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Additionally, 10% of patients will have an uncommon EGFR mutation, and response to EGFR TKI therapy is highly variable depending on the mutation.
No correlation was found between the presence of tumour D-Loop mutation and response to neoadjuvant chemotherapy (Table 1).
In non-small cell lung cancer, the relationship between KRAS mutation and response to EGFR inhibitors is less clear.
No previous studies have investigated the association between CHEK2 germline mutation and response to neoadjuvant chemotherapy in breast cancer.
Farnesyltransferase inhibitors were designed for RAS inhibition, but both preclinical and clinical studies have been disappointing, with no correlation between RAS mutation and response.
Multivariate analysis revealed that only EGFR expression and increased copy number were associated with erlotinib response and no correlation between base-pair mutation and response was found [ 15].
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Thus, despite the limited size of our patient cohort, these results support the notion that the dramatic differences in sensitivity strongly skew the association between the presence of EGFR mutations and response to erlotinib.
The 10 most studied cancer cell gene variants were TP53 and cisplatin/5-fluorouracil/paclitaxel response, ERBB2 (HER2/neu) and anthracyclines/trastuzumab response, EGFR and gefitinib response, and RAS, FLT3, ABCB1, BCL2 and t(9 22) and other karyotype and cytogenetic mutations and response to a variety of combination chemotherapy regimens.
A significant negative correlation between PIK3CA mutations and response to anti-EGFR moAbs has been documented in the Sartore-Bianchi's et al [21] and the Perone's et al [30] reports, whereas, Prenen et al [26] could not find a clear association between the presence of PIK3CA mutation status and an impaired efficacy of anti-EGFR moAbs.
No associations between HER2-status or detected mutations and response were observed.
A clear association was demonstrated between loss of PTEN/ PIK3CA mutations and response to different regimes of EGFR-tageted MoAbs.
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