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Biomedicines
Special Issues
Genomic and Epigenomic Alterations in Gastrointestinal (GI) Cancers
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Genomic and Epigenomic Alterations in Gastrointestinal (GI) Cancers

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (31 May 2023) | Viewed by 14077

Special Issue Editors

Prof. Dr. Jun Yu

E-Mail Website
Guest Editor
Institute of Digestive Disease, Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong, China
Interests: epigenetic and genetic alterations in gastrointestinal (GI) cancers; biomarkers for early detection and prognostication of GI cancer; role of gut microbiome in GI cancers; non-alcoholic steatohepatitis-associated liver cancer
Dr. Chi Chun Wong

E-Mail Website
Guest Editor
Institute of Digestive Disease, Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong, China
Interests: tumor metabolism and epigenetic interplay in gastrointestinal (GI) cancers; KRAS-mutant colorectal cancer; therapeutic targets in GI cancers

Special Issue Information

Dear Colleagues,

Gastrointestinal cancer (GI) (stomach, colon, liver) constitutes about 50% of all malignancies globally. Moreover, the incidence of GI cancers has been rising over the past 5 to 10 years, thus posing a serious threat to human health and representing a healthcare burden. Over the past decade, multiple international genetic, transcriptomic and epigenetic sequencing projects have established that aberrant genetic and epigenetic regulation plays key roles in the pathogenesis of GI cancers. More recently, the emergence of epitranscriptomics—the epigenetic modification of RNA—has provided an additional dimension for gene regulation in GI cancers. Genetic mutations, as well as epigenetic and epitranscriptomic alterations, are all fundamental to processes involved in the multifaceted aspects of GI cancer, including cancer cell proliferation, metastatic potential, adaptation to tumor microenvironment, modulation of antitumor immune response, and interaction with the gut microbiome. Understanding of genetic and epigenetic alterations in GI cancers will be critical to unveil novel therapeutic targets and molecular biomarkers to improve disease diagnosis and treatment.

The aim of this Special Issue is to gather reviews and research papers focusing on the role of genetic, epigenetic and epitranscriptomic alterations in the regulation of GI cancers, highlighting new insights into their roles in tumor initiation and progression, and how novel these discoveries can be translated to the clinic to improve patient care in GI cancers.

Prof. Dr. Jun Yu
Dr. Chi Chun Wong
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 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. Biomedicines 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 2600 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

  • epigenetics
  • epitranscriptomics
  • genetics
  • gastrointestinal cancers
  • tumorigenesis
  • tumor microenvironment
  • tumor microbiome

Published Papers (6 papers)

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Research

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12 pages, 1646 KiB  
Article
Role of IL-6/STAT3 Axis in Resistance to Cisplatin in Gastric Cancers
by Simona Laurino, Mariarita Brancaccio, Tiziana Angrisano, Giovanni Calice, Sabino Russi, Pellegrino Mazzone, Giuseppina Di Paola, Michele Aieta, Vitina Grieco, Gabriella Bianchino, Geppino Falco and Tiziana Notarangelo
Biomedicines 2023, 11(3), 694; https://doi.org/10.3390/biomedicines11030694 - 24 Feb 2023
Cited by 6 | Viewed by 1495
Abstract
Gastric cancer, the second most common cause of death worldwide, is characterized by poor prognosis and low responsiveness to chemotherapy. Indeed, multidrug resistance, based mainly on cellular and molecular factors, remains one of the most limiting factors of the current approach to gastric [...] Read more.
Gastric cancer, the second most common cause of death worldwide, is characterized by poor prognosis and low responsiveness to chemotherapy. Indeed, multidrug resistance, based mainly on cellular and molecular factors, remains one of the most limiting factors of the current approach to gastric cancer (GC) therapy. We employed a comprehensive gene expression analysis through data mining of publicly available databases to assess the role of the signal transducer and activator of transcription 3 (STAT3) in gastric cancer drug efficiency. It has been proposed that gastric cancer cells are less sensitive to these drugs because they develop resistance to these agents through activating alternative signalling pathways responsible for overcoming pharmacological inhibition. Our study evaluated the hypothesis that activating STAT3 signalling in response to cisplatin reduces the reaction to the drug. Consistent with this hypothesis, inhibition of interleukin 6 (IL-6)/STAT3 in combination therapy with cisplatin prevented both STAT3 activation and more lethality than induction by a single agent. The data suggest that the IL-6/STAT3 axis block associated with cisplatin treatment may represent a strategy to overcome resistance. Full article
(This article belongs to the Special Issue Genomic and Epigenomic Alterations in Gastrointestinal (GI) Cancers)
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Review

