After the sixth line of therapy, a woman with metastatic triple-negative breast cancer (TNBC) experienced disease progression, but when the identification of an EGFR gene amplification via comparative genomic hybridization led to the decision to treat her with EGFR inhibitor cetuximab, she responded. Her response was quick and dramatic, but short-lived. Her disease progressed 8 months after cetuximab initiation and she died several months later.1
The details of this patient’s treatment were described in a case report recently published in JCO Precision Oncology, and while the experience represents but a single person, the exceptional response resurfaces the question: Is EGFR amplification a potential biomarker for cetuximab, and perhaps other EGFR inhibitors, in TNBC? More specifically, is using comparative genomic hybridization to detect EGFR gene copy number the key to identifying TNBC patients who will respond to cetuximab?
TNBC represents 15% to 20% of breast cancers, and the EGFR amplification seen in the case report is believed to occur in approximately 8% of basal-like TNBC tumors, according to information drawn from The Cancer Genome Atlas database that was highlighted by the study authors.
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“Remember, for every 1 of these cases, unfortunately there’s going to be 9 other people who have not responded to cetuximab,” cautioned Vikram Gorantla, MD, medical oncologist, University of Pittsburgh School of Medicine (UPMC) Hillman Cancer Center, Pittsburgh, Pennsylvania, during an interview with Cancer Therapy Advisor. Dr Gorantla, who was not involved in the case report, said the real question is: how can we find out whether people will respond to treatment with cetuximab?
