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Genomic Instability and the DNA Damage Repair Response in Malignant...
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Genomic Instability and the DNA Damage Repair Response in Malignant Brain Tumors: Factors Underpinning Cancer Progression, Treatment Resistance, and Inter/Intra-Tumoral Heterogeneity

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

Deadline for manuscript submissions: closed (30 October 2021) | Viewed by 9371

Special Issue Editor

Dr. Sachin Katyal

E-Mail Website
Guest Editor
Deptartment of Pharmacology and Therapeutics, University of Manitoba, Research Institute in Oncology and Hematology, CancerCare Manitoba; Winnipeg, MB, Canada
Interests: DNA damage and repair; brain tumors; brain tumour initiating cells (BTICs); high-throughput methodologies; drug screening/testing; animals models; primary cultures; treatment resistance; personalized medicine

Special Issue Information

Dear Colleagues,

Although comprising a small percentage (~2%) of all cancer types, malignant brain tumors affect both young and old, are often lethal, and account for a high degree of worldwide cancer mortality. Pediatric brain tumors, including gliomas and embryonal tumors, are the leading cause of cancer-related death among children and adolescents, while gliomas and meningiomas account for significant mortality in adults. Whereas precision medicine approaches are emerging, these tumors are usually treated with combinations of radiation; chemotherapy; and, more recently, immunotherapy. Recurrence of these malignant tumors is pervasive due to resistance to anticancer therapeutics, which may involve pronounced genomic instability or alteration in DNA damage repair responses elicited by chemoradiotherapy.

This Special Issue invites short reports, original research, and review articles that highlight recent advances using in vitro, in vivo, animal models, and clinical studies that expand our understanding of how genomic instability and DNA damage repair responses affect brain tumor initiation, progression, heterogeneity and treatment resistance.

Dr. Sachin Katyal
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

  • brain tumors
  • DNA damage repair
  • genomic instability
  • chemoradiotherapy
  • alkylating agents
  • immunotherapy
  • tumor heterogeneity
  • treatment resistance
  • targeted therapy
  • glioblastoma multiforme
  • medulloblastoma
  • ependymoma
  • AT/RT
  • meningioma

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Published Papers (3 papers)

