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Genetics of cancer
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Genetics of cancer

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cell Biology".

Deadline for manuscript submissions: closed (30 June 2020) | Viewed by 24976

Special Issue Editors

Dr. Angabin Matin

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Guest Editor
Department of Pharmaceutical and Environmental Health Sciences, College of Pharmacy, Texas Southern University, 3100 Cleburne St, Houston, TX 77004, USA
Interests: cancer genetics; genetically modified mouse models; RNA binding proteins; germ cell tumors
Dr. Yun Zhang

E-Mail
Guest Editor
Department of Pharmaceutical Sciences, Joan M. Lafleur College of Pharmacy and Health Sciences, Texas Southern University, 3100 Cleburne St, Houston, TX 77004, USA
Interests: cancer genetics; breast cancer; genetically modified mouse models; tumor suppressors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The last decade has witnessed remarkable scientific breakthroughs and discoveries, especially using genomic, proteomic, and CRISPR/Cas9 technologies that have enhanced our understanding of the genetic basis of cancer. The hope is that such knowledge will translate into improved cancer prevention, diagnosis, and treatments with consideration of the individual’s genetic profile.

This Special Issue on “Genetics of Cancer” focuses on the broad topic of the genetic, molecular, and cellular defects in cancers. We welcome original scientific reports, research articles, communications, and reviews that illustrate how genetic alterations affect molecular pathways and result in cellular defects and cancer pathology. We seek to also highlight technological progresses, current challenges, and perspectives in unraveling the complex genetics of cancer. We hope to feature articles that overview the exciting and interdisciplinary field of cancer research.

Dr. Angabin Matin
Dr. Yun Zhang
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. Biology is an international peer-reviewed open access monthly 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 2700 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

  • Multistep tumorigenesis
  • Invasion and metastasis
  • Molecular pathways
  • Susceptibility genes
  • Cancer epigenetics
  • Immunogenetics
  • Cancer stem cells
  • Cancer microenvironment
  • Cancer heterogeneity

Published Papers (4 papers)

