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Vol.17 No.2
March, 2023
Frequency : Bimonthly
pISSN 1976-2283
eISSN 2005-1212 
Gut and Liver is an international journal of gastroenterology, focusing on the gastrointestinal tract, liver, biliary tree, pancreas, motility, and neurogastroenterology. Gut atnd Liver delivers up-to-date, authoritative papers on both clinical and research-based topics in gastroenterology. The Journal publishes original articles, case reports, brief communications, letters to the editor and invited review articles in the field of gastroenterology. The Journal is operated by internationally renowned editorial boards and designed to provide a global opportunity to promote academic developments in the field of gastroenterology and hepatology. +MORE
| Yong Chan Lee |
Professor of Medicine Director, Gastrointestinal Research Laboratory Veterans Affairs Medical Center, Univ. California San Francisco San Francisco, USA |
| Jong Pil Im | Seoul National University College of Medicine, Seoul, Korea |
| Robert S. Bresalier | University of Texas M. D. Anderson Cancer Center, Houston, USA |
| Steven H. Itzkowitz | Mount Sinai Medical Center, NY, USA |
All papers submitted to Gut and Liver are reviewed by the editorial team before being sent out for an external peer review to rule out papers that have low priority, insufficient originality, scientific flaws, or the absence of a message of importance to the readers of the Journal. A decision about these papers will usually be made within two or three weeks.
The remaining articles are usually sent to two reviewers. It would be very helpful if you could suggest a selection of reviewers and include their contact details. We may not always use the reviewers you recommend, but suggesting reviewers will make our reviewer database much richer; in the end, everyone will benefit. We reserve the right to return manuscripts in which no reviewers are suggested.
The final responsibility for the decision to accept or reject lies with the editors. In many cases, papers may be rejected despite favorable reviews because of editorial policy or a lack of space. The editor retains the right to determine publication priorities, the style of the paper, and to request, if necessary, that the material submitted be shortened for publication.
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Hyun Joo Jang 
Correspondence to: Hyun Joo Jang (
Department of Gastroenterology, Hallym University School of Medicine, 7 Keunjaebong-gil, Hwaseong 18450, Korea
Tel: +82-31-8086-2450, Fax: +82-31-8086-2029, E-mail: jhj1229@hallym.or.kr
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Gut Liver 2019;13(2):138-139. https://doi.org/10.5009/gnl19003
Published online March 15, 2019, Published date March 31, 2019
Copyright © Gut and Liver.
The risk for dysplasia and colorectal cancer (CRC) is increased in patients with long-standing ulcerative colitis (UC) and extensive Crohn’s disease (CD). CRC is one of important causes of death in patients with inflammatory bowel disease (IBD). Patients with long-standing UC and colonic CD have about 1- to 6-fold increase in lifetime risk of CRC compared to the general population.1 The risk factors for IBD-associated CRC include: prolonged duration of colitis, extent and severity of colitis, coexistence of primary sclerosing cholangitis (PSC), and family history of CRC.2 Oncogenic mechanism of IBD-related CRC has been known that chronic or repeated inflammation to the intestinal mucosa leads to the development of CRC via low- and high-grade dysplasia.
There is a controversial issue about whether statins have chemopreventive potentials against CRC, but it still remains a debate. Statins, one of cholesterol-lowering drugs, are used to prevent and treat cardiovascular diseases. Some experimental results recently suggest that statins provide an additional chemopreventive effect by inducing apoptosis, inhibiting angiogenesis, increasing the antitumor effects of several cytokines, and preventing metastasis.3,4 Two recent meta-analyses including 40 and 42 individual studies suggested a risk reduction of CRC among statin users.5,6
Statins reduce synthesis of cholesterol in liver and reduce the level of serum cholesterol by 3-hydroxy-3-methylglutaryl-coenzyme A reductase which is a rate-limiting enzyme in the mevalonate pathway. Its downstream mevalonate products (such as isoprenoid molecules, farnesyl pyrophosphate and geranyl-geranyl pyrophosphate) are necessary for post-translational modification and isoprenylation of a variety of proteins such as Ras and RhoA, which are important for cell growth, cell proliferation, angiogenesis or cell migration.7 These proteins are over-expressed in CRC and are associated with tumor invasion. Statin induces apoptosis and suppresses the β subunits of insulin-like growth factor 1 receptor (IGF-1R) and IGF-1-induced ERK/Akt activation.3 Non HMG-CoA reductase-mediated effects of statins may be through inhibition of inflammation, angiogenesis and cell adhesion, and an antioxidant effect.
There are limited studies investigating the chemopreventive effect of statins against CRC in IBD patients. One study showed that long-term statin use was associated with a reduced risk of both IBD-associated CRC (odds ratio [OR], 0.07; 95% confidence interval [CI], 0.01 to 0.78) and non-IBD CRC (OR, 0.49; 95% CI, 0.39 to 0.62).8 The limitations of this study were recall bias and misclassifications based on self-reporting data. It also did not report disease duration, location of disease, medications, extent of disease and severity. Another recent study of Ananthakrishnan
In previous issue of
In summary, statin use as chemopreventive agents in IBD patients remains controversial. Well-designed and large prospective studies would be needed to prove the chemopreventive role of statin in IBD patients.
No potential conflict of interest relevant to this article was reported.
