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MET overexpression and amplification define a distinct molecular subgroup for targeted therapies in gastric cancer
Background Currently, only trastuzumab, ramucirumab, and apatinib effectively treat gastric cancer. Thus, additional novel targets are required for this disease. Methods We investigated the immunohistochemical and fluorescence in situ hybridization expression of MET, ROS1, and ALK in four gastric ce...
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| Published in: | Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association 2016-07, Vol.19 (3), p.778-788 |
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| container_title | Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association |
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| creator | Yang, Yang Wu, Nandie Shen, Jie Teixido, Cristina Sun, Xia Lin, Zihan Qian, Xiaoping Zou, Zhengyun Guan, Wenxian Yu, Lixia Rosell, Rafael Liu, Baorui Wei, Jia |
| description | Background
Currently, only trastuzumab, ramucirumab, and apatinib effectively treat gastric cancer. Thus, additional novel targets are required for this disease.
Methods
We investigated the immunohistochemical and fluorescence in situ hybridization expression of MET, ROS1, and ALK in four gastric cell lines and a cohort of 98 gastric cancer patients. Crizotinib response was studied in vitro and in vivo.
Results
Crizotinib potently inhibited in vitro cell growth in only one cell line, which also showed MET amplification. A positive correlation between crizotinib sensitivity and MET overexpression was observed (
P
= 0.045) in the histoculture drug response assay. Meanwhile, patient-derived tumor xenograft mouse models transplanted with tissues with higher MET protein expression displayed a highly selective sensitivity to crizotinib. In the 98 patients, MET overexpression was found in 42 (42.9 %) and MET was amplified in 4 (4.1 %). ROS1 and ALK overexpression were found in 25 (25.5 %) and 0 patients, respectively. However, none of the patients screened harbored ALK or ROS1 rearrangements. No significant association was found between overall survival and MET or ROS1 status. We also observed a stage IV gastric cancer patient with MET amplification who experienced tumor shrinkage and clinical benefit after 3 weeks of crizotinib as fourth-line treatment.
Conclusions
Crizotinib may induce clinically relevant anticancer effects in MET-overexpressed or MET-amplified gastric cancer patients. |
| doi_str_mv | 10.1007/s10120-015-0545-5 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1797257056</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>4087836071</sourcerecordid><originalsourceid>FETCH-LOGICAL-c466t-4c0f0dfbe6ee77eba498ef56603ca8c8746fe223672a362ada9573be3dd9b8e13</originalsourceid><addsrcrecordid>eNp1kU9LHjEQxkOpqLV-gF5KoJdeVvM_7x5FrBaUXuw5ZJPJ28husk2yRb999-XVIgVPM8z85plhHoQ-UXJGCdHnlRLKSEeo7IgUspPv0DEVXHWcE_n-JWc9PUIfan0gK9hTdYiOmBJE9IQdo3J3dY_zHyjwOBeoNeaEbfLYTvMYQ3S27SoeQkyALfaxtphcw1MewS2jLbguw7bkZcYhF9xs2UIDj9svKHaOUHFMeGtrK9FhZ5OD8hEdBDtWOH2OJ-jnt6v7y5vu9sf198uL284JpVonHAnEhwEUgNYwWNFvIEilCHd24zZaqACMcaWZ5YpZb3up-QDc-37YAOUn6Otedy759wK1mSlWB-NoE-SlGqp7zaQmUq3ol__Qh7yUtF63oxRlQhGxUnRPuZJrLRDMXOJky5OhxOwMMXtDzPpnszPEyHXm87PyMkzg_028OLACbA_UtZW2UF6tflP1L_SXl44</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1796124604</pqid></control><display><type>article</type><title>MET overexpression and amplification define a distinct molecular subgroup for targeted therapies in gastric cancer</title><source>Springer Nature</source><creator>Yang, Yang ; Wu, Nandie ; Shen, Jie ; Teixido, Cristina ; Sun, Xia ; Lin, Zihan ; Qian, Xiaoping ; Zou, Zhengyun ; Guan, Wenxian ; Yu, Lixia ; Rosell, Rafael ; Liu, Baorui ; Wei, Jia</creator><creatorcontrib>Yang, Yang ; Wu, Nandie ; Shen, Jie ; Teixido, Cristina ; Sun, Xia ; Lin, Zihan ; Qian, Xiaoping ; Zou, Zhengyun ; Guan, Wenxian ; Yu, Lixia ; Rosell, Rafael ; Liu, Baorui ; Wei, Jia</creatorcontrib><description>Background
Currently, only trastuzumab, ramucirumab, and apatinib effectively treat gastric cancer. Thus, additional novel targets are required for this disease.
