Wild-Type BRAF Is Required for Response to Panitumumab or Cetuximab in Metastatic Colorectal Cancer
PURPOSE Cetuximab or panitumumab are effective in 10% to 20% unselected metastatic colorectal cancer (CRC) patients. KRAS mutations account for approximately 30% to 40% patients who are not responsive. The serine-threonine kinase BRAF is the principal effector of KRAS. We hypothesized that, in KRAS...
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Published in | Journal of clinical oncology Vol. 26; no. 35; pp. 5705 - 5712 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Alexandria, VA
American Society of Clinical Oncology
10.12.2008
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Subjects | |
Online Access | Get full text |
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Abstract | PURPOSE Cetuximab or panitumumab are effective in 10% to 20% unselected metastatic colorectal cancer (CRC) patients. KRAS mutations account for approximately 30% to 40% patients who are not responsive. The serine-threonine kinase BRAF is the principal effector of KRAS. We hypothesized that, in KRAS wild-type patients, BRAF mutations could have a predictive/prognostic value. PATIENTS AND METHODS We retrospectively analyzed objective tumor responses, time to progression, overall survival (OS), and the mutational status of KRAS and BRAF in 113 tumors from cetuximab- or panitumumab-treated metastatic CRC patients. The effect of the BRAF V600E mutation on cetuximab or panitumumab response was also assessed using cellular models of CRC. Results KRAS mutations were present in 30% of the patients and were associated with resistance to cetuximab or panitumumab (P = .011). The BRAF V600E mutation was detected in 11 of 79 patients who had wild-type KRAS. None of the BRAF-mutated patients responded to treatment, whereas none of the responders carried BRAF mutations (P = .029). BRAF-mutated patients had significantly shorter progression-free survival (P = .011) and OS (P < .0001) than wild-type patients. In CRC cells, the introduction of BRAF V600E allele impaired the therapeutic effect of cetuximab or panitumumab. Treatment with the BRAF inhibitor sorafenib restored sensitivity to panitumumab or cetuximab of CRC cells carrying the V600E allele. CONCLUSION BRAF wild-type is required for response to panitumumab or cetuximab and could be used to select patients who are eligible for the treatment. Double-hit therapies aimed at simultaneous inhibition of epidermal growth factor receptor and BRAF warrant exploration in CRC patients carrying the V600E oncogenic mutation. |
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AbstractList | PURPOSE Cetuximab or panitumumab are effective in 10% to 20% unselected metastatic colorectal cancer (CRC) patients. KRAS mutations account for approximately 30% to 40% patients who are not responsive. The serine-threonine kinase BRAF is the principal effector of KRAS. We hypothesized that, in KRAS wild-type patients, BRAF mutations could have a predictive/prognostic value. PATIENTS AND METHODS We retrospectively analyzed objective tumor responses, time to progression, overall survival (OS), and the mutational status of KRAS and BRAF in 113 tumors from cetuximab- or panitumumab-treated metastatic CRC patients. The effect of the BRAF V600E mutation on cetuximab or panitumumab response was also assessed using cellular models of CRC. Results KRAS mutations were present in 30% of the patients and were associated with resistance to cetuximab or panitumumab (P = .011). The BRAF V600E mutation was detected in 11 of 79 patients who had wild-type KRAS. None of the BRAF-mutated patients responded to treatment, whereas none of the responders carried BRAF mutations (P = .029). BRAF-mutated patients had significantly shorter progression-free survival (P = .011) and OS (P < .0001) than wild-type patients. In CRC cells, the introduction of BRAF V600E allele impaired the therapeutic effect of cetuximab or panitumumab. Treatment with the BRAF inhibitor sorafenib restored sensitivity to panitumumab or cetuximab of CRC cells carrying the V600E allele. CONCLUSION BRAF wild-type is required for response to panitumumab