Is Codon 13 KRAS Mutation Biologically Different from Codon 12 Mutation?
Abstract The introduction into clinical practice of KRAS mutational status for selection of patients has dramatically improved the results from use of anti-EGFR monoclonal antibodies cetuximab or panitumumab for metastatic colorectal cancer. More refined selection of patients by means of other molec...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Amatu, Alessio [verfasserIn] Sartore-Bianchi, Andrea [verfasserIn] Bencardino, Katia [verfasserIn] Cassingena, Andrea [verfasserIn] Venturini, Filippo [verfasserIn] Giacobbe, Felicia [verfasserIn] Pietrogiovanna, Lisa [verfasserIn] Marrapese, Giovanna [verfasserIn] Gambaro, Alessandra [verfasserIn] Belotti, Alessandro [verfasserIn] Siena, Salvatore [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2012 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Current colorectal cancer reports - Heidelberg [u.a.] : Springer, 2005, 8(2012), 4 vom: 06. Sept., Seite 272-276 |
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| Übergeordnetes Werk: |
volume:8 ; year:2012 ; number:4 ; day:06 ; month:09 ; pages:272-276 |
| Links: |
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| DOI / URN: |
10.1007/s11888-012-0140-7 |
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| Katalog-ID: |
SPR02288839X |
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| 520 | |a Abstract The introduction into clinical practice of KRAS mutational status for selection of patients has dramatically improved the results from use of anti-EGFR monoclonal antibodies cetuximab or panitumumab for metastatic colorectal cancer. More refined selection of patients by means of other molecular alterations, for example BRAF, PIK3CA, and NRAS has enabled further increases in responses to first-line and other therapy for metastatic disease. Elucidation of differences among specific subtypes of KRAS mutations affecting sensitivity, and identification of other mechanisms by which tumor cell resistance is acquired, revealing “druggable” molecular targets to overcome resistance, are clearly a priority of clinical research. Recent data have revealed potentially different activity of the G13D KRAS mutation in conferring resistance to cetuximab. This review examines the most recent evidence available on codon 13 mutation in metastatic colorectal cancer, including both preclinical and available clinical data, indicating differences between codon 13 and other KRAS mutations and analyzing its prognostic and predictive use in EGFR-targeted therapy. | ||
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| 650 | 4 | |a Panitumumab |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Cetuximab |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Monoclonal antibodies |7 (dpeaa)DE-He213 | |
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| 700 | 1 | |a Bencardino, Katia |e verfasserin |4 aut | |
| 700 | 1 | |a Cassingena, Andrea |e verfasserin |4 aut | |
| 700 | 1 | |a Venturini, Filippo |e verfasserin |4 aut | |
| 700 | 1 | |a Giacobbe, Felicia |e verfasserin |4 aut | |
| 700 | 1 | |a Pietrogiovanna, Lisa |e verfasserin |4 aut | |
| 700 | 1 | |a Marrapese, Giovanna |e verfasserin |4 aut | |
| 700 | 1 | |a Gambaro, Alessandra |e verfasserin |4 aut | |
| 700 | 1 | |a Belotti, Alessandro |e verfasserin |4 aut | |
| 700 | 1 | |a Siena, Salvatore |e verfasserin |4 aut | |
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10.1007/s11888-012-0140-7 doi (DE-627)SPR02288839X (SPR)s11888-012-0140-7-e DE-627 ger DE-627 rakwb eng 610 ASE 44.87 bkl Amatu, Alessio verfasserin aut Is Codon 13 KRAS Mutation Biologically Different from Codon 12 Mutation? 