Gut and Liver 2019; 13(2): 138-139
Published online March 31, 2019 https://doi.org/10.5009/gnl19003
Copyright © Gut and Liver.
Hyun Joo Jang
Department of Gastroenterology, Hallym University School of Medicine, Hwasung, Korea
Correspondence to:Hyun Joo Jang (
Department of Gastroenterology, Hallym University School of Medicine, 7 Keunjaebong-gil, Hwaseong 18450, Korea
Tel: +82-31-8086-2450, Fax: +82-31-8086-2029, E-mail: jhj1229@hallym.or.kr
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
The risk for dysplasia and colorectal cancer (CRC) is increased in patients with long-standing ulcerative colitis (UC) and extensive Crohn’s disease (CD). CRC is one of important causes of death in patients with inflammatory bowel disease (IBD). Patients with long-standing UC and colonic CD have about 1- to 6-fold increase in lifetime risk of CRC compared to the general population.1 The risk factors for IBD-associated CRC include: prolonged duration of colitis, extent and severity of colitis, coexistence of primary sclerosing cholangitis (PSC), and family history of CRC.2 Oncogenic mechanism of IBD-related CRC has been known that chronic or repeated inflammation to the intestinal mucosa leads to the development of CRC via low- and high-grade dysplasia.
There is a controversial issue about whether statins have chemopreventive potentials against CRC, but it still remains a debate. Statins, one of cholesterol-lowering drugs, are used to prevent and treat cardiovascular diseases. Some experimental results recently suggest that statins provide an additional chemopreventive effect by inducing apoptosis, inhibiting angiogenesis, increasing the antitumor effects of several cytokines, and preventing metastasis.3,4 Two recent meta-analyses including 40 and 42 individual studies suggested a risk reduction of CRC among statin users.5,6
Statins reduce synthesis of cholesterol in liver and reduce the level of serum cholesterol by 3-hydroxy-3-methylglutaryl-coenzyme A reductase which is a rate-limiting enzyme in the mevalonate pathway. Its downstream mevalonate products (such as isoprenoid molecules, farnesyl pyrophosphate and geranyl-geranyl pyrophosphate) are necessary for post-translational modification and isoprenylation of a variety of proteins such as Ras and RhoA, which are important for cell growth, cell proliferation, angiogenesis or cell migration.7 These proteins are over-expressed in CRC and are associated with tumor invasion. Statin induces apoptosis and suppresses the β subunits of insulin-like growth factor 1 receptor (IGF-1R) and IGF-1-induced ERK/Akt activation.3 Non HMG-CoA reductase-mediated effects of statins may be through inhibition of inflammation, angiogenesis and cell adhesion, and an antioxidant effect.
There are limited studies investigating the chemopreventive effect of statins against CRC in IBD patients. One study showed that long-term statin use was associated with a reduced risk of both IBD-associated CRC (odds ratio [OR], 0.07; 95% confidence interval [CI], 0.01 to 0.78) and non-IBD CRC (OR, 0.49; 95% CI, 0.39 to 0.62).8 The limitations of this study were recall bias and misclassifications based on self-reporting data. It also did not report disease duration, location of disease, medications, extent of disease and severity. Another recent study of Ananthakrishnan
In previous issue of
In summary, statin use as chemopreventive agents in IBD patients remains controversial. Well-designed and large prospective studies would be needed to prove the chemopreventive role of statin in IBD patients.
No potential conflict of interest relevant to this article was reported.
pISSN 1976-2283
eISSN 2005-1212
Gut and Liver is an international journal of gastroenterology, focusing on the gastrointestinal tract, liver, biliary tree, pancreas, motility, and neurogastroenterology. Gut atnd Liver delivers up-to-date, authoritative papers on both clinical and research-based topics in gastroenterology. The Journal publishes original articles, case reports, brief communications, letters to the editor and invited review articles in the field of gastroenterology. The Journal is operated by internationally renowned editorial boards and designed to provide a global opportunity to promote academic developments in the field of gastroenterology and hepatology. +MORE
| Yong Chan Lee |
Professor of Medicine Director, Gastrointestinal Research Laboratory Veterans Affairs Medical Center, Univ. California San Francisco San Francisco, USA |
| Jong Pil Im | Seoul National University College of Medicine, Seoul, Korea |
| Robert S. Bresalier | University of Texas M. D. Anderson Cancer Center, Houston, USA |
| Steven H. Itzkowitz | Mount Sinai Medical Center, NY, USA |
All papers submitted to Gut and Liver are reviewed by the editorial team before being sent out for an external peer review to rule out papers that have low priority, insufficient originality, scientific flaws, or the absence of a message of importance to the readers of the Journal. A decision about these papers will usually be made within two or three weeks.
The remaining articles are usually sent to two reviewers. It would be very helpful if you could suggest a selection of reviewers and include their contact details. We may not always use the reviewers you recommend, but suggesting reviewers will make our reviewer database much richer; in the end, everyone will benefit. We reserve the right to return manuscripts in which no reviewers are suggested.
The final responsibility for the decision to accept or reject lies with the editors. In many cases, papers may be rejected despite favorable reviews because of editorial policy or a lack of space. The editor retains the right to determine publication priorities, the style of the paper, and to request, if necessary, that the material submitted be shortened for publication.
