Cancer and Inflammation in the Gastrointestinal Tract

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Gastroenterology & Hepatopancreatobiliary Medicine".

Deadline for manuscript submissions: closed (1 June 2023) | Viewed by 5685

Special Issue Editors


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Guest Editor
Department of Digestive Tract Diseases, Medical University of Lodz, 90-153 Lodz, Poland
Interests: pancreatitis; pancreatic cancer; inflammatory bowel disease; faecal microbiota transplantation
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Guest Editor
1. Central Clinical Hospital of Ministry of Internal Affairs and Administration, 02-507 Warsaw, Poland
2. Collegium Medicum, Jak Kochanowski University, 25-516 Kielce, Poland
Interests: IBD; COVID and GI disease; chronic pancreatitis; acute pancreatitis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Inflammatory and malignant diseases of the GI tract are becoming the leading causes of morbidity, death and disability worldwide. In last few decades, progress has been achieved regarding their pathogenesis and management. Nevertheless, treatment results remain unsatisfactory.

Inflammatory reactions can stimulate antitumor immune responses, but also have the capacity to promote tumor development. Data have shown that many of the processes involved in inflammation, such as leucocyte migration, local vascular dilation and enhanced permeability and angiogenesis, may contribute to tumor growth, progression and metastasis.

Numerous studies confirm an increased risk of certain cancers in the setting of chronic inflammation. Epidemiological studies show that about 15–20% of all cancers are associated with chronic inflammation. Primary examples of this phenomenon concern the GI system: hepatocellular carcinoma as a result of viral hepatitis, adenocarcinoma and gastric lymphoma connected to Helicobacter pylori infection, colitis-associated cancer, pancreatic adenocarcinoma as a result of chronic pancreatitis and esophageal adenocarcinoma from Barrett’s esophagus.

While normal inflammatory processes are self-limiting, for many reasons, acute inflammation may develop into a chronic state: the inflammatory stimulus may persist (as seen in inflammatory bowel diseases or gastroesophageal reflux disease) or the dysregulation of the control mechanisms may occur.

It has been suggested that humans accumulate somatic mutations in different cell types, which arise spontaneously or are induced by the exposure to carcinogens. The inflammation may cause more mutation or promote proliferation. The precise mechanisms and signals stimulated by inflammation for the promotion of tumor progression are largely unclear.

The current pandemic, caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has severely impacted human society, causing, in addition to respiratory tract diseases, diseases associated with the digestive tract. Patients with COVID-19 experienced an increase in the number and severity of GI symptoms. It also had a significant impact on patients with chronic digestive tract pathologies, in particular, inflammatory bowel diseases (IBD) and autoimmune and neoplastic diseases in patients receiving immunosuppressive drugs.

Therefore, studies on GI inflammation and carcinogenesis are necessary to promote global health and well-being.

Prof. Dr. Ewa Małecka-Wojciesko
Prof. Dr. Grażyna Rydzewska
Guest Editors

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Keywords

  • GI cancer
  • GI inflammation
  • ulcerative colitis
  • Crohn's disease
  • gene mutation
  • pancreatic ductal adenocarcinoma
  • chronic pancreatitis
  • acute pancreatitis
  • colorectal cancer

Published Papers (3 papers)

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Research

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11 pages, 1117 KiB  
Article
Association of Hepatitis B and C Virus with the Risk of Coronary Artery Disease and Cerebrovascular Disease in Patients with Hepatocellular Carcinoma
by Meng-Chuan Lu, Ying-Hsuen Wu, Chi-Hsiang Chung, Hsuan-Hwai Lin, Tsai-Yuan Hsieh, Peng-Jen Chen, Wu-Chien Chien and Hsuan-Wei Chen
J. Clin. Med. 2023, 12(7), 2602; https://doi.org/10.3390/jcm12072602 - 30 Mar 2023
Cited by 1 | Viewed by 1437
Abstract
Background: Hepatocellular carcinoma accounts for approximately 90% of primary liver cancers and hepatitis virus was believed to have the potential for altering the pathogenesis of arteriosclerosis. However, the influence of the hepatitis virus on coronary artery disease or cerebral vascular disease remains unclear. [...] Read more.
Background: Hepatocellular carcinoma accounts for approximately 90% of primary liver cancers and hepatitis virus was believed to have the potential for altering the pathogenesis of arteriosclerosis. However, the influence of the hepatitis virus on coronary artery disease or cerebral vascular disease remains unclear. This study used the Taiwan National Health Insurance Research Database to clarify the virus-associated risk of coronary artery disease and cerebral vascular disease in patients with hepatocellular carcinoma (HCC). Methods: A total of 188,039 HCC individuals, age 20 years or older, were enrolled from the Longitudinal Health Insurance Database between 2000 and 2017 for cohort analysis. A total of 109,348 with hepatitis B virus (HBV) infection, 37,506 with hepatitis C virus (HCV) infection, 34,110 without HBV or HCV, and 7075 with both HBV and HCV were recorded. Statistically, propensity score matched by sex, age, and index year at a ratio of 15:5:5:1 and a sensitivity test using multivariable Cox regression were used. Results: The risk of coronary artery disease in the HCV-related HCC group was 1.516-fold (95% CI: 1.328–2.034, p < 0.001) higher than in the HBV-related HCC group, followed by the HBV/HCV-related HCC group and the non-B/C HCC group; the cerebral vascular disease risk in the HCV-related HCC group was 1.467-fold higher than in the HBV-related HCC group (95% CI: 1.335 to 1.786, p < 0.001), followed by the HBV/HCV-related HCC group and the non-B/C HCC group. Conclusion: Hepatitis C virus infection was found to have a higher risk of developing coronary artery disease or cerebral vascular disease in patients with hepatocellular carcinoma. For patients with hepatocellular carcinoma, our findings warrant the importance in preventing artherosclerotic disease in the setting of hepatitis C virus infection. Full article
(This article belongs to the Special Issue Cancer and Inflammation in the Gastrointestinal Tract)
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Review