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12 pages, 4666 KiB  
Review
Interplay between the m6A Epitranscriptome and Tumor Metabolism: Mechanisms and Therapeutic Implications
by Asa Sergei Fong, Yasi Pan, Jun Yu and Chi Chun Wong
Biomedicines 2022, 10(10), 2589; https://doi.org/10.3390/biomedicines10102589 - 15 Oct 2022
Cited by 1 | Viewed by 1987
Abstract
N6-methyladenosine (m6A) modification of messenger RNA (mRNA) influences the stability and translation of the transcripts into functional proteins. Recent studies reveal the role of m6A modifications in regulating the metabolism of basic biomolecules such as glucose, lipids [...] Read more.
N6-methyladenosine (m6A) modification of messenger RNA (mRNA) influences the stability and translation of the transcripts into functional proteins. Recent studies reveal the role of m6A modifications in regulating the metabolism of basic biomolecules such as glucose, lipids and amino acids. Such mechanisms are not only important for physiological functions of normal cells but also prove to be pivotal for the pathogenesis of cancers by driving dysregulated metabolism. M6A writers, readers and erasers function co-operatively to promote aberrant glucose, lipid and amino acid metabolism in cancer cells, which in turn support increased proliferative and metastatic potential. Better understanding of the relationship between m6A and metabolism in malignancy may unravel novel therapeutic targets as well as biomarkers in cancer. In this review, we summarize the recent evidence demonstrating the interplay between m6A modification and cancer metabolism and their therapeutic implications. Full article
(This article belongs to the Special Issue Genomic and Epigenomic Alterations in Gastrointestinal (GI) Cancers)
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22 pages, 1471 KiB  
Review
Targeting the Hippo Pathway in Gastric Cancer and Other Malignancies in the Digestive System: From Bench to Bedside
by Xiaoli Liu, Yifei Wang, Bonan Chen, Wai Nok Chan, Chun Wai Mui, Alvin H.K. Cheung, Jinglin Zhang, Kit Yee Wong, Jun Yu, Wei Kang and Ka Fai To
Biomedicines 2022, 10(10), 2512; https://doi.org/10.3390/biomedicines10102512 - 8 Oct 2022
Cited by 9 | Viewed by 3007
Abstract
The Hippo pathway is an evolutionally conserved signaling cascade that controls organ size and tissue regeneration under physiological conditions, and its aberrations have been well studied to promote tumor initiation and progression. Dysregulation of the Hippo tumor suppressor signaling frequently occurs in gastric [...] Read more.
The Hippo pathway is an evolutionally conserved signaling cascade that controls organ size and tissue regeneration under physiological conditions, and its aberrations have been well studied to promote tumor initiation and progression. Dysregulation of the Hippo tumor suppressor signaling frequently occurs in gastric cancer (GC) and other solid tumors and contributes to cancer development through modulating multiple aspects, including cell proliferation, survival, metastasis, and oncotherapy resistance. In the clinic, Hippo components also possess diagnostic and prognostic values for cancer patients. Considering its crucial role in driving tumorigenesis, targeting the Hippo pathway may greatly benefit developing novel cancer therapies. This review summarizes the current research progress regarding the core components and regulation of the Hippo pathway, as well as the mechanism and functional roles of their dysregulation in gastrointestinal malignancies, especially in GC, and discusses the therapeutic potential of targeting the Hippo pathway against cancers. Full article
(This article belongs to the Special Issue Genomic and Epigenomic Alterations in Gastrointestinal (GI) Cancers)
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22 pages, 3060 KiB  
Review
Exploiting the Molecular Basis of Oesophageal Cancer for Targeted Therapies and Biomarkers for Drug Response: Guiding Clinical Decision-Making
by Sikhumbuzo Mbatha, Rodney Hull and Zodwa Dlamini
Biomedicines 2022, 10(10), 2359; https://doi.org/10.3390/biomedicines10102359 - 22 Sep 2022
Cited by 2 | Viewed by 1820
Abstract
Worldwide, oesophageal cancer is the sixth leading cause of deaths related to cancer and represents a major health concern. Sub-Saharan Africa is one of the regions of the world with the highest incidence and mortality rates for oesophageal cancer and most of the [...] Read more.
Worldwide, oesophageal cancer is the sixth leading cause of deaths related to cancer and represents a major health concern. Sub-Saharan Africa is one of the regions of the world with the highest incidence and mortality rates for oesophageal cancer and most of the cases of oesophageal cancer in this region are oesophageal squamous cell carcinoma (OSCC). The development and progression of OSCC is characterized by genomic changes which can be utilized as diagnostic or prognostic markers. These include changes in the expression of various genes involved in signaling pathways that regulate pathways that regulate processes that are related to the hallmarks of cancer, changes in the tumor mutational burden, changes in alternate splicing and changes in the expression of non-coding RNAs such as miRNA. These genomic changes give rise to characteristic profiles of altered proteins, transcriptomes, spliceosomes and genomes which can be used in clinical applications to monitor specific disease related parameters. Some of these profiles are characteristic of more aggressive forms of cancer or are indicative of treatment resistance or tumors that will be difficult to treat or require more specialized specific treatments. In Sub-Saharan region of Africa there is a high incidence of viral infections such as HPV and HIV, which are both risk factors for OSCC. The genomic changes that occur due to these infections can serve as diagnostic markers for OSCC related to viral infection. Clinically this is an important distinction as it influences treatment as well as disease progression and treatment monitoring practices. This underlines the importance of the characterization of the molecular landscape of OSCC in order to provide the best treatment, care, diagnosis and screening options for the management of OSCC. Full article
(This article belongs to the Special Issue Genomic and Epigenomic Alterations in Gastrointestinal (GI) Cancers)
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15 pages, 979 KiB  
Review
RNA Modifications in Gastrointestinal Cancer: Current Status and Future Perspectives
by Xiaoting Zhang, Hao Su, Hongyan Chen, Qing Li, Xiaodong Liu, Lin Zhang, William Ka Kei Wu, Matthew Tak Vai Chan and Huarong Chen
Biomedicines 2022, 10(8), 1918; https://doi.org/10.3390/biomedicines10081918 - 8 Aug 2022
Cited by 6 | Viewed by 2915
Abstract
Gastrointestinal (GI) cancer, referring to cancers of the digestive system such as colorectal cancer (CRC), gastric cancer (GC), and liver cancer, is a major cause of cancer-related deaths in the world. A series of genetic, epigenetic, and epitranscriptomic changes occur during the development [...] Read more.
Gastrointestinal (GI) cancer, referring to cancers of the digestive system such as colorectal cancer (CRC), gastric cancer (GC), and liver cancer, is a major cause of cancer-related deaths in the world. A series of genetic, epigenetic, and epitranscriptomic changes occur during the development of GI cancer. The identification of these molecular events provides potential diagnostic, prognostic, and therapeutic targets for cancer patients. RNA modification is required in the posttranscriptional regulation of RNA metabolism, including splicing, intracellular transport, degradation, and translation. RNA modifications such as N6-methyladenosine (m6A) and N1-methyladenosine (m1A) are dynamically regulated by three different types of regulators named methyltransferases (writers), RNA binding proteins (readers), and demethylases (erasers). Recent studies have pointed out that abnormal RNA modification contributes to GI tumorigenesis and progression. In this review, we summarize the latest findings on the functional significance of RNA modification in GI cancer and discuss the therapeutic potential of epitranscriptomic inhibitors for cancer treatment. Full article
(This article belongs to the Special Issue Genomic and Epigenomic Alterations in Gastrointestinal (GI) Cancers)
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Other

