1. Molecular heterogeneity drives secondary resistance to anti-EGFR therapies in mCRC.
Molecular heterogeneity drives secondary resistance to anti-EGFR therapies in mCRC. Response to anti-EGFR targeted therapies in mCRC is accompanied by selection of preexisting resistant clones present in the initial metastasis burden. Conceivably, resistant clones can also emerge during treatment. Clones carrying distinct molecular alterations such as KRAS, NRAS, EGFR, and BRAF mutations or KRAS, HER2, or MET amplifications can coexist in the same metastatic site or in different metastatic sites. CT scans were obtained from a colorectal cancer patient who showed the first response to cetuximab observed at Ospedale Niguarda Ca' Granda in 2001.
Sandra Misale et al. Cancer Discovery 2014;4:
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