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Pathogens
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Inflammation and Gastrointestinal/Hepatobiliary Cancers
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Inflammation and Gastrointestinal/Hepatobiliary Cancers

A special issue of Pathogens (ISSN 2076-0817).

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 22620

Special Issue Editor

Dr. Hiroyuki Marusawa

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Guest Editor
Department of Gastroenterology, Red Cross Osaka Hospital, Osaka, Japan
Interests: Infection; inflammation and cancers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Epidemiologic studies have clearly demonstrated that chronic inflammation predisposes to tumor formation in various organs, including hepatocellular carcinoma (HCC) caused by hepatitis B virus (HBV) or hepatitis C virus (HCV) infection, gastric cancer caused by Helicobacter pylori (H. pylori) infection, colorectal cancer caused by inflammatory bowel diseases, bile duct cancer by primary sclerosing cholangitis, and esophageal cancer caused by Barrett’s esophagus. In this special issue, we will focus on the role of inflammation on the pathogenesis of gastrointestinal / heapatobiliary cancers. We welcome submissions of original research and review manuscripts that cover basic and/or clinical aspects of inflammation-associated cancers in digestive organs.

Dr. Hiroyuki Marusawa
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. Pathogens 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

  • Inflammation
  • hepatitis virus
  • hepatocellular carcinoma
  • Helicobacter pylori
  • gastric cancer
  • Barrett’s esophagus
  • esophageal cancer
  • inflammatory bowel diseases
  • colorectal cancer
  • pancreatic cancer
  • bile duct cancer

Published Papers (6 papers)

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Research

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15 pages, 4151 KiB  
Article
Metformin Improves Biochemical and Pathophysiological Changes in Hepatocellular Carcinoma with Pre-Existed Diabetes Mellitus Rats
by Maysa A. Mobasher, Mousa O. Germoush, Hala Galal El-Tantawi and Karim Samy El-Said
Pathogens 2021, 10(1), 59; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens10010059 - 11 Jan 2021
Cited by 6 | Viewed by 2203
Abstract
Hepatocellular carcinoma (HCC) is one of the world’s most widely recognized malignant tumors that accounts for 90% of all the primary liver cancers and is a major cause of death from cancer, representing half a million deaths per year. Obesity and associated metabolic [...] Read more.
Hepatocellular carcinoma (HCC) is one of the world’s most widely recognized malignant tumors that accounts for 90% of all the primary liver cancers and is a major cause of death from cancer, representing half a million deaths per year. Obesity and associated metabolic irregularities, particularly diabetes mellitus (DM) and insulin resistance, are important risk factors for the advancement of HCC. Recently, retrospective studies showed that metformin (MET) could protect the hepatic tissues in pre-existing diabetes mellitus from HCC. The purpose of this study was to assess the role of MET treatment in the pre-existing diabetic rats before and after HCC induction by diethylnitrosamine (DEN). Thirty-five male Sprague Dawley albino rats were partitioned into the following groups: Group 1 (Gp1) was the control. Gp2 was injected intraperitoneally (i.p) with streptozotocin (STZ) (80 mg/kg) and DEN (50 mg/kg/7 weeks). Gp3, Gp4, and Gp5 were injected as in Gp2 and treated with MET (150 mg/kg) before and/or after HCC induction. Biochemical parameters including liver functions, lipid profile, and oxidative stress biomarkers were determined. Furthermore, histological and immunohistochemical changes were assessed in all groups. Our results illustrated that the group of rats that were treated with STZ and DEN had significant changes in both liver functions and were associated with alterations in the liver histopathological architectures. Treatment with MET before or after HCC induction ameliorated the cellular changes in the liver tissues; however, the utmost protection was found in a group of rats, which were treated with MET before and after HCC induction. Full article
(This article belongs to the Special Issue Inflammation and Gastrointestinal/Hepatobiliary Cancers)
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Review