Methods
We investigated the immunohistochemical and fluorescence in situ hybridization expression of MET, ROS1, and ALK in four gastric cell lines and a cohort of 98 gastric cancer patients. Crizotinib response was studied in vitro and in vivo.
Results
Crizotinib potently inhibited in vitro cell growth in only one cell line, which also showed MET amplification. A positive correlation between crizotinib sensitivity and MET overexpression was observed (
P
= 0.045) in the histoculture drug response assay. Meanwhile, patient-derived tumor xenograft mouse models transplanted with tissues with higher MET protein expression displayed a highly selective sensitivity to crizotinib. In the 98 patients, MET overexpression was found in 42 (42.9 %) and MET was amplified in 4 (4.1 %). ROS1 and ALK overexpression were found in 25 (25.5 %) and 0 patients, respectively. However, none of the patients screened harbored ALK or ROS1 rearrangements. No significant association was found between overall survival and MET or ROS1 status. We also observed a stage IV gastric cancer patient with MET amplification who experienced tumor shrinkage and clinical benefit after 3 weeks of crizotinib as fourth-line treatment.
Conclusions
Crizotinib may induce clinically relevant anticancer effects in MET-overexpressed or MET-amplified gastric cancer patients.</description><identifier>ISSN: 1436-3291</identifier><identifier>EISSN: 1436-3305</identifier><identifier>DOI: 10.1007/s10120-015-0545-5</identifier><identifier>PMID: 26404902</identifier><language>eng</language><publisher>Tokyo: Springer Japan</publisher><subject>Abdominal Surgery ; Adult ; Aged ; Aged, 80 and over ; Animals ; Apoptosis ; Biomarkers, Tumor - metabolism ; Blotting, Western ; Cancer Research ; Cell Proliferation ; Drug Resistance, Neoplasm - genetics ; Female ; Fluorescent Antibody Technique ; Follow-Up Studies ; Gastric cancer ; Gastroenterology ; Humans ; Immunoenzyme Techniques ; In Situ Hybridization, Fluorescence ; Male ; Medicine ; Medicine & Public Health ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Middle Aged ; Neoplasm Grading ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Neoplasm Staging ; Oncology ; Original Article ; Prognosis ; Protein Kinase Inhibitors - therapeutic use ; Proto-Oncogene Proteins c-met - metabolism ; Pyrazoles - therapeutic use ; Pyridines - therapeutic use ; Stomach Neoplasms - drug therapy ; Stomach Neoplasms - metabolism ; Stomach Neoplasms - pathology ; Surgical Oncology ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays</subject><ispartof>Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2016-07, Vol.19 (3), p.778-788</ispartof><rights>The International Gastric Cancer Association and The Japanese Gastric Cancer Association 2015</rights><rights>The International Gastric Cancer Association and The Japanese Gastric Cancer Association 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c466t-4c0f0dfbe6ee77eba498ef56603ca8c8746fe223672a362ada9573be3dd9b8e13</citedby><cites>FETCH-LOGICAL-c466t-4c0f0dfbe6ee77eba498ef56603ca8c8746fe223672a362ada9573be3dd9b8e13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26404902$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Yang</creatorcontrib><creatorcontrib>Wu, Nandie</creatorcontrib><creatorcontrib>Shen, Jie</creatorcontrib><creatorcontrib>Teixido, Cristina</creatorcontrib><creatorcontrib>Sun, Xia</creatorcontrib><creatorcontrib>Lin, Zihan</creatorcontrib><creatorcontrib>Qian, Xiaoping</creatorcontrib><creatorcontrib>Zou, Zhengyun</creatorcontrib><creatorcontrib>Guan, Wenxian</creatorcontrib><creatorcontrib>Yu, Lixia</creatorcontrib><creatorcontrib>Rosell, Rafael</creatorcontrib><creatorcontrib>Liu, Baorui</creatorcontrib><creatorcontrib>Wei, Jia</creatorcontrib><title>MET overexpression and amplification define a distinct molecular subgroup for targeted therapies in gastric cancer</title><title>Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association</title><addtitle>Gastric Cancer</addtitle><addtitle>Gastric Cancer</addtitle><description>Background
Currently, only trastuzumab, ramucirumab, and apatinib effectively treat gastric cancer. Thus, additional novel targets are required for this disease.
