...] Read more.
Cell division is crucial for the survival of living organisms. Human cells undergo three types of cell division: mitosis, meiosis, and amitosis. The former two types occur in somatic cells and germ cells, respectively. Amitosis involves nuclear budding and occurs in cells that exhibit abnormal nuclear morphology (e.g., polyploidy) with increased cell size. In the early 2000s, Kirsten Walen and Rengaswami Rajaraman and his associates independently reported that polyploid human cells are capable of producing progeny via amitotic cell division, and that a subset of emerging daughter cells proliferate rapidly, exhibit stem cell-like properties, and can contribute to tumorigenesis. Polyploid cells that arise in solid tumors/tumor-derived cell lines are referred to as polyploid giant cancer cells (PGCCs) and are known to contribute to therapy resistance and disease recurrence following anticancer treatment. This commentary provides an update on some of these intriguing discoveries as a tribute to Drs. Walen and Rajaraman. Full article
(This article belongs to the Special Issue The Role of Chromosomal Instability in Cancer)
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8 pages, 1705 KiB  
Opinion
Macromutations Yielding Karyotype Alterations (and the Process(es) behind Them) Are the Favored Route of Carcinogenesis and Speciation
by Ingo Schubert
Cancers 2024, 16(3), 554; https://doi.org/10.3390/cancers16030554 - 28 Jan 2024
Cited by 3 | Viewed by 1401
Abstract
It is argued that carcinogenesis and speciation are evolutionary events which are based on changes in the ‘karyotypic code’ through a phase of ‘genome instability’, followed by a bottleneck of selection for the viability and adaptability of the initial cells. Genomic (i.e., chromosomal) [...] Read more.
It is argued that carcinogenesis and speciation are evolutionary events which are based on changes in the ‘karyotypic code’ through a phase of ‘genome instability’, followed by a bottleneck of selection for the viability and adaptability of the initial cells. Genomic (i.e., chromosomal) instability is caused by (massive) DNA breakage and the subsequent mis-repair of DNA double-strand breaks (DSBs) resulting in various chromosome rearrangements. Potential tumor cells are selected for rapid somatic proliferation. Cells eventually yielding a novel species need not only to be viable and proliferation proficient, but also to have a balanced genome which, after passing meiosis as another bottleneck and fusing with an identical gamete, can result in a well-adapted organism. Such new organisms should be genetically or geographically isolated from the ancestral population and possess or develop an at least partial sexual barrier. Full article
(This article belongs to the Special Issue The Role of Chromosomal Instability in Cancer)
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