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10 pages, 850 KiB  
Review
Clinical and Molecular Basis of Hepatocellular Carcinoma after Hepatitis C Virus Eradication
by Natsumi Oe, Haruhiko Takeda, Yuji Eso, Atsushi Takai and Hiroyuki Marusawa
Pathogens 2022, 11(4), 430; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens11040430 - 01 Apr 2022
Cited by 5 | Viewed by 2352
Abstract
Hepatocellular carcinoma (HCC) arises in the background of chronic liver diseases, including hepatitis and liver cirrhosis caused by hepatitis C virus (HCV) infection. It is well known that HCV eradication using antiviral drugs can efficiently inhibit hepatocarcinogenesis. Recent advances in and development of [...] Read more.
Hepatocellular carcinoma (HCC) arises in the background of chronic liver diseases, including hepatitis and liver cirrhosis caused by hepatitis C virus (HCV) infection. It is well known that HCV eradication using antiviral drugs can efficiently inhibit hepatocarcinogenesis. Recent advances in and development of direct-acting antiviral (DAA) drugs has revolutionized the treatment of HCV infection, and the vast majority of HCV patients can achieve HCV eradication using DAAs. However, mounting evidence clearly indicates that HCC inevitably occurs in a subset of patients after successful viral eradication using DAA therapy. Cancer is a genetic disease, and the accumulation of genetic and epigenetic aberrations may cause hepatocarcinogenesis in chronically damaged liver, even after virus elimination. In this review, we highlight HCC development after HCV eradication and discuss the current understanding of the molecular mechanisms of tumorigenesis after virus elimination, focusing on the genetic and epigenetic background of chronically damaged liver tissues. Full article
(This article belongs to the Special Issue Inflammation and Gastrointestinal/Hepatobiliary Cancers)
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16 pages, 2644 KiB  
Review
Helicobacter pylori-Induced Inflammation: Possible Factors Modulating the Risk of Gastric Cancer
by Sushil Kumar, Girijesh Kumar Patel and Uday C. Ghoshal
Pathogens 2021, 10(9), 1099; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens10091099 - 29 Aug 2021
Cited by 31 | Viewed by 6585
Abstract
Chronic inflammation and long-term tissue injury are related to many malignancies, including gastric cancer (GC). Helicobacter pylori (H. pylori), classified as a class I carcinogen, induces chronic superficial gastritis followed by gastric carcinogenesis. Despite a high prevalence of H. pylori infection, [...] Read more.
Chronic inflammation and long-term tissue injury are related to many malignancies, including gastric cancer (GC). Helicobacter pylori (H. pylori), classified as a class I carcinogen, induces chronic superficial gastritis followed by gastric carcinogenesis. Despite a high prevalence of H. pylori infection, only about 1–3% of people infected with this bacterium develop GC worldwide. Furthermore, the development of chronic gastritis in some, but not all, H. pylori-infected subjects remains unexplained. These conflicting findings indicate that clinical outcomes of aggressive inflammation (atrophic gastritis) to gastric carcinogenesis are influenced by several other factors (in addition to H. pylori infection), such as gut microbiota, co-existence of intestinal helminths, dietary habits, and host genetic factors. This review has five goals: (1) to assess our current understanding of the process of H. pylori-triggered inflammation and gastric precursor lesions; (2) to present a hypothesis on risk modulation by the gut microbiota and infestation with intestinal helminths; (3) to identify the dietary behavior of the people at risk of GC; (4) to check the inflammation-related genetic polymorphisms and role of exosomes together with other factors as initiators of precancerous lesions and gastric carcinoma; and (5) finally, to conclude and suggest a new direction for future research. Full article
(This article belongs to the Special Issue Inflammation and Gastrointestinal/Hepatobiliary Cancers)
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20 pages, 1660 KiB  
Review
Impact of Dietary Patterns on H. pylori Infection and the Modulation of Microbiota to Counteract Its Effect. A Narrative Review
by Ascensión Rueda-Robles, Teresa Rubio-Tomás, Julio Plaza-Diaz and Ana I. Álvarez-Mercado
Pathogens 2021, 10(7), 875; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens10070875 - 10 Jul 2021
Cited by 12 | Viewed by 5695
Abstract
Helicobacter pylori (H. pylori) is a Gram-negative bacterium that colonizes the stomach and can induce gastric disease and intra-gastric lesions, including chronic gastritis, peptic ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. This bacterium is responsible for long-term complications of gastric disease. The [...] Read more.