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The introduction into clinical practice of KRAS mutational status for selection of patients has dramatically improved the results from use of anti-EGFR monoclonal antibodies cetuximab or panitumumab for metastatic colorectal cancer. More refined selection of patients by means of other molecular alterations, for example BRAF, PIK3CA, and NRAS has enabled further increases in responses to first-line and other therapy for metastatic disease. Elucidation of differences among specific subtypes of KRAS mutations affecting sensitivity, and identification of other mechanisms by which tumor cell resistance is acquired, revealing “druggable” molecular targets to overcome resistance, are clearly a priority of clinical research. Recent data have revealed potentially different activity of the G13D KRAS mutation in conferring resistance to cetuximab. This review examines the most recent evidence available on codon 13 mutation in metastatic colorectal cancer, including both preclinical and available clinical data, indicating differences between codon 13 and other KRAS mutations and analyzing its prognostic and predictive use in EGFR-targeted therapy. G13D (dpeaa)DE-He213 EGFR (dpeaa)DE-He213 Metastatic colorectal cancer (dpeaa)DE-He213 Panitumumab (dpeaa)DE-He213 Cetuximab (dpeaa)DE-He213 Monoclonal antibodies (dpeaa)DE-He213 Sartore-Bianchi, Andrea verfasserin aut Bencardino, Katia verfasserin aut Cassingena, Andrea verfasserin aut Venturini, Filippo verfasserin aut Giacobbe, Felicia verfasserin aut Pietrogiovanna, Lisa verfasserin aut Marrapese, Giovanna verfasserin aut Gambaro, Alessandra verfasserin aut Belotti, Alessandro verfasserin aut Siena, Salvatore verfasserin aut Enthalten in Current colorectal cancer reports Heidelberg [u.a.] : Springer, 2005 8(2012), 4 vom: 06. Sept., Seite 272-276 (DE-627)511638213 (DE-600)2233562-6 1556-3804 nnns volume:8 year:2012 number:4 day:06 month:09 pages:272-276 https://dx.doi.org/10.1007/s11888-012-0140-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.87 ASE AR 8 2012 4 06 09 272-276 |
| spelling |
10.1007/s11888-012-0140-7 doi (DE-627)SPR02288839X (SPR)s11888-012-0140-7-e DE-627 ger DE-627 rakwb eng 610 ASE 44.87 bkl Amatu, Alessio verfasserin aut Is Codon 13 KRAS Mutation Biologically Different from Codon 12 Mutation? 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The introduction into clinical practice of KRAS mutational status for selection of patients has dramatically improved the results from use of anti-EGFR monoclonal antibodies cetuximab or panitumumab for metastatic colorectal cancer. More refined selection of patients by means of other molecular alterations, for example BRAF, PIK3CA, and NRAS has enabled further increases in responses to first-line and other therapy for metastatic disease. Elucidation of differences among specific subtypes of KRAS mutations affecting sensitivity, and identification of other mechanisms by which tumor cell resistance is acquired, revealing “druggable” molecular targets to overcome resistance, are clearly a priority of clinical research. Recent data have revealed potentially different activity of the G13D KRAS mutation in conferring resistance to cetuximab. This review examines the most recent evidence available on codon 13 mutation in metastatic colorectal cancer, including both preclinical and available clinical data, indicating differences between codon 13 and other KRAS mutations and analyzing its prognostic and predictive use in EGFR-targeted therapy. G13D (dpeaa)DE-He213 EGFR (dpeaa)DE-He213 Metastatic colorectal cancer (dpeaa)DE-He213 Panitumumab (dpeaa)DE-He213 Cetuximab (dpeaa)DE-He213 Monoclonal antibodies (dpeaa)DE-He213 Sartore-Bianchi, Andrea verfasserin aut Bencardino, Katia verfasserin aut Cassingena, Andrea verfasserin aut Venturini, Filippo verfasserin aut Giacobbe, Felicia verfasserin aut Pietrogiovanna, Lisa verfasserin aut Marrapese, Giovanna verfasserin aut Gambaro, Alessandra verfasserin aut Belotti, Alessandro verfasserin aut Siena, Salvatore verfasserin aut Enthalten in Current colorectal cancer reports Heidelberg [u.a.] : Springer, 2005 8(2012), 4 vom: 06. Sept., Seite 272-276 (DE-627)511638213 (DE-600)2233562-6 1556-3804 nnns volume:8 year:2012 number:4 day:06 month:09 pages:272-276 https://dx.doi.org/10.1007/s11888-012-0140-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.87 ASE AR 8 2012 4 06 09 272-276 |
