Pub Date : 2023-10-01DOI: 10.1016/j.esmogo.2023.08.004
F. van Bömmel , T. Berg , F. Lordick
Immune checkpoint inhibition (ICI) has revolutionized cancer therapy, including treatment of hepatocellular carcinoma (HCC) which comprises 80%-90% of all liver cancers, the third most common cause of cancer-related death worldwide. The main targeted pathways are the cytotoxic T-lymphocyte-associated protein-4 (CTLA-4) and the programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) checkpoints. Blockade of CTLA-4 with monoclonal antibodies leads to an activation and increase in effector T cells that can interact with tumor cells. Additionally, inhibitory regulatory T cells are reduced, leading to an immunosupportive tumor microenvironment. PD-1/PD-L1 inhibition reduces immunosuppression directly within the tumor tissue and reactivates the immune response to tumor cells. Recently, the HIMALAYA trial has shown that dual ICI with the CTLA-4-blocking antibody tremelimumab and the PD-L1-directed antibody durvalumab (STRIDE regimen) is superior to sorafenib regarding efficacy and safety in advanced HCC and has shown unprecedented long-term survival data for these patients. The combination of PD-L1-directed ICI (atezolizumab) and anti-vascular endothelial growth factor (bevacizumab) significantly improved outcomes compared to sorafenib and has been in clinical use since 2020. Looking at outcome measures for ICI, radiologically assessed endpoints such as progression-free survival and objective response rate only modestly correlate with overall survival. The modified RECIST criteria seem to better identify ICI responders in HCC compared to conventional imaging evaluation criteria. So far, predictive biomarkers in HCC and a robust understanding of the impact of underlying liver diseases are largely lacking. An accurate stratification of patients based on biomarkers and etiology has the potential to further improve outcomes in HCC.
{"title":"Immune checkpoint inhibition (ICI) in current systemic therapies for hepatocellular carcinoma (HCC)","authors":"F. van Bömmel , T. Berg , F. Lordick","doi":"10.1016/j.esmogo.2023.08.004","DOIUrl":"https://doi.org/10.1016/j.esmogo.2023.08.004","url":null,"abstract":"<div><p>Immune checkpoint inhibition (ICI) has revolutionized cancer therapy, including treatment of hepatocellular carcinoma (HCC) which comprises 80%-90% of all liver cancers, the third most common cause of cancer-related death worldwide. The main targeted pathways are the cytotoxic T-lymphocyte-associated protein-4 (CTLA-4) and the programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) checkpoints. Blockade of CTLA-4 with monoclonal antibodies leads to an activation and increase in effector T cells that can interact with tumor cells. Additionally, inhibitory regulatory T cells are reduced, leading to an immunosupportive tumor microenvironment. PD-1/PD-L1 inhibition reduces immunosuppression directly within the tumor tissue and reactivates the immune response to tumor cells. Recently, the HIMALAYA trial has shown that dual ICI with the CTLA-4-blocking antibody tremelimumab and the PD-L1-directed antibody durvalumab (STRIDE regimen) is superior to sorafenib regarding efficacy and safety in advanced HCC and has shown unprecedented long-term survival data for these patients. The combination of PD-L1-directed ICI (atezolizumab) and anti-vascular endothelial growth factor (bevacizumab) significantly improved outcomes compared to sorafenib and has been in clinical use since 2020. Looking at outcome measures for ICI, radiologically assessed endpoints such as progression-free survival and objective response rate only modestly correlate with overall survival. The modified RECIST criteria seem to better identify ICI responders in HCC compared to conventional imaging evaluation criteria. So far, predictive biomarkers in HCC and a robust understanding of the impact of underlying liver diseases are largely lacking. An accurate stratification of patients based on biomarkers and etiology has the potential to further improve outcomes in HCC.</p></div>","PeriodicalId":100490,"journal":{"name":"ESMO Gastrointestinal Oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71779383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-01-01DOI: 10.1080/1475956021000020206
