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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.
Chang Min Cho
Correspondence to: Chang Min Cho, Department of Internal Medicine, Kyungpook National University Chilgok Hospital, School of Medicine, Kyungpook National University, 807 Hoguk-ro, Buk-gu, Daegu 41404, Korea, Tel: +82-53-200-2608, Fax: +82-53-200-2028, E-mail: cmcho@knu.ac.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 2018;12(3):223-224. https://doi.org/10.5009/gnl18113
Published online May 15, 2018, Published date May 31, 2018
Copyright © Gut and Liver.
Pancreatic cancer is one of the worst tumors, and is the fourth leading cause of cancer-related deaths worldwide, with an overall 5-year survival rate of less than 5%.1 Since nearly four decades, the survival rates have not improved substantially. Only 10% to 20% of individuals present with the disease in a potentially operable stage, and despite resection with curative intent, the median survival remains between 12 and 18 months.2,3 Although great efforts have been made in the early diagnosis and treatment of pancreatic cancer, the prognostic outcomes of pancreatic cancer remain disappointing. There are several reasons for poor prognosis: (1) a highly invasive tumor, which usually shows metastases at diagnosis; (2) relatively resistant to chemotherapy, radiotherapy, and targeted therapy; (3) harboring multiple genetic and epigenetic alterations; and (4) extremely complicated tumor-microenvironment due to close interaction with host immune system.4 Several studies focusing on cancer-related response to immunity and inflammation may provide some suggestions on the possible explanation for poor prognosis.5 Inflammation, as a major feature of tumors, has been proven to play a crucial role in the progression of malignancies, including proliferation, angiogenesis, metastasis, and chemotherapy-resistance. A variety of prognostic scores based on systemic inflammation have been proposed in the last decade.
Previous studies have demonstrated the association of systemic inflammatory response (SIR) with adverse outcomes in a variety of solid organ malignancies, including pancreatic cancer.6 It has been proven that the levels of neutrophils, lymphocytes and platelets in peripheral venous blood could be affected by tumor-induced SIR. While neutrophils function as tumor-promoting factors via the signaling pathway triggered by inflammatory cytokines, platelets also play a crucial role in the proliferation and metastasis of tumors by promoting angiogenesis, extracellular matrix degradation, and the release of growth factors and adhesion molecules. Therefore, quantitative hematological parameters have been analyzed as prognostic markers in various tumors, including pancreatic cancer.
In this issue of
NLR and PLR show promise for the prediction of prognosis and response to treatment of cancers, and they are easily calculated, reproducible, and inexpensive. However, as mentioned in this article, there are several issues that should be addressed to consider NLR and PLR as prognostic factors. First, there is no consensus on the cutoff values of NLR and PLR, and thus, various cutoff values have been used in previous studies; while the receiver-operating characteristic curve was used to determine the cutoff value in some studies, median values were used in other studies. Second, most previous studies retrospectively enrolled patients with different stages and a variety of treatment modalities were applied. The heterogeneity of the study group and cutoff values may be attributed to the prognosis of patients with cancer. Finally, the mechanisms responsible for the association between NLR and PLR and poor outcomes of patients with cancer are not entirely understood. Additionally, variable factors such as infection and several host factors might affect the levels of inflammatory parameters.
Although the study by Lee
No potential conflict of interest relevant to this article was reported.
Gut and Liver 2018; 12(3): 223-224
Published online May 31, 2018 https://doi.org/10.5009/gnl18113
Copyright © Gut and Liver.
Chang Min Cho
Department of Internal Medicine, Kyungpook National University Chilgok Hospital, School of Medicine, Kyungpook National University, Daegu, Korea
Correspondence to:Chang Min Cho, Department of Internal Medicine, Kyungpook National University Chilgok Hospital, School of Medicine, Kyungpook National University, 807 Hoguk-ro, Buk-gu, Daegu 41404, Korea, Tel: +82-53-200-2608, Fax: +82-53-200-2028, E-mail: cmcho@knu.ac.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.
Pancreatic cancer is one of the worst tumors, and is the fourth leading cause of cancer-related deaths worldwide, with an overall 5-year survival rate of less than 5%.1 Since nearly four decades, the survival rates have not improved substantially. Only 10% to 20% of individuals present with the disease in a potentially operable stage, and despite resection with curative intent, the median survival remains between 12 and 18 months.2,3 Although great efforts have been made in the early diagnosis and treatment of pancreatic cancer, the prognostic outcomes of pancreatic cancer remain disappointing. There are several reasons for poor prognosis: (1) a highly invasive tumor, which usually shows metastases at diagnosis; (2) relatively resistant to chemotherapy, radiotherapy, and targeted therapy; (3) harboring multiple genetic and epigenetic alterations; and (4) extremely complicated tumor-microenvironment due to close interaction with host immune system.4 Several studies focusing on cancer-related response to immunity and inflammation may provide some suggestions on the possible explanation for poor prognosis.5 Inflammation, as a major feature of tumors, has been proven to play a crucial role in the progression of malignancies, including proliferation, angiogenesis, metastasis, and chemotherapy-resistance. A variety of prognostic scores based on systemic inflammation have been proposed in the last decade.
Previous studies have demonstrated the association of systemic inflammatory response (SIR) with adverse outcomes in a variety of solid organ malignancies, including pancreatic cancer.6 It has been proven that the levels of neutrophils, lymphocytes and platelets in peripheral venous blood could be affected by tumor-induced SIR. While neutrophils function as tumor-promoting factors via the signaling pathway triggered by inflammatory cytokines, platelets also play a crucial role in the proliferation and metastasis of tumors by promoting angiogenesis, extracellular matrix degradation, and the release of growth factors and adhesion molecules. Therefore, quantitative hematological parameters have been analyzed as prognostic markers in various tumors, including pancreatic cancer.
In this issue of
NLR and PLR show promise for the prediction of prognosis and response to treatment of cancers, and they are easily calculated, reproducible, and inexpensive. However, as mentioned in this article, there are several issues that should be addressed to consider NLR and PLR as prognostic factors. First, there is no consensus on the cutoff values of NLR and PLR, and thus, various cutoff values have been used in previous studies; while the receiver-operating characteristic curve was used to determine the cutoff value in some studies, median values were used in other studies. Second, most previous studies retrospectively enrolled patients with different stages and a variety of treatment modalities were applied. The heterogeneity of the study group and cutoff values may be attributed to the prognosis of patients with cancer. Finally, the mechanisms responsible for the association between NLR and PLR and poor outcomes of patients with cancer are not entirely understood. Additionally, variable factors such as infection and several host factors might affect the levels of inflammatory parameters.
Although the study by Lee
No potential conflict of interest relevant to this article was reported.