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10.1007/s11888-012-0140-7 doi (DE-627)SPR02288839X (SPR)s11888-012-0140-7-e DE-627 ger DE-627 rakwb eng 610 ASE 44.87 bkl Amatu, Alessio verfasserin aut Is Codon 13 KRAS Mutation Biologically Different from Codon 12 Mutation? 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The introduction into clinical practice of KRAS mutational status for selection of patients has dramatically improved the results from use of anti-EGFR monoclonal antibodies cetuximab or panitumumab for metastatic colorectal cancer. More refined selection of patients by means of other molecular alterations, for example BRAF, PIK3CA, and NRAS has enabled further increases in responses to first-line and other therapy for metastatic disease. Elucidation of differences among specific subtypes of KRAS mutations affecting sensitivity, and identification of other mechanisms by which tumor cell resistance is acquired, revealing “druggable” molecular targets to overcome resistance, are clearly a priority of clinical research. Recent data have revealed potentially different activity of the G13D KRAS mutation in conferring resistance to cetuximab. This review examines the most recent evidence available on codon 13 mutation in metastatic colorectal cancer, including both preclinical and available clinical data, indicating differences between codon 13 and other KRAS mutations and analyzing its prognostic and predictive use in EGFR-targeted therapy. G13D (dpeaa)DE-He213 EGFR (dpeaa)DE-He213 Metastatic colorectal cancer (dpeaa)DE-He213 Panitumumab (dpeaa)DE-He213 Cetuximab (dpeaa)DE-He213 Monoclonal antibodies (dpeaa)DE-He213 Sartore-Bianchi, Andrea verfasserin aut Bencardino, Katia verfasserin aut Cassingena, Andrea verfasserin aut Venturini, Filippo verfasserin aut Giacobbe, Felicia verfasserin aut Pietrogiovanna, Lisa verfasserin aut Marrapese, Giovanna verfasserin aut Gambaro, Alessandra verfasserin aut Belotti, Alessandro verfasserin aut Siena, Salvatore verfasserin aut Enthalten in Current colorectal cancer reports Heidelberg [u.a.] : Springer, 2005 8(2012), 4 vom: 06. Sept., Seite 272-276 (DE-627)511638213 (DE-600)2233562-6 1556-3804 nnns volume:8 year:2012 number:4 day:06 month:09 pages:272-276 https://dx.doi.org/10.1007/s11888-012-0140-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.87 ASE AR 8 2012 4 06 09 272-276 |
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Enthalten in Current colorectal cancer reports 8(2012), 4 vom: 06. Sept., Seite 272-276 volume:8 year:2012 number:4 day:06 month:09 pages:272-276 |
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Enthalten in Current colorectal cancer reports 8(2012), 4 vom: 06. Sept., Seite 272-276 volume:8 year:2012 number:4 day:06 month:09 pages:272-276 |
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G13D EGFR Metastatic colorectal cancer Panitumumab Cetuximab Monoclonal antibodies |
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Amatu, Alessio @@aut@@ Sartore-Bianchi, Andrea @@aut@@ Bencardino, Katia @@aut@@ Cassingena, Andrea @@aut@@ Venturini, Filippo @@aut@@ Giacobbe, Felicia @@aut@@ Pietrogiovanna, Lisa @@aut@@ Marrapese, Giovanna @@aut@@ Gambaro, Alessandra @@aut@@ Belotti, Alessandro @@aut@@ Siena, Salvatore @@aut@@ |
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Amatu, Alessio |
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Amatu, Alessio ddc 610 bkl 44.87 misc G13D misc EGFR misc Metastatic colorectal cancer misc Panitumumab misc Cetuximab misc Monoclonal antibodies Is Codon 13 KRAS Mutation Biologically Different from Codon 12 Mutation? |
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610 ASE 44.87 bkl Is Codon 13 KRAS Mutation Biologically Different from Codon 12 Mutation? G13D (dpeaa)DE-He213 EGFR (dpeaa)DE-He213 Metastatic colorectal cancer (dpeaa)DE-He213 Panitumumab (dpeaa)DE-He213 Cetuximab (dpeaa)DE-He213 Monoclonal antibodies (dpeaa)DE-He213 |
