Sentence examples for mutations are predictive from inspiring English sources

KRAS mutations are predictive markers for the efficacy of anti-EGFR antibody therapies in patients with metastatic colorectal cancer.

In contrast, whether BRAF and PIK3CA mutations are predictive of the efficacy of anti-EGFR therapy remains controversial [ 19- 22].

Activating EGFR mutations are predictive of response to EGFR inhibitors with reported response rates of upto 75%.

Moreover, KRAS mutations are predictive of the lack of efficacy of anti-EGFR antibody in treatment of metastatic CRC (Lievre et al, 2008).

This study suggests that TP53 mutations are predictive of cetuximab sensitivity, particularly in patients without KRAS mutation, and that TP53 genotyping could have a clinical interest to select patients who should benefit from cetuximab-based CT.

In contrast, this study, performed in 64 MCRC patients, suggests that TP53 mutations are predictive markers of cetuximab sensitivity, particularly in the subgroup of patients without detectable KRAS mutation.

However, when types of mutations were analysed separately for each gene, KRAS codon 12 mutations were predictive for increased risk of death (HR 1.62, p=0.014).

A large adjuvant trial of 595 patients showed that p53 mutations were predictive for a better effect of a higher dose of doxorubicin [ 15], but this was not confirmed in a preoperative trial of 329 patients [ 16].

Interestingly, AR alterations accompanied enzalutamide resistance, and the presence of pre-treatment AR amplifications or mutations were predictive for adverse outcomes on enzalutamide (Azad et al, 2015b; Gleave & Chi, 2015).

However, this report does not necessarily refute the role of EGFR mutations as a predictive factor because EGFR mutations only failed to significantly affect overall survival (P=0.09), whereas EGFR mutations were predictive of response rate and time to progression (Cappuzzo et al, 2005a).

The impact of RAS mutations in KRAS exon 3 and 4 and NRAS exons 2, 3 and 4 appears to be similar to that of KRAS exon 2 mutations, with all mutations being predictive of a lack of response to panitumumab therapy.