Cancer therapy: can the challenge be MET?
The deregulation of tyrosine kinase receptors (RTKs) is frequent in human tumors and is often associated with the acquisition of an aggressive phenotype. The Met oncogene, encoding the RTK for hepatocyte growth factor (HGF), controls genetic programs leading to cell growth, invasion and protection f...
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| Veröffentlicht in: | Trends in molecular medicine 2005-06, Vol.11 (6), p.284-292 |
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| creator | Corso, Simona Comoglio, Paolo M. Giordano, Silvia |
| description | The deregulation of tyrosine kinase receptors (RTKs) is frequent in human tumors and is often associated with the acquisition of an aggressive phenotype. The
Met oncogene, encoding the RTK for hepatocyte growth factor (HGF), controls genetic programs leading to cell growth, invasion and protection from apoptosis. The deregulated activation of Met is crucial not only for the acquisition of tumorigenic properties but also to achieve an invasive phenotype. The involvement of MET in human tumors has been definitively established and can be achieved through several mechanisms, including MET interaction with unrelated membrane receptors, such as integrins, plexins, CD44, FAS and other RTKs. Interfering with
Met activation is thus a new and challenging approach to hamper tumorigenic and metastatic processes. |
| doi_str_mv | 10.1016/j.molmed.2005.04.005 |
| format | Article |
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Met oncogene, encoding the RTK for hepatocyte growth factor (HGF), controls genetic programs leading to cell growth, invasion and protection from apoptosis. The deregulated activation of Met is crucial not only for the acquisition of tumorigenic properties but also to achieve an invasive phenotype. The involvement of MET in human tumors has been definitively established and can be achieved through several mechanisms, including MET interaction with unrelated membrane receptors, such as integrins, plexins, CD44, FAS and other RTKs. Interfering with
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Met oncogene, encoding the RTK for hepatocyte growth factor (HGF), controls genetic programs leading to cell growth, invasion and protection from apoptosis. The deregulated activation of Met is crucial not only for the acquisition of tumorigenic properties but also to achieve an invasive phenotype. The involvement of MET in human tumors has been definitively established and can be achieved through several mechanisms, including MET interaction with unrelated membrane receptors, such as integrins, plexins, CD44, FAS and other RTKs. Interfering with
Met activation is thus a new and challenging approach to hamper tumorigenic and metastatic processes.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Cell Adhesion</subject><subject>Cell Adhesion Molecules - metabolism</subject><subject>Hepatocyte Growth Factor - metabolism</subject><subject>Humans</subject><subject>Hyaluronan Receptors - biosynthesis</subject><subject>Hyaluronan Receptors - metabolism</subject><subject>Models, Biological</subject><subject>Neoplasm Invasiveness</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - therapy</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Phenotype</subject><subject>Proto-Oncogene Proteins c-met - physiology</subject><subject>Signal Transduction</subject><issn>1471-4914</issn><issn>1471-499X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkN9LwzAQx4Mobk7_A5E-CT60Xpq0SX1QZMwfMPFlgm8hTa-uo11n0gn7703p2KM-fe_I5-7Ch5BLChEFmt6uoqatGyyiGCCJgEc-jsiYckFDnmWfx4ea8hE5c24FQBMh5CkZ0STjmRAwJjdTvTZog26JVm92d4HR674JzFLXNa6_MMgxeJstHs7JSalrhxf7nJCPp9li-hLO359fp4_z0PAYujCOJde0oNLoAktWUCalYBzyPNEMEqbLkvp_SYBYFGkiIJWmzOJSM5pDLjWbkOth78a231t0nWoqZ7Cu9RrbrVOpyOKUMvgXpCLlLJXSg3wAjW2ds1iqja0abXeKgupdqpUaXKrepQKufPixq_3-bd6_HYb28jxwPwDodfxUaJUzFXqdRWXRdKpoq78v_AIfzIP-</recordid><startdate>20050601</startdate><enddate>20050601</enddate><creator>Corso, Simona</creator><creator>Comoglio, Paolo M.</creator><creator>Giordano, Silvia</creator><general>Elsevier Ltd</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>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20050601</creationdate><title>Cancer therapy: can the challenge be MET?</title><author>Corso, Simona ; Comoglio, Paolo M. ; Giordano, Silvia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c420t-2284a1d18cadef3d13887340bb5a3053aff114780027d657068cf92fa31b0b8a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Cell Adhesion</topic><topic>Cell Adhesion Molecules - metabolism</topic><topic>Hepatocyte Growth Factor - metabolism</topic><topic>Humans</topic><topic>Hyaluronan Receptors - biosynthesis</topic><topic>Hyaluronan Receptors - metabolism</topic><topic>Models, Biological</topic><topic>Neoplasm Invasiveness</topic><topic>Neoplasms - metabolism</topic><topic>Neoplasms - therapy</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Phenotype</topic><topic>Proto-Oncogene Proteins c-met - physiology</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Corso, Simona</creatorcontrib><creatorcontrib>Comoglio, Paolo M.</creatorcontrib><creatorcontrib>Giordano, Silvia</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Trends in molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Corso, Simona</au><au>Comoglio, Paolo M.</au><au>Giordano, Silvia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cancer therapy: can the challenge be MET?</atitle><jtitle>Trends in molecular medicine</jtitle><addtitle>Trends Mol Med</addtitle><date>2005-06-01</date><risdate>2005</risdate><volume>11</volume><issue>6</issue><spage>284</spage><epage>292</epage><pages>284-292</pages><issn>1471-4914</issn><eissn>1471-499X</eissn><abstract>The deregulation of tyrosine kinase receptors (RTKs) is frequent in human tumors and is often associated with the acquisition of an aggressive phenotype. The
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| subjects | Animals Apoptosis Cell Adhesion Cell Adhesion Molecules - metabolism Hepatocyte Growth Factor - metabolism Humans Hyaluronan Receptors - biosynthesis Hyaluronan Receptors - metabolism Models, Biological Neoplasm Invasiveness Neoplasms - metabolism Neoplasms - therapy Nerve Tissue Proteins - metabolism Phenotype Proto-Oncogene Proteins c-met - physiology Signal Transduction |
| title | Cancer therapy: can the challenge be MET? |
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