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6 pages, 609 KiB  
Case Report
Heterozygous Pathogenic Nonsense Variant in the ATM Gene in a Family with Unusually High Gastric Cancer Susceptibility
by Daniele Guadagnolo, Gioia Mastromoro, Enrica Marchionni, Aldo Germani, Fabio Libi, Soha Sadeghi, Camilla Savio, Simona Petrucci, Laura De Marchis, Maria Piane and Antonio Pizzuti
Biomedicines 2023, 11(7), 2062; https://doi.org/10.3390/biomedicines11072062 - 22 Jul 2023
Cited by 1 | Viewed by 2216
Abstract
Germline pathogenic variants (PVs) in the Ataxia Telangiectasia mutated (ATM) gene (MIM* 607585) increase the risk for breast, pancreatic, gastric, and prostatic cancer and, to a reduced extent, ovarian and colon cancer and melanoma, with moderate penetrance and variable expressivity. We [...] Read more.
Germline pathogenic variants (PVs) in the Ataxia Telangiectasia mutated (ATM) gene (MIM* 607585) increase the risk for breast, pancreatic, gastric, and prostatic cancer and, to a reduced extent, ovarian and colon cancer and melanoma, with moderate penetrance and variable expressivity. We describe a family presenting early-onset gastric cancer and harboring a heterozygous pathogenic ATM variant. The proband had gastric cancer (age 45) and reported a sister deceased due to diffuse gastric cancer (age 30) and another sister who developed diffuse gastric cancer (age 52) and ovarian serous cancer. Next generation sequencing for cancer susceptibility genes (APC, ATM, BRD1, BRIP1, CDH1, CDK4, CDKN2A, CHEK2, EPCAM, MLH1, MRE11, MSH2, MSH6, MUTYH, NBN, PALB2, PMS2, PTEN, RAD50, RAD51C, RAD51D, RECQL1, SMAD4, STK11, and TP53) was performed. Molecular analysis identified the truncating c.5944C>T, p.(Gln1982*) variant in the ATM (NM_000051.3; NP_000042.3) in the proband. The variant had segregated in the living affected sister and in the unaffected daughter of the deceased affected sister. Familial early-onset gastric cancer is an unusual presentation for ATM-related malignancies. Individual variants may result in different specific risks. Genotype–phenotype correlations are challenging given the low penetrance and variable expressivity. Careful family history assessments are pivotal for prevention planning and are strengthened by the availability of molecular diagnoses. Full article
(This article belongs to the Special Issue Genomic and Epigenomic Alterations in Gastrointestinal (GI) Cancers)
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