Established and Emerging Biomarkers of Immunotherapy in Renal Cell Carcinoma

Abstract

Immunotherapies, such as immune checkpoint inhibitors, have heralded impressive progress for patient care in renal cell carcinoma (RCC). Despite this success, some patients’ disease fails to respond, and other patients experience significant side effects. Thus, development of biomarkers is needed to ensure that patients can be selected to maximize benefit from immunotherapies. Improving clinicians’ ability to predict which patients will respond to immunotherapy and which are most at risk of adverse events – namely through clinical biomarkers – is indispensable for patient safety and therapeutic efficacy. Accordingly, an evolving suite of therapeutic biomarkers continues to be investigated. This review discusses biomarkers for immunotherapy in RCC, highlighting current practices and emerging innovations, aiming to contribute to improved outcomes for patients with RCC.

Plain language summary

Renal cell carcinoma (RCC) is a type of kidney cancer. Treatments that target the body’s immune system, called immunotherapies, are generally effective in RCC, but not all patients’ cancer will respond (shrink or disappear) after receiving this treatment. Because of this, signals, called biomarkers, are needed to signal which patients’ cancer will respond and which patients may experience unwanted side effects after treatment. This article highlights biomarkers that have been or are being studied for understanding immunotherapy in RCC.

Graphical abstract

Keywords::

• cancer immunology
• checkpoint inhibitors
• clinical immunology
• immunological markers
• immunotherapy

Author contributions

Y Jani and CS Jansen drafted and revised the manuscript. MA Bilen provided critical input and oversight. MB Gerke revised the manuscript. All authors edited, reviewed and approved the final manuscript.

Financial disclosure

The authors have no financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties. C.S.J. is supported by National Cancer Institute Grant (F30CA243250) and by the Medical Scientist Training Program Grant (T32 GM008169).

Competing interests disclosure

Author MA Bilen has acted as a paid consultant for and/or as a member of the advisory boards of Exelixis, Bayer, BMS, Eisai, Pfizer, AstraZeneca, Janssen, Calithera Biosciences, Genomic Health, Nektar, EMD Serono, SeaGen, and Sanofi, and his institution has received grants from Merck, Xencor, Bayer, Bristol-Myers Squibb, Genentech/Roche, SeaGen, Incyte, Nektar, AstraZeneca, Tricon Pharmaceuticals, Genome & Company, AAA, Peloton Therapeutics, and Pfizer for work performed outside of the current study. BN serves on the scientific advisory board for Exelixis. BCC reported consulting/advisory relationships with Astellas Medivation, Pfizer, and Blue Earth Diagnostics, and travel expenses from Bristol-Myers Squibb. All other authors declare no conflicts of interest.

Writing disclosure

No writing assistance was utilized in the production of this manuscript.