or cetuximab and could be used to select patients who are eligible for the treatment. Double-hit therapies aimed at simultaneous inhibition of epidermal growth factor receptor and BRAF warrant exploration in CRC patients carrying the V600E oncogenic mutation. PURPOSE Cetuximab or panitumumab are effective in 10% to 20% unselected metastatic colorectal cancer (CRC) patients. KRAS mutations account for approximately 30% to 40% patients who are not responsive. The serine-threonine kinase BRAF is the principal effector of KRAS. We hypothesized that, in KRAS wild-type patients, BRAF mutations could have a predictive/prognostic value. PATIENTS AND METHODS We retrospectively analyzed objective tumor responses, time to progression, overall survival (OS), and the mutational status of KRAS and BRAF in 113 tumors from cetuximab- or panitumumab-treated metastatic CRC patients. The effect of the BRAF V600E mutation on cetuximab or panitumumab response was also assessed using cellular models of CRC. Results KRAS mutations were present in 30% of the patients and were associated with resistance to cetuximab or panitumumab (P = .011). The BRAF V600E mutation was detected in 11 of 79 patients who had wild-type KRAS. None of the BRAF-mutated patients responded to treatment, whereas none of the responders carried BRAF mutations (P = .029). BRAF-mutated patients had significantly shorter progression-free survival (P = .011) and OS (P < .0001) than wild-type patients. In CRC cells, the introduction of BRAF V600E allele impaired the therapeutic effect of cetuximab or panitumumab. Treatment with the BRAF inhibitor sorafenib restored sensitivity to panitumumab or cetuximab of CRC cells carrying the V600E allele. CONCLUSION BRAF wild-type is required for response to panitumumab or cetuximab and could be used to select patients who are eligible for the treatment. Double-hit therapies aimed at simultaneous inhibition of epidermal growth factor receptor and BRAF warrant exploration in CRC patients carrying the V600E oncogenic mutation. Purpose Cetuximab or panitumumab are effective in 10% to 20% unselected metastatic colorectal cancer (CRC) patients. KRAS mutations account for approximately 30% to 40% patients who are not responsive. The serine-threonine kinase BRAF is the principal effector of KRAS. We hypothesized that, in KRAS wild-type patients, BRAF mutations could have a predictive/prognostic value. Patients and Methods We retrospectively analyzed objective tumor responses, time to progression, overall survival (OS), and the mutational status of KRAS and BRAF in 113 tumors from cetuximab- or panitumumab-treated metastatic CRC patients. The effect of the BRAF V600E mutation on cetuximab or panitumumab response was also assessed using cellular models of CRC. Results KRAS mutations were present in 30% of the patients and were associated with resistance to cetuximab or panitumumab (P = .011). The BRAF V600E mutation was detected in 11 of 79 patients who had wild-type KRAS. None of the BRAF-mutated patients responded to treatment, whereas none of the responders carried BRAF mutations (P = .029). BRAF-mutated patients had significantly shorter progression-free survival (P = .011) and OS (P < .0001) than wild-type patients. In CRC cells, the introduction of BRAF V600E allele impaired the therapeutic effect of cetuximab or panitumumab. Treatment with the BRAF inhibitor sorafenib restored sensitivity to panitumumab or cetuximab of CRC cells carrying the V600E allele. Conclusion BRAF wild-type is required for response to panitumumab or cetuximab and could be used to select patients who are eligible for the treatment. Double-hit therapies aimed at simultaneous inhibition of epidermal growth factor receptor and BRAF warrant exploration in CRC patients carrying the V600E oncogenic mutation. |
Author | Francesca Molinari Salvatore Siena Federica Di Nicolantonio Miriam Martini Piercarlo Saletti Andrea Sartore-Bianchi Sabrina Arena Sara De Dosso Milo Frattini Alberto Bardelli Luca Mazzucchelli |