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Research

12 pages, 2444 KiB  
Article
Loss of CENP-I Impairs Homologous Recombination and Sensitizes Cells to PARP1 Inhibition
by Tuyen T. Dang and Julio C. Morales
Cancers 2021, 13(13), 3202; https://doi.org/10.3390/cancers13133202 - 26 Jun 2021
Cited by 2 | Viewed by 2461
Abstract
Centromere Protein I (CENP-I) is a member of the CENP-H/I/K complex. CENP-H/I/K is a major component of the inner kinetochore and aids in ensuring proper chromosomal segregation during mitosis. In addition to this chromosomal segregation function, CENP-I also plays a role in DNA [...] Read more.
Centromere Protein I (CENP-I) is a member of the CENP-H/I/K complex. CENP-H/I/K is a major component of the inner kinetochore and aids in ensuring proper chromosomal segregation during mitosis. In addition to this chromosomal segregation function, CENP-I also plays a role in DNA double-strand break (DSB) repair. Loss of CENP-I leads to increased endogenous 53BP1 foci and R-loop formation, while reducing cellular survival after ionizing radiation and Niraparib, a PARP1 small molecule inhibitor, exposures. Cells lacking CENP-I display delayed 53BP1 foci regression, an indication that DSB repair is impaired. Additionally, loss of CENP-I impairs the homologous recombination DSB repair pathway, while having no effect on the non-homologous end-joining pathway. Interestingly, we find that RNaseH1 expression restores HR capacity in CENP-I deficient cells. Importantly, CENP-I expression is elevated in glioma tissue as compared to normal brain tissue. This elevated expression also correlates with poor overall patient survival. These data highlight the multi-functional role CENP-I plays in maintaining genetic, as well as chromosomal, stability and tumor survival. Full article
(This article belongs to the Special Issue Genomic Instability and the DNA Damage Repair Response in Malignant Brain Tumors: Factors Underpinning Cancer Progression, Treatment Resistance, and Inter/Intra-Tumoral Heterogeneity)
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21 pages, 3467 KiB  
Article
Multiregional Sequencing of IDH-WT Glioblastoma Reveals High Genetic Heterogeneity and a Dynamic Evolutionary History
by Sara Franceschi, Prospero Civita, Francesco Pasqualetti, Francesca Lessi, Martina Modena, Serena Barachini, Mariangela Morelli, Orazio Santonocito, Riccardo Vannozzi, Geoffrey J. Pilkington, Valerio Ortenzi, Antonio Giuseppe Naccarato, Paolo Aretini and Chiara Maria Mazzanti
Cancers 2021, 13(9), 2044; https://doi.org/10.3390/cancers13092044 - 23 Apr 2021
Cited by 4 | Viewed by 3156
Abstract
Glioblastoma is one of the most common and lethal primary neoplasms of the brain. Patient survival has not improved significantly over the past three decades and the patient median survival is just over one year. Tumor heterogeneity is thought to be a major [...] Read more.
Glioblastoma is one of the most common and lethal primary neoplasms of the brain. Patient survival has not improved significantly over the past three decades and the patient median survival is just over one year. Tumor heterogeneity is thought to be a major determinant of therapeutic failure and a major reason for poor overall survival. This work aims to comprehensively define intra- and inter-tumor heterogeneity by mapping the genomic and mutational landscape of multiple areas of three primary IDH wild-type (IDH-WT) glioblastomas. Using whole exome sequencing, we explored how copy number variation, chromosomal and single loci amplifications/deletions, and mutational burden are spatially distributed across nine different tumor regions. The results show that all tumors exhibit a different signature despite the same diagnosis. Above all, a high inter-tumor heterogeneity emerges. The evolutionary dynamics of all identified mutations within each region underline the questionable value of a single biopsy and thus the therapeutic approach for the patient. Multiregional collection and subsequent sequencing are essential to try to address the clinical challenge of precision medicine. Especially in glioblastoma, this approach could provide powerful support to pathologists and oncologists in evaluating the diagnosis and defining the best treatment option. Full article
(This article belongs to the Special Issue Genomic Instability and the DNA Damage Repair Response in Malignant Brain Tumors: Factors Underpinning Cancer Progression, Treatment Resistance, and Inter/Intra-Tumoral Heterogeneity)
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20 pages, 4329 KiB  
Article
Mapping and Quantification of Non-Coding RNA Originating from the rDNA in Human Glioma Cells
by Anastasia A. Sadova, Natalia S. Kupriyanova and Galina V. Pavlova
Cancers 2020, 12(8), 2090; https://doi.org/10.3390/cancers12082090 - 28 Jul 2020
Cited by 8 | Viewed by 3249
Abstract
Ribosomal DNA is one of the most conserved parts of the genome, especially in its rRNA coding regions, but some puzzling pieces of its noncoding repetitive sequences harbor secrets of cell growth and development machinery. Disruptions in the neat mechanisms of rDNA orchestrating [...] Read more.
Ribosomal DNA is one of the most conserved parts of the genome, especially in its rRNA coding regions, but some puzzling pieces of its noncoding repetitive sequences harbor secrets of cell growth and development machinery. Disruptions in the neat mechanisms of rDNA orchestrating the cell functioning result in malignant conversion. In cancer cells, the organization of rRNA coding genes and their transcription somehow differ from that of normal cells, but little is known about the particular mechanism for this switch. In this study, we demonstrate that the region ~2 kb upstream of the rDNA promoter is transcriptionally active in one type of the most malignant human brain tumors, and we compare its expression rate to that of healthy human tissues and cell cultures. Sense and antisense non-coding RNA transcripts were detected and mapped, but their secondary structure and functions remain to be elucidated. We propose that the transcripts may relate to a new class of so-called promoter-associated RNAs (pRNAs), or have some other regulatory functions. We also hope that the expression of these non-coding RNAs can be used as a marker in glioma diagnostics and prognosis. Full article
(This article belongs to the Special Issue Genomic Instability and the DNA Damage Repair Response in Malignant Brain Tumors: Factors Underpinning Cancer Progression, Treatment Resistance, and Inter/Intra-Tumoral Heterogeneity)
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