A new drug that harnesses the immune system to attack tumors is highly effective against advanced bladder cancer, according to a recent study.
As part of the latest study findings to be presented at the Chicago meeting, injections of the experimental agent atezolizumab were found to shrink tumors by at least 30 percent and stall new tumor growth in 28 of 119 (or 24 percent of) patients.
All had received the medication as their initial therapy for the disease. Part of a new class of drugs known as checkpoint inhibitors, atezolizumab, also known by its brand name, Tecentriq, was last month approved by the Food and Drug Administration based on recent research from a related clinical trial presented in 2015.
“Our new study results argue that atezolizumab represents a major advance in the treatment of bladder cancer,” says lead investigator Arjun Balar of NYU Langone Medical Center.
“Atezolizumab is the first therapy to be approved in more three decades for this disease, and it is the new standard of care for patients whose initial therapy with platinum-based chemotherapy drugs has failed,” says Balar. “Indeed, it may be the only therapy some patients need.”
The current “first-line” standard of care in bladder cancer, Balar says, is cisplatin, a drug that kills tumor cells by preventing them from repairing damage to their DNA.
Half the patients who responded to the new therapy did so within 15 weeks, with almost all (21 out of 28) remaining on therapy without any detectable signs of cancer growth (at a dose of 1,200 milligrams every three weeks). As part of the study, all 21 patients still in cancer remission continue to be monitored, with some having continued to receive atezolizumab since the study started in May 2014.
Seven patients who initially responded to therapy eventually saw their cancer return and were referred for other therapies, along with those who did not initially respond to atezolizumab.
Patients who responded to therapy saw their tumors shrink or disappear altogether as part of a sustained immune response, with the shrinkages confirmed by radiological scans.
While the drug’s precise mechanism of action is subject to further research by the team, the scientists say the new medication primarily blocks the interaction of the protein PD-L1, or programmed death ligand-1, with its programmed death receptor partner and checkpoint, PD-1. This “lock and key” connection, Balar says, is critical to the detection of tumor cells by immune system T cells.