When tyrosine kinase inhibitor sunitinib can be discontinued in metastatic renal cell carcinoma to pancreas: a case report

Yassir Sbitti, Adil Debbagh, Khaoula Slimani, Mohamed Mahi, Hassan Errihani, Mohamed Ichou

Long-term survival with durable response remains possible in the area of targeted therapies. Discontinuation of sunitinib could improve quality of life and reduce treatment costs in metastatic renal cell carcinoma with long-term disease stabilization. We discuss a case of successful interruption of antiangiogenic therapy in a patient with persisting evidence of metastases. The discontinuation of antiangiogenic therapy seems to be an option, even in indolent oligo-metastatic renal cell carcinoma with long disease stabilization before sunitinib. This observation contributes important data to the ongoing discussion on the discontinuation of treatment with kinase inhibitors in selected patients with metastatic renal cell carcinoma. We report a case of an 80-year-old Moroccan man treated for renal clear cell carcinoma with multiple pancreatic metastases. He was not on any other medications. He underwent active surveillance with deferred sunitinib at disease progression. He showed significant disease control on sunitinib therapy demonstrating partial response with stable disease after a total of 28 months of therapy. He experienced toxicities which were manageable with supportive care and dose adjustments. Our patient asked for a break of the sunitinib administration, and the treatment was stopped. The disease remained stable after 13 months' discontinuation of sunitinib therapy. The patient was in excellent overall health. All available agents for metastatic renal cell carcinoma have side effects, which may become serious in a minority of patients. Clinicians and patients must therefore carefully balance the goals of maximal efficacy with minimal toxicity. Sunitinib can be discontinued without negatively impacting outcomes in indolent disease. Further research is needed to characterize the molecular determinants of response and resistance to targeted therapy.