Abstract
Colorectal cancer (CRC) is one of the most common cancers worldwide. Despite the improvement in overall survival (OS) due to new treatments and targeted therapies alone or in combination with chemotherapy up-to–date, little is known about cellular mechanisms, both of primary and acquired resistance of CRC to anti-Epidermal Growth Factor Receptor (EGFR) antibodies. EGFR is characterized by tyrosine kinase activity and occupies a key-role in the control of cellular transduction pathways. Its activation triggers both the RAS-RAF and PIK3CA pathways and is required to promote cell growth, differentiation, proliferation, and invasion. Cetuximab and panitumumab are both monoclonal antibodies (MoAbs) directed against the extracellular domain of EGFR, thus leading to inhibition of the downstream signaling pathways. Mutations in oncogene Kirsten-RAS (KRAS) are frequently associated with resistance to anti-EGFR therapy. However, a significant number of KRAS wild-type (WT) tumors fail to obtain disease control with anti-EGFR agents. Therefore, additional biomarkers of response/resistance to these drugs such as BRAF, NRAS, PIK3CA and PTEN have been investigated. This review will point attention on Neuroblastoma-RAS (NRAS) status in metastatic CRC (mCRC) patients (pts) selected for anti-EGFR therapy.
Keywords: Colorectal cancer, epidermal growth factor receptor, mutations, KRAS, NRAS, anti-EGFR, monoclonal antibodies, cetuximab, panitumumab.
Reviews on Recent Clinical Trials
Title:The Emerging Role of NRAS Mutations in Colorectal Cancer Patients Selected for Anti-EGFR Therapies
Volume: 9 Issue: 1
Author(s): Fausto Meriggi, William Vermi, Paola Bertocchi and Alberto Zaniboni
Affiliation:
Keywords: Colorectal cancer, epidermal growth factor receptor, mutations, KRAS, NRAS, anti-EGFR, monoclonal antibodies, cetuximab, panitumumab.
Abstract: Colorectal cancer (CRC) is one of the most common cancers worldwide. Despite the improvement in overall survival (OS) due to new treatments and targeted therapies alone or in combination with chemotherapy up-to–date, little is known about cellular mechanisms, both of primary and acquired resistance of CRC to anti-Epidermal Growth Factor Receptor (EGFR) antibodies. EGFR is characterized by tyrosine kinase activity and occupies a key-role in the control of cellular transduction pathways. Its activation triggers both the RAS-RAF and PIK3CA pathways and is required to promote cell growth, differentiation, proliferation, and invasion. Cetuximab and panitumumab are both monoclonal antibodies (MoAbs) directed against the extracellular domain of EGFR, thus leading to inhibition of the downstream signaling pathways. Mutations in oncogene Kirsten-RAS (KRAS) are frequently associated with resistance to anti-EGFR therapy. However, a significant number of KRAS wild-type (WT) tumors fail to obtain disease control with anti-EGFR agents. Therefore, additional biomarkers of response/resistance to these drugs such as BRAF, NRAS, PIK3CA and PTEN have been investigated. This review will point attention on Neuroblastoma-RAS (NRAS) status in metastatic CRC (mCRC) patients (pts) selected for anti-EGFR therapy.
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Cite this article as:
Meriggi Fausto, Vermi William, Bertocchi Paola and Zaniboni Alberto, The Emerging Role of NRAS Mutations in Colorectal Cancer Patients Selected for Anti-EGFR Therapies, Reviews on Recent Clinical Trials 2014; 9 (1) . https://dx.doi.org/10.2174/1568026614666140423121525
DOI https://dx.doi.org/10.2174/1568026614666140423121525 |
Print ISSN 1574-8871 |
Publisher Name Bentham Science Publisher |
Online ISSN 1876-1038 |
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