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The recent identification of HER2 gene amplification as a novel predictorof resistance to the EGFR (HER2)-targeted antibody cetuximab and of response tocombination therapies against EGFR and HER2 in wild-type KRAS tumor settings mayrepresent a further step toward personalized medicine for patients with colorectalcancer. Herein, we show that transcriptional upregulation of HER2 expression inthe absence of HER2 gene amplification is a molecular phenomenon that takes placein EGFR-dependent, wild-type KRAS squamous cell carcinoma (SCC) cells that acquireresistance to cetuximab. Since cetuximab activity against cetuximab-refractorySCC cells can be fully restored in the presence of the anti-HER2 monoclonal antibodytrastuzumab, our findings suggest that, beyond HER2 gene amplification, we mightneed to redefine the threshold values for HER2 positivity to improve the accuracyof the selection of cetuximab-refractory patients with wild-type KRAS that maybenefit from receiving a cetuximab/trastuzumab combination.

oncology reports

Transcriptional upregulation of HER2 expression in the absence of HER2 gene amplification results in cetuximab resistance that is reversed by trastuzumab treatment