Methods
We investigated the immunohistochemical and fluorescence in situ hybridization expression of MET, ROS1, and ALK in four gastric cell lines and a cohort of 98 gastric cancer patients. Crizotinib response was studied in vitro and in vivo.
Results
Crizotinib potently inhibited in vitro cell growth in only one cell line, which also showed MET amplification. A positive correlation between crizotinib sensitivity and MET overexpression was observed (
P
= 0.045) in the histoculture drug response assay. Meanwhile, patient-derived tumor xenograft mouse models transplanted with tissues with higher MET protein expression displayed a highly selective sensitivity to crizotinib. In the 98 patients, MET overexpression was found in 42 (42.9 %) and MET was amplified in 4 (4.1 %). ROS1 and ALK overexpression were found in 25 (25.5 %) and 0 patients, respectively. However, none of the patients screened harbored ALK or ROS1 rearrangements. No significant association was found between overall survival and MET or ROS1 status. We also observed a stage IV gastric cancer patient with MET amplification who experienced tumor shrinkage and clinical benefit after 3 weeks of crizotinib as fourth-line treatment.
Conclusions
Crizotinib may induce clinically relevant anticancer effects in MET-overexpressed or MET-amplified gastric cancer patients.</description><subject>Abdominal Surgery</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Blotting, Western</subject><subject>Cancer Research</subject><subject>Cell Proliferation</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Female</subject><subject>Fluorescent Antibody Technique</subject><subject>Follow-Up Studies</subject><subject>Gastric cancer</subject><subject>Gastroenterology</subject><subject>Humans</subject><subject>Immunoenzyme Techniques</subject><subject>In Situ Hybridization, Fluorescence</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Middle Aged</subject><subject>Neoplasm Grading</subject><subject>Neoplasm Invasiveness</subject><subject>Neoplasm Metastasis</subject><subject>Neoplasm Staging</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Prognosis</subject><subject>Protein Kinase Inhibitors - therapeutic use</subject><subject>Proto-Oncogene Proteins c-met - metabolism</subject><subject>Pyrazoles - therapeutic use</subject><subject>Pyridines - therapeutic use</subject><subject>Stomach Neoplasms - drug therapy</subject><subject>Stomach Neoplasms - metabolism</subject><subject>Stomach Neoplasms - pathology</subject><subject>Surgical Oncology</subject><subject>Tumor Cells, Cultured</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1436-3291</issn><issn>1436-3305</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNp1kU9LHjEQxkOpqLV-gF5KoJdeVvM_7x5FrBaUXuw5ZJPJ28husk2yRb999-XVIgVPM8z85plhHoQ-UXJGCdHnlRLKSEeo7IgUspPv0DEVXHWcE_n-JWc9PUIfan0gK9hTdYiOmBJE9IQdo3J3dY_zHyjwOBeoNeaEbfLYTvMYQ3S27SoeQkyALfaxtphcw1MewS2jLbguw7bkZcYhF9xs2UIDj9svKHaOUHFMeGtrK9FhZ5OD8hEdBDtWOH2OJ-jnt6v7y5vu9sf198uL284JpVonHAnEhwEUgNYwWNFvIEilCHd24zZaqACMcaWZ5YpZb3up-QDc-37YAOUn6Otedy759wK1mSlWB-NoE-SlGqp7zaQmUq3ol__Qh7yUtF63oxRlQhGxUnRPuZJrLRDMXOJky5OhxOwMMXtDzPpnszPEyHXm87PyMkzg_028OLACbA_UtZW2UF6tflP1L_SXl44</recordid><startdate>20160701</startdate><enddate>20160701</enddate><creator>Yang, Yang</creator><creator>Wu, Nandie</creator><creator>Shen, Jie</creator><creator>Teixido, Cristina</creator><creator>Sun, Xia</creator><creator>Lin, Zihan</creator><creator>Qian, Xiaoping</creator><creator>Zou, Zhengyun</creator><creator>Guan, Wenxian</creator><creator>Yu, Lixia</creator><creator>Rosell, Rafael</creator><creator>Liu, Baorui</creator><creator>Wei, Jia</creator><general>Springer