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Research

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14 pages, 2197 KiB  
Article
Isolation and Identification of Long Non-Coding RNAs in Exosomes Derived from the Serum of Colorectal Carcinoma Patients
by Chin Tat Ng, Shamin Azwar, Wai Kien Yip, Siti Yazmin Zahari Sham, Mohd Faisal Jabar, Norren Haneezah Sahak, Norhafizah Mohtarrudin and Heng Fong Seow
Biology 2021, 10(9), 918; https://0-doi-org.brum.beds.ac.uk/10.3390/biology10090918 - 15 Sep 2021
Cited by 11 | Viewed by 2611
Abstract
Long non-coding RNAs (lncRNAs) are non-coding RNAs consisting of more than 200 nucleotides in length. LncRNAs present in exosomes may play a critical role in the cellular processes involved in cancer pathogenesis and progression including proliferation, invasion, and migration of tumor cells. This [...] Read more.
Long non-coding RNAs (lncRNAs) are non-coding RNAs consisting of more than 200 nucleotides in length. LncRNAs present in exosomes may play a critical role in the cellular processes involved in cancer pathogenesis and progression including proliferation, invasion, and migration of tumor cells. This paper aims to identify the differential expression of exosomal lncRNAs derived from the sera of non-cancer individuals and patients diagnosed with colorectal carcinoma. These differentially-expressed exosomal serum lncRNAs may provide an insight into the pathogenesis and progression of colorectal cancer (CRC). Serum exosomes and exosomes from SW480-7 cell culture supernatants were isolated and viewed by transmission electron microscope (TEM). The particle size distribution and protein markers of exosomes derived from SW480-7 were further analyzed using the Zetasizer Nano S instrument and western blotting technique. TEM showed that exosomes derived from serum and SW480-7 cells were round vesicles with sizes ranging from 50–200 nm. The exosomes derived from SW480-7 had an average diameter of 274.6 nm and contained the exosomal protein, ALIX/PDCD6IP. In our clinical studies, six lncRNAs, namely GAS5, H19, LINC00152, SNHG16, RMRP, and ZFAS1 were detected in the exosomes from sera of 18 CRC patients. Among these six lncRNAs, the expression level of LINC00152 was found to be significantly lower in CRC patients as compared to non-cancer individuals (p = 0.04) while lncRNA H19 was significantly up-regulated in advanced-stages (stage III and IV) of CRC (p = 0.04) as compared to early-stages (stage I and II). In conclusion, the detection of lower LINC00152 in exosomes of sera from CRC patients versus non-cancer individuals and H19 upregulation in advanced stages suggests that they may play important roles in pathogenesis and progression of CRC. Full article
(This article belongs to the Special Issue Genetics of cancer)
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13 pages, 2092 KiB  
Article
Deficiency of Splicing Factor 1 (SF1) Reduces Intestinal Polyp Incidence in ApcMin/+ Mice
by Jyotsna D. Godavarthi, Shahrazad Polk, Lisa Nunez, Amruthesh Shivachar, Nancy L. Glenn Griesinger and Angabin Matin
Biology 2020, 9(11), 398; https://0-doi-org.brum.beds.ac.uk/10.3390/biology9110398 - 13 Nov 2020
Cited by 1 | Viewed by 2236
Abstract
Background: Splicing factor 1 (SF1) is a conserved alternative splicing factor expressed in many different mammalian cell types. The genetically modified Sf1+/− (or Sf1β-geo/+) mice express reduced levels of SF1 protein in mouse tissues, including in cells of the intestines. Mutational [...] Read more.
Background: Splicing factor 1 (SF1) is a conserved alternative splicing factor expressed in many different mammalian cell types. The genetically modified Sf1+/− (or Sf1β-geo/+) mice express reduced levels of SF1 protein in mouse tissues, including in cells of the intestines. Mutational inactivation of human adenomatous polyposis coli (APC) gene deregulates the Wnt signaling pathway and is a frequent genetic event in colon cancers. Mice with a point mutation in the Apc gene (ApcMin/+) also develop numerous intestinal polyps at a young age. Our aim was to determine the effect of reduced SF1 levels on polyp development due to the strong driver ApcMin/+ mutation. Methods: We utilized mice genetically deficient for expression of SF1 to assess how SF1 levels affect intestinal tumorigenesis. We crossed ApcMin/+ to Sf1+/− mice to generate a cohort of heterozygous mutant ApcMin/+;Sf1+/− mice and compared intestinal polyp development in these mice to that in a control cohort of sibling ApcMin/+ mice. We compared total polyp numbers, sizes of polyps and gender differences in polyp numbers between ApcMin/+;Sf1+/− and ApcMin/+ mice. Results: Our results showed that ApcMin/+ mice with lower SF1 expression developed 25–30% fewer intestinal polyps compared to their ApcMin/+ siblings with normal SF1 levels. Interestingly, this difference was most significant for females (ApcMin/+;Sf1+/− and ApcMin/+ females developed 39 and 55 median number of polyps, respectively). Furthermore, the difference in polyp numbers between ApcMin/+;Sf1+/− and ApcMin/+ mice was significant for smaller polyps with a size of 2 mm or less, whereas both groups developed similar numbers of larger polyps. Conclusions: Our results suggest that lower SF1 levels likely inhibit the rate of initiation of polyp development due to ApcMin/+ driver mutation in the mouse intestine. Thus, therapeutic lowering of SF1 levels in the intestine could attenuate intestinal polyp development. Full article
(This article belongs to the Special Issue Genetics of cancer)
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Review