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Amatu, Alessio Sartore-Bianchi, Andrea Bencardino, Katia Cassingena, Andrea Venturini, Filippo Giacobbe, Felicia Pietrogiovanna, Lisa Marrapese, Giovanna Gambaro, Alessandra Belotti, Alessandro Siena, Salvatore |
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is codon 13 kras mutation biologically different from codon 12 mutation? |
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Is Codon 13 KRAS Mutation Biologically Different from Codon 12 Mutation? |
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Abstract The introduction into clinical practice of KRAS mutational status for selection of patients has dramatically improved the results from use of anti-EGFR monoclonal antibodies cetuximab or panitumumab for metastatic colorectal cancer. More refined selection of patients by means of other molecular alterations, for example BRAF, PIK3CA, and NRAS has enabled further increases in responses to first-line and other therapy for metastatic disease. Elucidation of differences among specific subtypes of KRAS mutations affecting sensitivity, and identification of other mechanisms by which tumor cell resistance is acquired, revealing “druggable” molecular targets to overcome resistance, are clearly a priority of clinical research. Recent data have revealed potentially different activity of the G13D KRAS mutation in conferring resistance to cetuximab. This review examines the most recent evidence available on codon 13 mutation in metastatic colorectal cancer, including both preclinical and available clinical data, indicating differences between codon 13 and other KRAS mutations and analyzing its prognostic and predictive use in EGFR-targeted therapy. |
| abstractGer |
Abstract The introduction into clinical practice of KRAS mutational status for selection of patients has dramatically improved the results from use of anti-EGFR monoclonal antibodies cetuximab or panitumumab for metastatic colorectal cancer. More refined selection of patients by means of other molecular alterations, for example BRAF, PIK3CA, and NRAS has enabled further increases in responses to first-line and other therapy for metastatic disease. Elucidation of differences among specific subtypes of KRAS mutations affecting sensitivity, and identification of other mechanisms by which tumor cell resistance is acquired, revealing “druggable” molecular targets to overcome resistance, are clearly a priority of clinical research. Recent data have revealed potentially different activity of the G13D KRAS mutation in conferring resistance to cetuximab. This review examines the most recent evidence available on codon 13 mutation in metastatic colorectal cancer, including both preclinical and available clinical data, indicating differences between codon 13 and other KRAS mutations and analyzing its prognostic and predictive use in EGFR-targeted therapy. |
| abstract_unstemmed |
Abstract The introduction into clinical practice of KRAS mutational status for selection of patients has dramatically improved the results from use of anti-EGFR monoclonal antibodies cetuximab or panitumumab for metastatic colorectal cancer. More refined selection of patients by means of other molecular alterations, for example BRAF, PIK3CA, and NRAS has enabled further increases in responses to first-line and other therapy for metastatic disease. Elucidation of differences among specific subtypes of KRAS mutations affecting sensitivity, and identification of other mechanisms by which tumor cell resistance is acquired, revealing “druggable” molecular targets to overcome resistance, are clearly a priority of clinical research. Recent data have revealed potentially different activity of the G13D KRAS mutation in conferring resistance to cetuximab. This review examines the most recent evidence available on codon 13 mutation in metastatic colorectal cancer, including both preclinical and available clinical data, indicating differences between codon 13 and other KRAS mutations and analyzing its prognostic and predictive use in EGFR-targeted therapy. |
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| score |
7.3998213 |