The Role of cMET in Gastric Cancer-A Review of the Literature
Gastric cancer (GC) is an important cause of cancer worldwide with over one million new cases yearly. The vast majority of cases present in stage IV disease, and it still bears a poor prognosis. However, since 2010, progress has been made with the introduction of targeted therapies against HER2 and...
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| Veröffentlicht in: | Cancers 2023-03, Vol.15 (7), p.1976 |
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| description | Gastric cancer (GC) is an important cause of cancer worldwide with over one million new cases yearly. The vast majority of cases present in stage IV disease, and it still bears a poor prognosis. However, since 2010, progress has been made with the introduction of targeted therapies against HER2 and with checkpoint inhibitors (PDL1). More agents interfering with other targets (FGFR2B, CLDN18.2) are being investigated. cMET is a less frequent molecular target that has been studied for gastric cancer. It is a proto-oncogene that leads to activation of the MAPK pathway and the PI3K pathway, which is responsible for activating the MTOR pathway. The prevalence of cMET is strongly debated as different techniques are being used to detect MET-driven tumors. Because of the difference in diagnostic assays, selecting patients who benefit from cMET inhibitors is difficult. In this review, we discuss the pathway of cMET, its clinical significance and the different diagnostic assays that are currently used, such as immunohistochemy (IHC), fluorescence in situ hybridization (FISH), the H-score and next-generation sequencing (NGS). Next, we discuss all the current data on cMET inhibitors in gastric cancer. Since the data on cMET inhibitors are very heterogenous, it is difficult to provide a general consensus on the outcome, as inclusion criteria differ between trials. Diagnosing cMET-driven gastric tumors is difficult, and potentially the only accurate determination of cMET overexpression/amplification may be next-generation sequencing (NGS). |
| doi_str_mv | 10.3390/cancers15071976 |
| format | Article |
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The vast majority of cases present in stage IV disease, and it still bears a poor prognosis. However, since 2010, progress has been made with the introduction of targeted therapies against HER2 and with checkpoint inhibitors (PDL1). More agents interfering with other targets (FGFR2B, CLDN18.2) are being investigated. cMET is a less frequent molecular target that has been studied for gastric cancer. It is a proto-oncogene that leads to activation of the MAPK pathway and the PI3K pathway, which is responsible for activating the MTOR pathway. The prevalence of cMET is strongly debated as different techniques are being used to detect MET-driven tumors. Because of the difference in diagnostic assays, selecting patients who benefit from cMET inhibitors is difficult. In this review, we discuss the pathway of cMET, its clinical significance and the different diagnostic assays that are currently used, such as immunohistochemy (IHC), fluorescence in situ hybridization (FISH), the H-score and next-generation sequencing (NGS). Next, we discuss all the current data on cMET inhibitors in gastric cancer. Since the data on cMET inhibitors are very heterogenous, it is difficult to provide a general consensus on the outcome, as inclusion criteria differ between trials. Diagnosing cMET-driven gastric tumors is difficult, and potentially the only accurate determination of cMET overexpression/amplification may be next-generation sequencing (NGS).</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers15071976</identifier><identifier>PMID: 37046637</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>1-Phosphatidylinositol 3-kinase ; Bone cancer ; c-Met protein ; Cancer therapies ; Cell growth ; Chemotherapy ; Clinical trials ; Development and progression ; Epstein-Barr virus ; ErbB-2 protein ; Fluorescence in situ hybridization ; Gastric cancer ; Gene amplification ; Genetic aspects ; Growth factors ; Health aspects ; Immune checkpoint inhibitors ; Kinases ; Ligands ; Literature reviews ; MAP kinase ; Medical prognosis ; Mutation ; Next-generation sequencing ; Oncogenes ; Phosphorylation ; Prognosis ; Protein-tyrosine kinase ; Proteins ; Review ; Stomach cancer ; TOR protein ; Tumors</subject><ispartof>Cancers, 2023-03, Vol.15 (7), p.1976</ispartof><rights>COPYRIGHT 2023 MDPI AG</rights><rights>2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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The