CRISPR in Cancer Biology and Therapy

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Methods and Technologies Development".

Deadline for manuscript submissions: 15 July 2024 | Viewed by 6407

Special Issue Editor


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Guest Editor
RNA Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA
Interests: cancer drug resistance; targeted-therapy; CRISPR screens; CRISPR-related technology; base eating; gene editing; prime editing; off-target analysis; AAV delivery

Special Issue Information

Dear Colleagues,

Cancer is a disease of the genome, initiated by the activation of oncogenes and the inactivation of tumor suppressors. It is also a disease of the cell, feeding off changes in metabolism and motility to be able to grow in different environments. Understanding how genomic changes drive the initiation of individual cancers is crucial for developing more effective treatment options and improving outcomes for cancer patients.

CRISPR has been realized as a tool for programmable genome modification in almost all cell types. The development of different CRISPR-mediated genome editing tools continues to drive major advances in the life sciences. Currently, four classes of CRISPR-Cas-derived genome editing agents—nucleases, base editors, transposases and prime editors—are currently available for modifying genomes. Each of them has its own capabilities, and a lot of efforts have expanded their targeting scope and enhanced editing specificity.

In cancer research, CRISPR-related tools have greatly advanced our understanding of cancer genetics and tumor heterogeneity, providing new insights into therapeutic vulnerabilities. This Special Issue will focus on the development of CRISPR systems as a tool to study cancers, and the emerging adaptation of these technologies to improve diagnosis and treatment.

Dr. Shunqing Liang
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 short 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

  • cancer drug resistance
  • CRISPR screens
  • CRISPR-related technology
  • base editing
  • prime editing
  • off-target analysis
  • adeno-associated virus

Published Papers (3 papers)

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Research

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14 pages, 2616 KiB  
Communication
Analysis of Cancer Genomic Amplifications Identifies Druggable Collateral Dependencies within the Amplicon
by Guillem Pons, Gabriel Gallo-Oller, Natalia Navarro, Patricia Zarzosa, Júlia Sansa-Girona, Lia García-Gilabert, Ainara Magdaleno, Miguel F. Segura, Josep Sánchez de Toledo, Soledad Gallego, Lucas Moreno and Josep Roma
Cancers 2023, 15(6), 1636; https://doi.org/10.3390/cancers15061636 - 7 Mar 2023
Viewed by 2808
Abstract
The identification of novel therapeutic targets for specific cancer molecular subtypes is crucial for the development of precision oncology. In the last few years, CRISPR/Cas9 screens have accelerated the discovery and validation of new targets associated with different tumor types, mutations, and fusions. [...] Read more.
The identification of novel therapeutic targets for specific cancer molecular subtypes is crucial for the development of precision oncology. In the last few years, CRISPR/Cas9 screens have accelerated the discovery and validation of new targets associated with different tumor types, mutations, and fusions. However, there are still many cancer vulnerabilities associated with specific molecular features that remain to be explored. Here, we used data from CRISPR/Cas9 screens in 954 cancer cell lines to identify gene dependencies associated with 16 common cancer genomic amplifications. We found that high-copy-number genomic amplifications generate multiple collateral dependencies within the amplified region in most cases. Further, to prioritize candidate targets for each chromosomal region amplified, we integrated gene dependency parameters with both druggability data and subcellular location. Finally, analysis of the relationship between gene expression and gene dependency led to the identification of genes, the expression of which may constitute predictive biomarkers of dependency. In conclusion, our study provides a set of druggable targets specific for each amplification, opening the possibility to specifically target amplified tumors on this basis. Full article
(This article belongs to the Special Issue CRISPR in Cancer Biology and Therapy)
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Review

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15 pages, 1260 KiB  
Review
CRISPRing KRAS: A Winding Road with a Bright Future in Basic and Translational Cancer Research
by Xian Gong, Jianting Du, Ren-Wang Peng, Chun Chen and Zhang Yang
Cancers 2024, 16(2), 460; https://doi.org/10.3390/cancers16020460 - 22 Jan 2024
Viewed by 1674
Abstract
Once considered “undruggable” due to the strong affinity of RAS proteins for GTP and the structural lack of a hydrophobic “pocket” for drug binding, the development of proprietary therapies for KRAS-mutant tumors has long been a challenging area of research. CRISPR technology, the [...] Read more.
Once considered “undruggable” due to the strong affinity of RAS proteins for GTP and the structural lack of a hydrophobic “pocket” for drug binding, the development of proprietary therapies for KRAS-mutant tumors has long been a challenging area of research. CRISPR technology, the most successful gene-editing tool to date, is increasingly being utilized in cancer research. Here, we provide a comprehensive review of the application of the CRISPR system in basic and translational research in KRAS-mutant cancer, summarizing recent advances in the mechanistic understanding of KRAS biology and the underlying principles of drug resistance, anti-tumor immunity, epigenetic regulatory networks, and synthetic lethality co-opted by mutant KRAS. Full article
(This article belongs to the Special Issue CRISPR in Cancer Biology and Therapy)
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13 pages, 1221 KiB  
Review
Pre-Clinical Models to Study Human Prostate Cancer
by Martin K. Thomsen and Morten Busk
Cancers 2023, 15(17), 4212; https://doi.org/10.3390/cancers15174212 - 22 Aug 2023
Cited by 1 | Viewed by 1417
Abstract
Prostate cancer is a common cancer among men and typically progresses slowly for several decades before becoming aggressive and spreading to other organs, leaving few treatment options. While large animals have been studied, the dog’s prostate is anatomically similar to humans and has [...] Read more.
Prostate cancer is a common cancer among men and typically progresses slowly for several decades before becoming aggressive and spreading to other organs, leaving few treatment options. While large animals have been studied, the dog’s prostate is anatomically similar to humans and has been used to study spontaneous prostate cancer. However, most research currently focuses on the mouse as a model organism due to the ability to genetically modify their prostatic tissues for molecular analysis. One milestone in this research was the identification of the prostate-specific promoter Probasin, which allowed for the prostate-specific expression of transgenes. This has led to the generation of mice with aggressive prostatic tumors through overexpression of the SV40 oncogene. The Probasin promoter is also used to drive Cre expression and has allowed researchers to generate prostate-specific loss-of-function studies. Another landmark moment in the process of modeling prostate cancer in mice was the orthoptic delivery of viral particles. This technology allows the selective overexpression of oncogenes from lentivirus or the use of CRISPR to generate complex loss-of-function studies. These genetically modified models are complemented by classical xenografts of human prostate tumor cells in immune-deficient mice. Overall, pre-clinical models have provided a portfolio of model systems to study and address complex mechanisms in prostate cancer for improved treatment options. This review will focus on the advances in each technique. Full article
(This article belongs to the Special Issue CRISPR in Cancer Biology and Therapy)
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