Japan</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20160701</creationdate><title>MET overexpression and amplification define a distinct molecular subgroup for targeted therapies in gastric cancer</title><author>Yang, Yang ; Wu, Nandie ; Shen, Jie ; Teixido, Cristina ; Sun, Xia ; Lin, Zihan ; Qian, Xiaoping ; Zou, Zhengyun ; Guan, Wenxian ; Yu, Lixia ; Rosell, Rafael ; Liu, Baorui ; Wei, Jia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c466t-4c0f0dfbe6ee77eba498ef56603ca8c8746fe223672a362ada9573be3dd9b8e13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Abdominal Surgery</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Blotting, Western</topic><topic>Cancer Research</topic><topic>Cell Proliferation</topic><topic>Drug Resistance, Neoplasm - genetics</topic><topic>Female</topic><topic>Fluorescent Antibody Technique</topic><topic>Follow-Up Studies</topic><topic>Gastric cancer</topic><topic>Gastroenterology</topic><topic>Humans</topic><topic>Immunoenzyme Techniques</topic><topic>In Situ Hybridization, Fluorescence</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Middle Aged</topic><topic>Neoplasm Grading</topic><topic>Neoplasm Invasiveness</topic><topic>Neoplasm Metastasis</topic><topic>Neoplasm Staging</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Prognosis</topic><topic>Protein Kinase Inhibitors - therapeutic use</topic><topic>Proto-Oncogene Proteins c-met - metabolism</topic><topic>Pyrazoles - therapeutic use</topic><topic>Pyridines - therapeutic use</topic><topic>Stomach Neoplasms - drug therapy</topic><topic>Stomach Neoplasms - metabolism</topic><topic>Stomach Neoplasms - pathology</topic><topic>Surgical Oncology</topic><topic>Tumor Cells, Cultured</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Yang</creatorcontrib><creatorcontrib>Wu, Nandie</creatorcontrib><creatorcontrib>Shen, Jie</creatorcontrib><creatorcontrib>Teixido, Cristina</creatorcontrib><creatorcontrib>Sun, Xia</creatorcontrib><creatorcontrib>Lin, Zihan</creatorcontrib><creatorcontrib>Qian, Xiaoping</creatorcontrib><creatorcontrib>Zou, Zhengyun</creatorcontrib><creatorcontrib>Guan, Wenxian</creatorcontrib><creatorcontrib>Yu, Lixia</creatorcontrib><creatorcontrib>Rosell, Rafael</creatorcontrib><creatorcontrib>Liu, Baorui</creatorcontrib><creatorcontrib>Wei, Jia</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database (Proquest)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</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>MEDLINE - Academic</collection><jtitle>Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Yang</au><au>Wu, Nandie</au><au>Shen, Jie</au><au>Teixido, Cristina</au><au>Sun, Xia</au><au>Lin, Zihan</au><au>Qian, Xiaoping</au><au>Zou, Zhengyun</au><au>Guan, Wenxian</au><au>Yu, Lixia</au><au>Rosell, Rafael</au><au>Liu, Baorui</au><au>Wei, Jia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MET overexpression and amplification define a distinct molecular subgroup for targeted therapies in gastric cancer</atitle><jtitle>Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association</jtitle><stitle>Gastric Cancer</stitle><addtitle>Gastric Cancer</addtitle><date>2016-07-01</date><risdate>2016</risdate><volume>19</volume><issue>3</issue><spage>778</spage><epage>788</epage><pages>778-788</pages><issn>1436-3291</issn><eissn>1436-3305</eissn><abstract>Background