vast majority of cases present in stage IV disease, and it still bears a poor prognosis. However, since 2010, progress has been made with the introduction of targeted therapies against HER2 and with checkpoint inhibitors (PDL1). More agents interfering with other targets (FGFR2B, CLDN18.2) are being investigated. cMET is a less frequent molecular target that has been studied for gastric cancer. It is a proto-oncogene that leads to activation of the MAPK pathway and the PI3K pathway, which is responsible for activating the MTOR pathway. The prevalence of cMET is strongly debated as different techniques are being used to detect MET-driven tumors. Because of the difference in diagnostic assays, selecting patients who benefit from cMET inhibitors is difficult. In this review, we discuss the pathway of cMET, its clinical significance and the different diagnostic assays that are currently used, such as immunohistochemy (IHC), fluorescence in situ hybridization (FISH), the H-score and next-generation sequencing (NGS). Next, we discuss all the current data on cMET inhibitors in gastric cancer. Since the data on cMET inhibitors are very heterogenous, it is difficult to provide a general consensus on the outcome, as inclusion criteria differ between trials. 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Van Cutsem, Eric</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c489t-c081144dd97c91e987736751ee0778ac94110710feaa245f44cfd7a1d5c44d343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Bone cancer</topic><topic>c-Met protein</topic><topic>Cancer therapies</topic><topic>Cell growth</topic><topic>Chemotherapy</topic><topic>Clinical trials</topic><topic>Development and progression</topic><topic>Epstein-Barr virus</topic><topic>ErbB-2 protein</topic><topic>Fluorescence in situ hybridization</topic><topic>Gastric cancer</topic><topic>Gene amplification</topic><topic>Genetic aspects</topic><topic>Growth factors</topic><topic>Health aspects</topic><topic>Immune checkpoint inhibitors</topic><topic>Kinases</topic><topic>Ligands</topic><topic>Literature reviews</topic><topic>MAP kinase</topic><topic>Medical prognosis</topic><topic>Mutation</topic><topic>Next-generation sequencing</topic><topic>Oncogenes</topic><topic>Phosphorylation</topic><topic>Prognosis</topic><topic>Protein-tyrosine kinase</topic><topic>Proteins</topic><topic>Review</topic><topic>Stomach cancer</topic><topic>TOR protein</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Van Herpe, Filip</creatorcontrib><creatorcontrib>Van Cutsem, Eric</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Van Herpe, Filip</au><au>Van Cutsem, Eric</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Role of cMET in Gastric Cancer-A Review of the Literature</atitle><jtitle>Cancers</jtitle><addtitle>Cancers (Basel)</addtitle><date>2023-03-26</date><risdate>2023</risdate><volume>15</volume><issue>7</issue><spage>1976</spage><pages>1976-</pages><issn>2072-6694</issn><eissn>2072-6694</eissn><abstract>Gastric cancer (GC) is an important cause of cancer worldwide with over one million new cases yearly. 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In this review, we discuss the pathway of cMET, its clinical significance and the different diagnostic assays that are currently used, such as immunohistochemy (IHC), fluorescence in situ hybridization (FISH), the H-score and next-generation sequencing (NGS). Next, we discuss all the current data on cMET inhibitors in gastric cancer. Since the data on cMET inhibitors are very heterogenous, it is difficult to provide a general consensus on the outcome, as inclusion criteria differ between trials. Diagnosing cMET-driven gastric tumors is difficult, and potentially the only accurate determination of cMET overexpression/amplification may be next-generation sequencing (NGS).</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>37046637</pmid><doi>10.3390/cancers15071976</doi><oa>free_for_read</oa></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase Bone cancer c-Met protein Cancer therapies Cell growth Chemotherapy Clinical trials Development and progression Epstein-Barr virus ErbB-2 protein Fluorescence in situ hybridization Gastric cancer Gene amplification Genetic aspects Growth factors Health aspects Immune checkpoint inhibitors Kinases Ligands Literature reviews MAP kinase Medical prognosis Mutation Next-generation sequencing Oncogenes Phosphorylation Prognosis Protein-tyrosine kinase Proteins Review Stomach cancer TOR protein Tumors |
| title | The Role of cMET in Gastric Cancer-A Review of the Literature |
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