Helicobacter pylori (H. pylori) is a Gram-negative bacterium that colonizes the stomach and can induce gastric disease and intra-gastric lesions, including chronic gastritis, peptic ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. This bacterium is responsible for long-term complications of gastric disease. The conjunction of host genetics, immune response, bacterial virulence expression, diet, micronutrient availability, and microbiome structure influence the disease outcomes related to chronic H. pylori infection. In this regard, the consumption of unhealthy and unbalanced diets can induce microbial dysbiosis, which infection with H. pylori may contribute to. However, to date, clinical trials have reported controversial results and current knowledge in this field is inconclusive. Here, we review preclinical studies concerning the changes produced in the microbiota that may be related to H. pylori infection, as well as the involvement of diet. We summarize and discuss the last approaches based on the modulation of the microbiota to improve the negative impact of H. pylori infection and their potential translation from bench to bedside. Full article
(This article belongs to the Special Issue Inflammation and Gastrointestinal/Hepatobiliary Cancers)
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13 pages, 725 KiB  
Review
Clinical Aspects of Gut Microbiota in Hepatocellular Carcinoma Management
by Jinghang Xu, Qiao Zhan, Yanan Fan, Emily Kwun Kwan Lo, Fangfei Zhang, Yanyan Yu, Hani El-Nezami and Zheng Zeng
Pathogens 2021, 10(7), 782; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens10070782 - 22 Jun 2021
Cited by 4 | Viewed by 2702
Abstract
Liver cancer, predominantly hepatocellular carcinoma (HCC), is the third leading cause of cancer-related deaths worldwide. Emerging data highlight the importance of gut homeostasis in the pathogenesis of HCC. Clinical and translational studies revealed the patterns of dysbiosis in HCC patients and their potential [...] Read more.
Liver cancer, predominantly hepatocellular carcinoma (HCC), is the third leading cause of cancer-related deaths worldwide. Emerging data highlight the importance of gut homeostasis in the pathogenesis of HCC. Clinical and translational studies revealed the patterns of dysbiosis in HCC patients and their potential role for HCC diagnosis. Research on underlying mechanisms of dysbiosis in HCC development pointed out the direction for improving the treatment and prevention. Despite missing clinical studies, animal models showed that modulation of the gut microbiota by probiotics may become a new way to treat or prevent HCC development. Full article
(This article belongs to the Special Issue Inflammation and Gastrointestinal/Hepatobiliary Cancers)
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10 pages, 1583 KiB  
Review
Genetic Pathogenesis of Inflammation-Associated Cancers in Digestive Organs
by Risa Nakanishi, Takahiro Shimizu, Ken Kumagai, Atsushi Takai and Hiroyuki Marusawa
Pathogens 2021, 10(4), 453; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens10040453 - 09 Apr 2021
Cited by 5 | Viewed by 2092
Abstract
Epidemiological, clinical, and biological studies convincingly demonstrate that chronic inflammation predisposes to the development of human cancers. In digestive organs, inflammation-associated cancers include colitis-associated colorectal cancers, Helicobacter pylori-associated gastric cancer, as well as Barrett’s esophagus and esophageal adenocarcinoma associated with chronic duodenogastric-esophageal [...] Read more.
Epidemiological, clinical, and biological studies convincingly demonstrate that chronic inflammation predisposes to the development of human cancers. In digestive organs, inflammation-associated cancers include colitis-associated colorectal cancers, Helicobacter pylori-associated gastric cancer, as well as Barrett’s esophagus and esophageal adenocarcinoma associated with chronic duodenogastric-esophageal reflux. Cancer is a genomic disease, and stepwise accumulation of genetic and epigenetic alterations of tumor-related genes leads to the development of tumor cells. Recent genome analyses show that genetic alterations, which are evoked by inflammation, are latently accumulated in inflamed epithelial cells of digestive organs. Production of reactive oxygen and aberrant expression of activation-induced cytidine deaminase, a nucleotide-editing enzyme, could be induced in inflamed gastrointestinal epithelial cells and play a role as a genomic modulator of inflammation-associated carcinogenesis. Understanding the molecular linkage between inflammation and genetic alterations will open up a new field of tumor biology and provide a novel strategy for the prevention of inflammation-associated tumorigenesis. Full article
(This article belongs to the Special Issue Inflammation and Gastrointestinal/Hepatobiliary Cancers)
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