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34 pages, 2428 KiB  
Review
Recent Updates on Mechanisms of Resistance to 5-Fluorouracil and Reversal Strategies in Colon Cancer Treatment
by Shamin Azwar, Heng Fong Seow, Maha Abdullah, Mohd Faisal Jabar and Norhafizah Mohtarrudin
Biology 2021, 10(9), 854; https://0-doi-org.brum.beds.ac.uk/10.3390/biology10090854 - 31 Aug 2021
Cited by 55 | Viewed by 11128
Abstract
5-Fluorouracil (5-FU) plus leucovorin (LV) remain as the mainstay standard adjuvant chemotherapy treatment for early stage colon cancer, and the preferred first-line option for metastatic colon cancer patients in combination with oxaliplatin in FOLFOX, or irinotecan in FOLFIRI regimens. Despite treatment success to [...] Read more.
5-Fluorouracil (5-FU) plus leucovorin (LV) remain as the mainstay standard adjuvant chemotherapy treatment for early stage colon cancer, and the preferred first-line option for metastatic colon cancer patients in combination with oxaliplatin in FOLFOX, or irinotecan in FOLFIRI regimens. Despite treatment success to a certain extent, the incidence of chemotherapy failure attributed to chemotherapy resistance is still reported in many patients. This resistance, which can be defined by tumor tolerance against chemotherapy, either intrinsic or acquired, is primarily driven by the dysregulation of various components in distinct pathways. In recent years, it has been established that the incidence of 5-FU resistance, akin to multidrug resistance, can be attributed to the alterations in drug transport, evasion of apoptosis, changes in the cell cycle and DNA-damage repair machinery, regulation of autophagy, epithelial-to-mesenchymal transition, cancer stem cell involvement, tumor microenvironment interactions, miRNA dysregulations, epigenetic alterations, as well as redox imbalances. Certain resistance mechanisms that are 5-FU-specific have also been ascertained to include the upregulation of thymidylate synthase, dihydropyrimidine dehydrogenase, methylenetetrahydrofolate reductase, and the downregulation of thymidine phosphorylase. Indeed, the successful modulation of these mechanisms have been the game plan of numerous studies that had employed small molecule inhibitors, plant-based small molecules, and non-coding RNA regulators to effectively reverse 5-FU resistance in colon cancer cells. It is hoped that these studies would provide fundamental knowledge to further our understanding prior developing novel drugs in the near future that would synergistically work with 5-FU to potentiate its antitumor effects and improve the patient’s overall survival. Full article
(This article belongs to the Special Issue Genetics of cancer)
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13 pages, 598 KiB  
Review
A Glance of p53 Functions in Brain Development, Neural Stem Cells, and Brain Cancer
by Yuqing Xiong, Yun Zhang, Shunbin Xiong and Abie E. Williams-Villalobo
Biology 2020, 9(9), 285; https://0-doi-org.brum.beds.ac.uk/10.3390/biology9090285 - 11 Sep 2020
Cited by 22 | Viewed by 8456
Abstract
p53 is one of the most intensively studied tumor suppressors. It transcriptionally regulates a broad range of genes to modulate a series of cellular events, including DNA damage repair, cell cycle arrest, senescence, apoptosis, ferroptosis, autophagy, and metabolic remodeling, which are fundamental for [...] Read more.
p53 is one of the most intensively studied tumor suppressors. It transcriptionally regulates a broad range of genes to modulate a series of cellular events, including DNA damage repair, cell cycle arrest, senescence, apoptosis, ferroptosis, autophagy, and metabolic remodeling, which are fundamental for both development and cancer. This review discusses the role of p53 in brain development, neural stem cell regulation and the mechanisms of inactivating p53 in gliomas. p53 null or p53 mutant mice show female biased exencephaly, potentially due to X chromosome inactivation failure and/or hormone-related gene expression. Oxidative cellular status, increased PI3K/Akt signaling, elevated ID1, and metabolism are all implicated in p53-loss induced neurogenesis. However, p53 has also been shown to promote neuronal differentiation. In addition, p53 mutations are frequently identified in brain tumors, especially glioblastomas. Mechanisms underlying p53 inactivation in brain tumor cells include disruption of p53 protein stability, gene expression and transactivation potential as well as p53 gene loss or mutation. Loss of p53 function and gain-of-function of mutant p53 are both implicated in brain development and tumor genesis. Further understanding of the role of p53 in the brain may provide therapeutic insights for brain developmental syndromes and cancer. Full article
(This article belongs to the Special Issue Genetics of cancer)
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