Commentary|Videos|June 4, 2026

Mitigating Skin Rash in RMC: De-Escalation of Panitumumab-Based Triplets

Proactive management of EGFR-mediated toxicities can help to prevent the escalation of grade 1/2 skin toxicities to higher grade events.

Renal medullary carcinoma (RMC) is an exceptionally aggressive, SMARCB1-deficient kidney cancer that predominantly affects young individuals and remains notoriously refractory to standard therapies. To address this critical unmet need, researchers explored wild-type EGFR mutational status as a therapeutic vulnerability in RMC.

In an interview with CancerNetwork® at the 2026 American Society of Clinical Oncology (ASCO) Annual Meeting, Pavlos Msaouel, MD, PhD, discussed the prospective toxicity and safety data from a collaborative, multi-institutional study evaluating panitumumab (Vectibix)-based EGFR blockade in patients with heavily pretreated RMC. First, Msaouel detailed the clinical evolution of the treatment regimen, explaining how a high rate of platinum-induced infusion reactions prompted investigators to drop carboplatin in favor of a safer, highly active doublet utilizing panitumumab and nab-paclitaxel.

Additionally, he shared insights into the management of EGFR-mediated toxicities, noting that proactive strategies successfully prevented transient grade 1/2 skin rashes from escalating into higher-grade adverse effects (AEs). Specifically, noting that managing these toxicities is the “bread and butter” of oncologists, he explained that prophylactic doxycycline among other strategies may serve to prevent or mitigate these events.

Msaouel is an assistant professor in the Department of Genitourinary Medical Oncology in the Division of Cancer Medicine at The University of Texas MD Anderson Cancer Center.

CancerNetwork: From a multidisciplinary perspective, what specific care coordination strategies should different specialists like medical oncologists, nephrologists, and nursing teams implement to proactively manage class-specific toxicities and maximize patient adherence in this setting?

Msaouel: This is an important question, and this is why it was so important to us that we gather toxicity data. The original version of the regimen that was developed for inflammatory breast cancer actually included 3 drugs together: panitumumab that targets EGFR; nab-paclitaxel…a second-generation type of taxane––we had noticed that heavily pretreated patients with RMC could respond to monotherapy with nab-paclitaxel, just not very impressively, but we knew that it is an active regimen, which again compelled us to combine it with panitumumab—and carboplatin. The breast cancer regimen used carboplatin as well.

We started bringing this to the clinic using the 3 drugs together; however, these patients were already heavily pretreated with platinum, including carboplatin. For this reason, for example, out of the 26 patients we are presenting at [the conference], 20 also received carboplatin, and 6 had infusion reactions. At the same time, our preclinical data suggested that you are not gaining much from carboplatin. For this reason, henceforth, once we did our data cutoff for the first 26 patients and realized this, we decided to instead bring to the [40+] subsequent patients…only the doublet of panitumumab and nab-paclitaxel.

Now, for panitumumab, what is the most common [adverse] effect in oncology practice? Skin rash, and that is exactly what we also observed with our study. About 80% of patients from those 26 had grade 1 or grade 2 skin rash. None of them progressed to grade 3, and part of the reason was because for oncologists, it is [their] bread and butter to know how to manage EGFR-targeting toxicity. Many of these patients were started on prophylactic doxycycline and other strategies to prevent or mitigate the skin rash.

Reference

Msaoeul P, Rupe ES, Chen X, et al. Prospective clinical activity and preclinical basis of panitumumab-based EGFR blockade in SMARCB1-deficient renal medullary carcinoma (RMC): a collaborative multi-institutional study. J Clin Oncol. 2026;44(suppl 16):4520. doi:10.1200/JCO.2026.44.16_suppl.4520


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