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Cancers
Special Issues
Applied Genomics and Cancer Therapeutics
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Applied Genomics and Cancer Therapeutics

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

Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 15043

Special Issue Editors

Dr. Jeremy Chien

E-Mail Website
Guest Editor
1. Department of Obstetrics and Gynecology, University of California, Davis, CA 95817, USA
2. Department of Biochemistry and Molecular Medicine, University of California, Davis, CA 95817, USA
Interests: ovarian cancer; applied genomics; cancer genomics; functional genomics; targeted therapies; PROTAC; synthetic lethalities; acquired dependencies
Dr. Rui Kuang

E-Mail Website
Guest Editor
Department of Computer Science and Engineering, Universityof Minnesota Twin Cities, Minneapolis, MN, USA
Interests: computational cancer genomics; machine learning; biological network analysis; phenome-genome association analysis

Special Issue Information

Dear Colleagues,

The advances in next-generation sequencing technologies and functional genomics are trailblazing new frontiers in Applied Genomics and Cancer Therapeutics. The single-cell sequencing, genome-wide RNAi screens, and genome-scale CRISPR/Cas9 screens are unveiling new insights into acquired dependencies, synthetic lethalities, and new target opportunities in cancer treatment. Acquired dependencies introduced by oncogenic mutations, loss of tumor suppressor genes function, and non-oncogene addiction are presenting new avenues for the development of targeted Precision Cancer Medicine. New advances in immuno-oncology are also giving new hope to cancer patients.

This Special Issue will feature the application of functional genomics and cancer genomics in the identification of cancer targets and the development of next-generation targeted therapies focusing on proteolysis-targeting chimera (PROTAC)-based targeted proteolysis, immuno-oncology, and combination therapies to enhance immunogenic cell death. This Special Issue will cover new bioinformatics tools, novel statistical and machine learning methods, and their applications that enable or demonstrate genome-wide interrogation of acquired dependencies and synthetic lethalities in cancer. Manuscripts focusing on new target opportunities discovered from the application of functional genomics and single-cell sequencing approaches will be featured. Drug repositioning, new drug development based on genomic analysis, and new therapeutics concepts will be featured.

Dr. Jeremy Chien
Dr. Rui Kuang
Guest Editors

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.

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Further information on MDPI's Special Issue polices can be found here.

Published Papers (3 papers)