R. Talar-Wojnarowska, A. Sasor, J. Strzelczyk, E. Małecka-Panas
{"title":"Molecular Basis of Pancreatic Cancer--Selected Issues","authors":"R. Talar-Wojnarowska, A. Sasor, J. Strzelczyk, E. Małecka-Panas","doi":"10.1080/1475956021000020206","DOIUrl":"https://doi.org/10.1080/1475956021000020206","url":null,"abstract":"","PeriodicalId":100490,"journal":{"name":"ESMO Gastrointestinal Oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84354508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-01-01DOI: 10.1080/1475956021000015086
J. Sayfan
{"title":"Surgery for Inflammatory Bowel Diseases and Prevention of Gastrointestinal Malignancies","authors":"J. Sayfan","doi":"10.1080/1475956021000015086","DOIUrl":"https://doi.org/10.1080/1475956021000015086","url":null,"abstract":"","PeriodicalId":100490,"journal":{"name":"ESMO Gastrointestinal Oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84149919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-01-01DOI: 10.1080/1475956021000015103
Mohamed M. Eida, Abd Elraouf El Deib, A. Saad, I. Perry, David Roland, M. Dixon, J. Jankowski
{"title":"Down-regulation of E-cadherin and β-catenin in Helicobacter pylori Associated Gastritis and Gastric Carcinoma: An Immunohistochemical Study","authors":"Mohamed M. Eida, Abd Elraouf El Deib, A. Saad, I. Perry, David Roland, M. Dixon, J. Jankowski","doi":"10.1080/1475956021000015103","DOIUrl":"https://doi.org/10.1080/1475956021000015103","url":null,"abstract":"","PeriodicalId":100490,"journal":{"name":"ESMO Gastrointestinal Oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79919843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-01-01DOI: 10.1080/1475956021000020215
I. Rácz, A. Szabó, M. Goda, A. Oláh
{"title":"Preliminary Colorectal Cancer Screening Program Model in Hungary","authors":"I. Rácz, A. Szabó, M. Goda, A. Oláh","doi":"10.1080/1475956021000020215","DOIUrl":"https://doi.org/10.1080/1475956021000020215","url":null,"abstract":"","PeriodicalId":100490,"journal":{"name":"ESMO Gastrointestinal Oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89588709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-01-01DOI: 10.1080/14759560290029614
Yoon Kim, Hanhui Yang, S. Oh
Purpose: Bombesin-like peptides are known to be important in the autocrine growth of a number of smlll cell lung cancer cell lines. The aim of this study was to investigate the extent of bombesin family ligands/receptors expression in human gastric cancer tissues and cell lines, and to evaluate the relationship between the expression of bombesin family Iigands/receptor and clinicopathologic parameters. Methods: We measured the expression of gstrin releasing peptide (GAP), neuromedin B (NMB), and their receptors, in human gastric cancer tissues and cell lines. Ligand and receptor mRNA studies were carried out on: 20 tumor and matched normal samples, and 9 gastric cell lines. The expression of mRNA of GRP/NMB, and their receptors, was examined by the reverse transcription-polymerase chain reaction (RT-PCR). Results: Expression of GRP, NMB and GRPR, NMBR mRNA was found in 55%, 100%, 40%, and 100% of gastric cancer tissue, respectively. GRP/GRPR co-expression was observed in 30% of gastric cancer tissues and expression of gastric cancer was higher than that of normal mucosa. GRP and GRPR were highly expressed in the differentiated type of gastric cancer. In gastric cancer cell lines, these peptides and receptors were expressed equally. Conclusion: The result demonstrate that GRP, NMB, GRPR, and NMBR were expressed in gastric cancer tissues and cell lines. This result suggests that these may have a role as growth factors in gastric cancer growth, and these peptides may act in an autocrine fashion as a morphogen in gastric cancer.