Currently, only trastuzumab, ramucirumab, and apatinib effectively treat gastric cancer. Thus, additional novel targets are required for this disease.
Methods
We investigated the immunohistochemical and fluorescence in situ hybridization expression of MET, ROS1, and ALK in four gastric cell lines and a cohort of 98 gastric cancer patients. Crizotinib response was studied in vitro and in vivo.
Results
Crizotinib potently inhibited in vitro cell growth in only one cell line, which also showed MET amplification. A positive correlation between crizotinib sensitivity and MET overexpression was observed (
P
= 0.045) in the histoculture drug response assay. Meanwhile, patient-derived tumor xenograft mouse models transplanted with tissues with higher MET protein expression displayed a highly selective sensitivity to crizotinib. In the 98 patients, MET overexpression was found in 42 (42.9 %) and MET was amplified in 4 (4.1 %). ROS1 and ALK overexpression were found in 25 (25.5 %) and 0 patients, respectively. However, none of the patients screened harbored ALK or ROS1 rearrangements. No significant association was found between overall survival and MET or ROS1 status. We also observed a stage IV gastric cancer patient with MET amplification who experienced tumor shrinkage and clinical benefit after 3 weeks of crizotinib as fourth-line treatment.
Conclusions
Crizotinib may induce clinically relevant anticancer effects in MET-overexpressed or MET-amplified gastric cancer patients.</abstract><cop>Tokyo</cop><pub>Springer Japan</pub><pmid>26404902</pmid><doi>10.1007/s10120-015-0545-5</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1436-3291 |
| ispartof | Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2016-07, Vol.19 (3), p.778-788 |
| issn | 1436-3291 1436-3305 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1797257056 |
| source | Springer Nature |
| subjects | Abdominal Surgery Adult Aged Aged, 80 and over Animals Apoptosis Biomarkers, Tumor - metabolism Blotting, Western Cancer Research Cell Proliferation Drug Resistance, Neoplasm - genetics Female Fluorescent Antibody Technique Follow-Up Studies Gastric cancer Gastroenterology Humans Immunoenzyme Techniques In Situ Hybridization, Fluorescence Male Medicine Medicine & Public Health Mice Mice, Inbred BALB C Mice, Nude Middle Aged Neoplasm Grading Neoplasm Invasiveness Neoplasm Metastasis Neoplasm Staging Oncology Original Article Prognosis Protein Kinase Inhibitors - therapeutic use Proto-Oncogene Proteins c-met - metabolism Pyrazoles - therapeutic use Pyridines - therapeutic use Stomach Neoplasms - drug therapy Stomach Neoplasms - metabolism Stomach Neoplasms - pathology Surgical Oncology Tumor Cells, Cultured Xenograft Model Antitumor Assays |
| title | MET overexpression and amplification define a distinct molecular subgroup for targeted therapies in gastric cancer |
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