Findings previously demonstrated that nivolumab plus ipilimumab prolongs overall survival and was better tolerated among patients with renal cell carcinoma, but its impact on health-related quality of life was not reported.
Nicholas J. Vogelzang, MD, FASCO, FACP, discusses the findings at the ASCO 2018 meeting.
The incorporation and efficacy of targeted therapies to management has called into question the conventional standard of using cytoreductive nephrectomy prior to sunitinib.
Researchers assigned 38 patients with metastatic renal cell carcinoma to receive pegilodecakin plus nivolumab or pembrolizumab.
Women with type 2 diabetes have a 1.5-fold higher risk of renal cell carcinoma compared with non-diabetic women.
An example of where biomarkers may help to select the best medication for a patient and also assist in drug development is the tyrosine kinase inhibitor (TKI) dovitinib for renal cell carcinoma (RCC).
The phase 3 METEOR study previously demonstrated that cabozantinib significantly improved survival outcomes among patients with relapsed renal cell carcinoma.
Recent research indicates that there were no significant differences in the genomic landscape of clear cell RCC primary tumors and metastases, or between the different sites of metastases.
Immunotherapy may supplant sunitinib in RCC, except for in patients who cannot tolerate checkpoint inhibition.
Approval was based on results from the randomized phase 3 CheckMate-214 study.
The standard schedule is associated with AEs including grade 3 to 4 fatigue, HFS, and diarrhea.
Several phase 3 clinical trials are likely to identify new frontline standards of care.
Previous studies showed that combination therapy with nivolumab and ipilimumab has promising efficacy for various cancers, including RCC, compared with either agent alone.
VEGF and PD-1 pathway inhibitors show promising improvements compared with single-agent VEGF pathway inhibitors.
Access a treatment regimen chart with detailed information for renal cell carcinoma, including tyrosine kinase inhibitors and cytokine therapy.
Researchers enrolled 6 and 49 patients into dose-finding and dose expansion stages, respectively.
Previous studies found that an elevated pH environment leads to nearly a 40% reduction in pazopanib exposure.
Close to 60% of all patients with VHL will develop RCC or renal cysts.
A shift toward multidisciplinary care is inevitable for the treatment of locally advanced and metastatic RCC.
Findings from the phase 2 CABOSUN study showed that, compared with sunitinib, cabozantinib improves PFS and the ORR among patients with advanced RCC.
Previous findings suggested that there were no benefits to overall survival or disease-free survival with VEGF-TKIs vs placebo.
Patients with PRCC1 frequently show MET mutations. Crizotinib, a dual inhibitor of MET and ALK, has shown promising activity in MET-altered cancers.
Patients receiving VEGF-TKIs are likely to have treatment dose reductions, delays, or interruptions because of diarrhea, which occurs in about 50% of cases.
The phase 3 METEOR trial demonstrated that cabozantinib prolonged PFS, OS, and ORR compared with everolimus, but the impact on QoL was not fully established.
The drug was, however, associated with a greater number of grade 3 to 4 adverse events.
Though uncommon, complete responses are seen among patients with metastatic disease, but CRs seem to occur more often with immune checkpoint inhibitors.
The FDA based its approval on data collected from the open-label, phase 2 CABOSUN study, for which researchers randomly assigned 157 patients with RCC to receive oral cabozantinib or sunitinib.
A cumulative-use analysis suggests that NSAIDs, ACEis, and SSRIs improve disease-specific outcomes among patients with kidney cancer, and further that NSAIDs improve overall survival.
A recent study into the relationship between glucose and cancer cell proliferation may be helping to identify a therapeutic route to starve tumors without killing normal cells.
Cigarettes may favor VHL-intact RCC, but it is unclear whether cigarette smoking selects for more aggressive histology of RCC in a similar way to, for example, the TP53 mutation in lung cancer.
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