{"title":"Expression of Bombesin Family Ligands and Receptors in Human Gastric Cancer Tissues and Cell Lines.","authors":"Yoon Kim, Hanhui Yang, S. Oh","doi":"10.1080/14759560290029614","DOIUrl":"https://doi.org/10.1080/14759560290029614","url":null,"abstract":"Purpose: Bombesin-like peptides are known to be important in the autocrine growth of a number of smlll cell lung cancer cell lines. The aim of this study was to investigate the extent of bombesin family ligands/receptors expression in human gastric cancer tissues and cell lines, and to evaluate the relationship between the expression of bombesin family Iigands/receptor and clinicopathologic parameters. Methods: We measured the expression of gstrin releasing peptide (GAP), neuromedin B (NMB), and their receptors, in human gastric cancer tissues and cell lines. Ligand and receptor mRNA studies were carried out on: 20 tumor and matched normal samples, and 9 gastric cell lines. The expression of mRNA of GRP/NMB, and their receptors, was examined by the reverse transcription-polymerase chain reaction (RT-PCR). Results: Expression of GRP, NMB and GRPR, NMBR mRNA was found in 55%, 100%, 40%, and 100% of gastric cancer tissue, respectively. GRP/GRPR co-expression was observed in 30% of gastric cancer tissues and expression of gastric cancer was higher than that of normal mucosa. GRP and GRPR were highly expressed in the differentiated type of gastric cancer. In gastric cancer cell lines, these peptides and receptors were expressed equally. Conclusion: The result demonstrate that GRP, NMB, GRPR, and NMBR were expressed in gastric cancer tissues and cell lines. This result suggests that these may have a role as growth factors in gastric cancer growth, and these peptides may act in an autocrine fashion as a morphogen in gastric cancer.","PeriodicalId":100490,"journal":{"name":"ESMO Gastrointestinal Oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76989426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-01-01DOI: 10.1080/14759560290019804
John W. C. Chen, D. Mirza
{"title":"Radiofrequency Ablation of Liver Tumours","authors":"John W. C. Chen, D. Mirza","doi":"10.1080/14759560290019804","DOIUrl":"https://doi.org/10.1080/14759560290019804","url":null,"abstract":"","PeriodicalId":100490,"journal":{"name":"ESMO Gastrointestinal Oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81994077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-01-01DOI: 10.1080/1475956021000018614
K. Yassin, E. Vlodavsky, R. Eliakim
{"title":"Recurrent Upper Gastrointestinal Bleeding Caused by a Giant Brunneroma--Report of a Case Treated Endoscopically","authors":"K. Yassin, E. Vlodavsky, R. Eliakim","doi":"10.1080/1475956021000018614","DOIUrl":"https://doi.org/10.1080/1475956021000018614","url":null,"abstract":"","PeriodicalId":100490,"journal":{"name":"ESMO Gastrointestinal Oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89392492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-01-01DOI: 10.1080/1475956021000017057
S. Böhm
{"title":"Hyperplastic Polyps of the Colorectum--Do They Possess a Malignant Potential?","authors":"S. Böhm","doi":"10.1080/1475956021000017057","DOIUrl":"https://doi.org/10.1080/1475956021000017057","url":null,"abstract":"","PeriodicalId":100490,"journal":{"name":"ESMO Gastrointestinal Oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78814487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-01-01DOI: 10.1080/14759560290032746
J. King, J. Caplehorn, J. Seifert, A. Preketes, P. Clingan, D. Morris
{"title":"A Randomised Placebo Control Double-blind Trial of Ranitidine in Patients with Colorectal Hepatic Metastases: Survival Advantage in Patients with Poor Cell Mediated Immunity","authors":"J. King, J. Caplehorn, J. Seifert, A. Preketes, P. Clingan, D. Morris","doi":"10.1080/14759560290032746","DOIUrl":"https://doi.org/10.1080/14759560290032746","url":null,"abstract":"","PeriodicalId":100490,"journal":{"name":"ESMO Gastrointestinal Oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77983759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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