<abstract xmlns="http://www.w3.org/1999/xhtml"><p>A major challenge in metastatic colorectal cancer (mCRC) is the identification of specific biomarkers that are likely to predict which patients will benefit from a specific treatment. To this date, a number of studies have shown that a tumour's mutational profile influences treatment outcome in patients with mCRC and should, therefore, be used to guide treatment decision. For more than 5 years now, we know that patients with tumours harbouring mutations in exon 2, codons 12 and 13 of the <italic>KRAS</italic> oncogene gain no benefit from the administration of anti-epidermal growth factor receptor (EGFR) monoclonal antibodies (moAbs), Cetuximab and Panitumumab. It has just recently being elucidated that <italic>KRAS</italic> mutations outside codons 12 and 13 and mutations in the <italic>NRAS</italic> gene confer resistance to Cetuximab and Panitumumab, as well. Thus, since June 2013, the analysis of exons 2, 3 and 4 of <italic>KRAS</italic> and <italic>NRAS</italic> has been incorporated in daily clinical practice to improve patients’ selection for anti-EGFR moAbs treatment. Nevertheless, even if patients’ outcome under anti-EGFR moAbs therapy is improved with better selection based on Ras mutational status, more research is needed in this field; the matter is far from being resolved, since there are still a minority of wt <italic>RAS</italic> patients who do not respond upfront to such a treatment.</p></abstract>

A major challenge in metastatic colorectal cancer (mCRC) is the identification of specific biomarkers that are likely to predict which patients will benefit from a specific treatment. To this date, a number of studies have shown that a tumour's mutational profile influences treatment outcome in patients with mCRC and should, therefore, be used to guide treatment decision. For more than 5 years now, we know that patients with tumours harbouring mutations in exon 2, codons 12 and 13 of the KRAS oncogene gain no benefit from the administration of anti-epidermal growth factor receptor (EGFR) monoclonal antibodies (moAbs), Cetuximab and Panitumumab. It has just recently being elucidated that KRAS mutations outside codons 12 and 13 and mutations in the NRAS gene confer resistance to Cetuximab and Panitumumab, as well. Thus, since June 2013, the analysis of exons 2, 3 and 4 of KRAS and NRAS has been incorporated in daily clinical practice to improve patients’ selection for anti-EGFR moAbs treatment. Nevertheless, even if patients’ outcome under anti-EGFR moAbs therapy is improved with better selection based on Ras mutational status, more research is needed in this field; the matter is far from being resolved, since there are still a minority of wt RAS patients who do not respond upfront to such a treatment.

Analysis of the role of RAS Family Mutations in Metastatic Colorectal Cancer (mCRC): Current Treatment Practice

Laboratory of Tumor Cell Biology, School of Medicine, University of Crete, 71110 Heraklion, Crete, Greece

Oncology Department “Asklepios”, 71303 Heraklion, Crete, Greece

Department of Medical Oncology, University General Hospital of Heraklion, 71110 Heraklion, Crete, Greece

Department of Medical Oncology, Centre René Gauducheau, Nantes

Forum of Clinical Oncology

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

A major challenge in metastatic colorectal cancer (mCRC) is the identification of specific biomarkers that are likely to predict which patients will benefit...

Analysis of the role of RAS Family Mutations in Metastatic Colorectal Cancer (mCRC): Current Treatment Practice

Publicado en línea: 10 dic 2014

Páginas: 12 - 15

DOI: https://doi.org/10.2478/fco-2014-0008

Palabras clave
RAS, Family mutations, Metastatic, Colorectal, Cancer

© 2014 Zenia Saridaki et. al.

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Analysis of the role of RAS Family Mutations in Metastatic Colorectal Cancer (mCRC): Current Treatment Practice

Publicado en línea: 10 dic 2014

Páginas: 12 - 15

DOI: https://doi.org/10.2478/fco-2014-0008

Palabras claveRAS, Family mutations, Metastatic, Colorectal, Cancer

© 2014 Zenia Saridaki et. al.

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Palabras clave
RAS, Family mutations, Metastatic, Colorectal, Cancer