ASCO 2026 | Panitumumab-based EGFR blockade in SMARCB1-deficient RMC
Pavlos Msaouel, MD, PhD, The University of Texas MD Anderson Cancer Center, Houston, TX, describes preclinical and prospective clinical findings evaluating panitumumab-based therapy in SMARCB1-deficient renal medullary carcinoma (RMC). Results demonstrated substantial antitumor activity, with a notably high overall response rate in heavily pretreated patients, alongside a manageable safety profile, establishing wild-type EGFR dependency as a foundational vulnerability and supporting panitumumab-based therapy as a new systemic standard of care in RMC. This interview took place during the 2026 American Society of Clinical Oncology (ASCO) Meeting in Chicago, IL.
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Transcript
One of the things that we looked into is exactly what is happening with EGFR. And the first thing that we noticed is that it appears that EGFR is uniformly very highly expressed across patients with RMC. So the vast majority of patients by immunohistochemistry would have in essentially 100% of the tumor cells 3 plus expression of EGFR. Rarely we would see some 2 plus expression...
One of the things that we looked into is exactly what is happening with EGFR. And the first thing that we noticed is that it appears that EGFR is uniformly very highly expressed across patients with RMC. So the vast majority of patients by immunohistochemistry would have in essentially 100% of the tumor cells 3 plus expression of EGFR. Rarely we would see some 2 plus expression. So highly expressed wild-type EGFR more so than many other cancers. Homogeneously expressed. Now as I mentioned RMC is defined by the loss of the SMARCB1 tumor suppressor. So we also looked to see if other cancers that also are defined by the loss of SMARCB1 express such high levels of EGFR and the answer is really no. It is RMC specific to have such high levels of EGFR and we believe that that has to do with the lineage of RMC, the putative cell of origin of RMC. We’re looking further into these biological questions. In the meantime, to your point, we’re interested to know why some patients do not respond either de novo or why some patients acquire resistance to the EGFR targeting so that we can develop the next generations of therapies. This is an ongoing process and an ongoing research and I’m looking forward in the coming years to hopefully discuss more about that.
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