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20 pages, 1070 KiB  
Review
Why Does Obesity as an Inflammatory Condition Predispose to Colorectal Cancer?
by Anna Maria Rychter, Liliana Łykowska-Szuber, Agnieszka Zawada, Aleksandra Szymczak-Tomczak, Alicja Ewa Ratajczak, Kinga Skoracka, Michalina Kolan, Agnieszka Dobrowolska and Iwona Krela-Kaźmierczak
J. Clin. Med. 2023, 12(7), 2451; https://doi.org/10.3390/jcm12072451 - 23 Mar 2023
Cited by 2 | Viewed by 2154
Abstract
Obesity is a complex and multifactorial problem of global importance. Additionally, obesity causes chronic inflammation, upregulates cell growth, disturbs the immune system, and causes genomic instability, increasing the risk of carcinogenesis. Colorectal cancer is one of the most common cancers, and it has [...] Read more.
Obesity is a complex and multifactorial problem of global importance. Additionally, obesity causes chronic inflammation, upregulates cell growth, disturbs the immune system, and causes genomic instability, increasing the risk of carcinogenesis. Colorectal cancer is one of the most common cancers, and it has become a global problem. In 2018, there were around 1.8 million new cases and around 881,000 deaths worldwide. Another risk factor of colorectal cancer associated with obesity is poor diet. A Western diet, including a high intake of red and processed meat and a low consumption of whole grains, fruits, vegetables, and fiber, may increase the risk of both colorectal cancer and obesity. Moreover, the Western diet is associated with a proinflammatory profile diet, which may also affect chronic low-grade inflammation. In fact, people with obesity often present gut dysbiosis, increased inflammation, and risk of colorectal cancer. In this article, the association between obesity and colorectal cancer is discussed, including the most important mechanisms, such as low-grade chronic inflammation, gut dysbiosis, and poor diet. Full article
(This article belongs to the Special Issue Cancer and Inflammation in the Gastrointestinal Tract)
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13 pages, 980 KiB  
Review
A Crosstalk between the Cannabinoid Receptors and Nociceptin Receptors in Colitis—Clinical Implications
by Maria Wołyniak, Ewa Małecka-Wojciesko, Marta Zielińska and Adam Fabisiak
J. Clin. Med. 2022, 11(22), 6675; https://doi.org/10.3390/jcm11226675 - 10 Nov 2022
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Abstract
Inflammatory bowel diseases (IBD) refer to a group of gastrointestinal (GI) disorders with complex pathogenesis characterized by chronic intestinal inflammation with a variety of symptoms. Cannabinoid and nociceptin opioid receptors (NOPs) and their ligands are widely distributed in the GI tract. The nociceptin [...] Read more.
Inflammatory bowel diseases (IBD) refer to a group of gastrointestinal (GI) disorders with complex pathogenesis characterized by chronic intestinal inflammation with a variety of symptoms. Cannabinoid and nociceptin opioid receptors (NOPs) and their ligands are widely distributed in the GI tract. The nociceptin opioid receptor is a newly discovered member of the opioid receptor family with unique characteristics. Both cannabinoid and NOP systems exhibit antinociceptive and anti-inflammatory activity and contribute to maintaining proper motility, secretion and absorption in the GI tract. Furthermore, they influence high and low voltage calcium channels, which play a crucial role in the processing of pain, and share at least two kinases mediating their action. Among them there is NF-κB, a key factor in the regulation of inflammatory processes. Therefore, based on functional similarities between cannabinoid and nociceptin receptors and the anti-inflammatory effects exerted by their ligands, there is a high likelihood that there is an interaction between cannabinoid receptors 1 and 2 and the nociceptin receptor in colitis. In this review, we discuss potential overlaps between these two systems on a molecular and functional level in intestinal inflammation to create the basis for novel treatments of IBD. Full article
(This article belongs to the Special Issue Cancer and Inflammation in the Gastrointestinal Tract)
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