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    Association details:
    Biomarker:PTEN mutation
    Cancer:Colorectal Cancer
    Drug:Erbitux (cetuximab) (EGFR inhibitor)
    Direction:Resistant
    Evidence:
    Evidence Level:
    Sensitive: C2 – Inclusion Criteria
    Source:
    clinicaltrialsregister.eu
    Title:

    PREDICTIVE MARKERS OF THE EFFICACY IN METASTATIC COLORECTAL TUMOR TREATED WITH CETUXIMAB - PHASE 2 STUDY

    Excerpt:
    ...Assessing in patients with metastatic colorectal cancer refractory to treatment with chemotherapy and Irinotecan 5FU the correlation between the response to treatment with Cetuximab in combination with chemotherapy based Irinotecan;search for mutations of K-RAS and odetermination of PTEN by immunohistochemistry;Gene amplification dell'EGFR determined by FISH;the intensity of expression dell'EGFR determined by immunohistochemistry test with DAKO and Zymed (monoclonal antibody clone 31G7)...
    Trial ID:
    2008-004904-29
    Evidence Level:
    Sensitive: C2 – Inclusion Criteria
    Source:
    clinicaltrials.gov
    Title:

    Safety and Efficacy Study of Combination Therapy With Cetuximab and FOLFOX4 in Patients With Colorectal Cancer

    Excerpt:
    ...Determine safety of combination, surgical resectability and R0 resections, clinical benefit, time to disease progression, time to onset of response, duration of response, time to treatment failure, overall survival time`determination of polymorphisms of the intron 1 of the EGFR gene, TS, XRCC1, XPD, serum levels of EGFR and ATP7A and ATP7B, nº of copies of EGFR gene, the levels of PTEN, EGFR, AKT y MAPK proteins, and mutations at EGFR, PI3KCA, K-RAS y B-RAF genes...
    Trial ID:
    NCT00202787
    Less C2 evidence
    Evidence Level:
    Resistant: C3 – Early Trials
    Source:
    Oncotarget
    Title:

    Mutations of KRAS/NRAS/BRAF predict cetuximab resistance in metastatic colorectal cancer patients

    Excerpt:
    In contrast, BRAF mutations (0% for responders vs. 26.1% for non-responders, p = 0.0044) and KRAS (0% for responders vs. 21.7% for non-responders, p = 0.0117) were observed exclusively in non-responders. Three of the 4 subjects with NRAS mutations were non-responders (p = 0.3053) while both PTEN mutations were detected in responders (p = 0.4993). Collective mutation frequencies of KRAS, NRAS, and BRAF combined were higher in non-responders (p = 0.0001).
    DOI:
    10.18632/oncotarget.8076