Author_xml | – sequence: 1 givenname: Federica surname: Di Nicolantonio fullname: Di Nicolantonio, Federica organization: Laboratory of Molecular Genetics, The Oncogenomics Center, Institute for Cancer Research and Treatment, University of Torino, Medical School, Candiolo, Torino, Italy – sequence: 2 givenname: Miriam surname: Martini fullname: Martini, Miriam – sequence: 3 givenname: Francesca surname: Molinari fullname: Molinari, Francesca – sequence: 4 givenname: Andrea surname: Sartore-Bianchi fullname: Sartore-Bianchi, Andrea – sequence: 5 givenname: Sabrina surname: Arena fullname: Arena, Sabrina – sequence: 6 givenname: Piercarlo surname: Saletti fullname: Saletti, Piercarlo – sequence: 7 givenname: Sara surname: De Dosso fullname: De Dosso, Sara – sequence: 8 givenname: Luca surname: Mazzucchelli fullname: Mazzucchelli, Luca – sequence: 9 givenname: Milo surname: Frattini fullname: Frattini, Milo – sequence: 10 givenname: Salvatore surname: Siena fullname: Siena, Salvatore – sequence: 11 givenname: Alberto surname: Bardelli fullname: Bardelli, Alberto |
BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20966513$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/19001320$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.1200/JCO.2007.12.5906 10.1200/JCO.2007.14.7116 10.1200/JCO.2006.08.2644 10.1158/0008-5472.CAN-07-0589 10.1158/0008-5472.CAN-06-4158 10.1056/NEJMoa033025 10.1002/cncr.21123 10.1158/0008-5472.CAN-05-0404 10.1074/jbc.273.37.24052 10.1056/NEJMra040958 10.1038/sj.onc.1207980 10.1158/0008-5472.CAN-04-1443 10.1158/1078-0432.CCR-07-4790 10.1016/S1470-2045(05)70102-9 10.1158/1078-0432.CCR-04-0031 10.1200/JCO.2004.10.182 10.1093/annonc/mdn058 10.1038/sj.bjc.6604009 10.1245/ASO.2004.03.585 10.1200/JCO.2006.08.1620 10.1093/jnci/92.3.205 10.1093/emboj/19.20.5429 10.1158/1078-0432.CCR-1118-3 10.1038/418934a 10.1200/JCO.2007.11.5956 10.1093/annonc/mdm399 10.1200/JCO.2006.10.5437 10.1093/annonc/mdm516 10.1093/annonc/mdm496 10.1158/1078-0432.CCR-07-0366 10.1200/JCO.2005.08.037 10.1016/S0959-8049(01)00233-7 10.1158/0008-5472.CAN-06-0191 10.1038/sj.bjc.6603685 10.1093/annonc/mdm492 |
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Keywords | Antineoplastic agent Rectal disease Panitumumab Colorectal cancer Monoclonal antibody Malignant tumor Metastasis Wild type Epidermal growth factor receptor Colonic disease BRAF Gene Cancerology C-Onc gene Digestive diseases Intestinal disease Advanced stage Cetuximab Protooncogene Cancer |
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Snippet | PURPOSE Cetuximab or panitumumab are effective in 10% to 20% unselected metastatic colorectal cancer (CRC) patients. KRAS mutations account for approximately... Purpose Cetuximab or panitumumab are effective in 10% to 20% unselected metastatic colorectal cancer (CRC) patients. KRAS mutations account for approximately... |
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SubjectTerms | Adult Aged Aged, 80 and over Antibodies, Monoclonal - therapeutic use Antibodies, Monoclonal, Humanized Antineoplastic Agents - therapeutic use Benzenesulfonates - pharmacology Biological and medical sciences Biomarkers, Tumor - genetics Cell Survival - drug effects Cetuximab Colorectal Neoplasms - drug therapy Colorectal Neoplasms - enzymology Colorectal Neoplasms - genetics Colorectal Neoplasms - pathology Disease-Free Survival Dose-Response Relationship, Drug Drug Resistance, Neoplasm - genetics Female Gastroenterology. Liver. Pancreas. Abdomen Gene Expression Profiling Gene Expression Regulation, Neoplastic HT29 Cells Humans Italy Male Medical sciences Middle Aged Mutation Neoplasm Metastasis Niacinamide - analogs & derivatives Patient Selection Phenylurea Compounds Protein Kinase Inhibitors - pharmacology Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins B-raf - antagonists & inhibitors Proto-Oncogene Proteins B-raf - genetics Proto-Oncogene Proteins p21(ras) Pyridines - pharmacology ras Proteins - genetics Receptor, Epidermal Growth Factor - antagonists & inhibitors Retrospective Studies Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Switzerland Time Factors Treatment Outcome Tumors |
Title | Wild-Type BRAF Is Required for Response to Panitumumab or Cetuximab in Metastatic Colorectal Cancer |
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