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Research

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24 pages, 7663 KiB  
Article
ABL Genomic Editing Sufficiently Abolishes Oncogenesis of Human Chronic Myeloid Leukemia Cells In Vitro and In Vivo
by Shu-Huey Chen, Yao-Yu Hsieh, Huey-En Tzeng, Chun-Yu Lin, Kai-Wen Hsu, Yun-Shan Chiang, Su-Mei Lin, Ming-Jang Su, Wen-Shyang Hsieh and Chia-Hwa Lee
Cancers 2020, 12(6), 1399; https://doi.org/10.3390/cancers12061399 - 29 May 2020
Cited by 17 | Viewed by 4391
Abstract
Chronic myelogenous leukemia (CML) is the most common type of leukemia in adults, and more than 90% of CML patients harbor the abnormal Philadelphia chromosome (Ph) that encodes the BCR-ABL oncoprotein. Although the ABL kinase inhibitor (imatinib) has proven to be very effective [...] Read more.
Chronic myelogenous leukemia (CML) is the most common type of leukemia in adults, and more than 90% of CML patients harbor the abnormal Philadelphia chromosome (Ph) that encodes the BCR-ABL oncoprotein. Although the ABL kinase inhibitor (imatinib) has proven to be very effective in achieving high remission rates and improving prognosis, up to 33% of CML patients still cannot achieve an optimal response. Here, we used CRISPR/Cas9 to specifically target the BCR-ABL junction region in K562 cells, resulting in the inhibition of cancer cell growth and oncogenesis. Due to the variety of BCR-ABL junctions in CML patients, we utilized gene editing of the human ABL gene for clinical applications. Using the ABL gene-edited virus in K562 cells, we detected 41.2% indels in ABL sgRNA_2-infected cells. The ABL-edited cells reveled significant suppression of BCR-ABL protein expression and downstream signals, inhibiting cell growth and increasing cell apoptosis. Next, we introduced the ABL gene-edited virus into a systemic K562 leukemia xenograft mouse model, and bioluminescence imaging of the mice showed a significant reduction in the leukemia cell population in ABL-targeted mice, compared to the scramble sgRNA virus-injected mice. In CML cells from clinical samples, infection with the ABL gene-edited virus resulted in more than 30.9% indels and significant cancer cell death. Notably, no off-target effects or bone marrow cell suppression was found using the ABL gene-edited virus, ensuring both user safety and treatment efficacy. This study demonstrated the critical role of the ABL gene in maintaining CML cell survival and tumorigenicity in vitro and in vivo. ABL gene editing-based therapy might provide a potential strategy for imatinib-insensitive or resistant CML patients. Full article
(This article belongs to the Special Issue Applied Genomics and Cancer Therapeutics)
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25 pages, 8643 KiB  
Article
Analysis of the Circadian Regulation of Cancer Hallmarks by a Cross-Platform Study of Colorectal Cancer Time-Series Data Reveals an Association with Genes Involved in Huntington’s Disease
by Müge Yalçin, Rukeia El-Athman, Koliane Ouk, Josef Priller and Angela Relógio
Cancers 2020, 12(4), 963; https://doi.org/10.3390/cancers12040963 - 13 Apr 2020
Cited by 16 | Viewed by 4592
Abstract
Accumulating evidence points to a link between circadian clock dysfunction and the molecular events that drive tumorigenesis. Here, we investigated the connection between the circadian clock and the hallmarks of cancer in an in vitro model of colorectal cancer (CRC). We used a [...] Read more.
Accumulating evidence points to a link between circadian clock dysfunction and the molecular events that drive tumorigenesis. Here, we investigated the connection between the circadian clock and the hallmarks of cancer in an in vitro model of colorectal cancer (CRC). We used a cross-platform data normalization method to concatenate and compare available microarray and RNA-sequencing time series data of CRC cell lines derived from the same patient at different disease stages. Our data analysis suggests differential regulation of molecular pathways between the CRC cells and identifies several of the circadian and likely clock-controlled genes (CCGs) as cancer hallmarks and circadian drug targets. Notably, we found links of the CCGs to Huntington’s disease (HD) in the metastasis-derived cells. We then investigated the impact of perturbations of our candidate genes in a cohort of 439 patients with colon adenocarcinoma retrieved from the Cancer Genome Atlas (TCGA). The analysis revealed a correlation of the differential expression levels of the candidate genes with the survival of patients. Thus, our study provides a bioinformatics workflow that allows for a comprehensive analysis of circadian properties at different stages of colorectal cancer, and identifies a new association between cancer and HD. Full article
(This article belongs to the Special Issue Applied Genomics and Cancer Therapeutics)
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Review

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15 pages, 2066 KiB  
Review
The Prowess of Andrographolide as a Natural Weapon in the War against Cancer
by Ammad Ahmad Farooqi, Rukset Attar, Uteuliyev Yerzhan Sabitaliyevich, Nada Alaaeddine, Damião Pergentino de Sousa, Baojun Xu and William C. Cho
Cancers 2020, 12(8), 2159; https://doi.org/10.3390/cancers12082159 - 4 Aug 2020
Cited by 32 | Viewed by 5553
Abstract
There has been a paradigm shift in our understanding about the multifaceted nature of cancer, and a wealth of information has revealed that single-target drugs are not good enough to provide satisfactory clinical outcomes and therapeutic effects for complex diseases which involve multiple [...] Read more.
There has been a paradigm shift in our understanding about the multifaceted nature of cancer, and a wealth of information has revealed that single-target drugs are not good enough to provide satisfactory clinical outcomes and therapeutic effects for complex diseases which involve multiple factors. Therefore, there has been a reignition to search for natural products having premium pharmacological activities aim to efficiently target multiple deregulated cellular signaling pathways. Andrographolide, a diterpene lactone from Andrographis paniculata was brought into to the limelight because of its ability to inhibit cancer cell proliferation and induce apoptosis. Here we reviewed andrographolide on cellular pathways regulation including Wnt/β-catenin, mTOR, VEGF-mediated intracellular signaling, as well as TRAIL-mediated apoptosis to inhibit cancer development. Full article
(This article belongs to the Special Issue Applied Genomics and Cancer Therapeutics)
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