Enabling The Immune System to Fight Cancer

Immunotherapy drugs for fighting cancer that work by rendering cancer detectable to the immune system and therefore actionable for destruction are now in “early clinical trials.”

One way of fighting cancer, since cancer plays tricks on the immune system to render it effectively invisible to that system, is to enable the immune system to detect tumor cells and destroy them. There is a class of drugs that does just this. They’re called immunotherapy drugs. Some of these drugs are already at the stage of “early clinical trials” and they’re “showing promise.” Of “several hundred patients” afflicted “with various kinds of advanced cancer” involved in the clinical trials, “up to one-quarter of those who received the treatment saw their tumors shrink and some are still alive more than a year later.”
The immunotherapy drugs involved in the clinical trials targeted specific proteins (one for each drug) that played roles in rendering cancer cells invisible to the immune system. One of the proteins – programmed death ligand-1 (PD-L1) – is produced by cancer cells on their surface. PD-L1 “locks onto a protein called PD-1 on T cells, a type of immune cell. (PD-1 is the other protein targeted for functional disruption in the clinical studies, as will presently be made clear.) When PD-L1 and PD-1 have locked, the effect is for the cancer cell to be rendered invisible to T cells, thus sparing them from attack by the immune system upon signals from T cells. It is therefore the most natural question to ask whether functional disruption of either protein could serve as a treatment modality for cancer. “[A] small initial clinical trial of an anti-PD-1 drug confirmed that this strategy holds promise for treating cancer.”
The initial clinical study was followed by “two larger, multicenter studies” that offered support for the results of the initial study. In one of the subsequent larger studies, “a group of 296 patients with five types of advanced cancer received an infusion of antibody [which is also a protein] targeting PD-1 every two weeks.” This regimen caused tumors to shrink “in 14 of 76 lung cancer patients, 26 of 94 melanoma patients, and 9 of 33 kidney cancer patients – an 18% to 28% response rate.” Further, the drug proved effective in many patients “for a year or longer.” Suzanne Topalian of Johns Hopkins University in Baltimore, Maryland, USA, a “melanoma researcher” and “leader of the multicenter study,” characterized the results as “ ‘encouraging’.”
In the other study (conducted “at Hopkins and elsewhere”) “207 cancer patients received an antibody” blocking PD-L1. The outcome saw “10% to 17% of those with one of three types of cancer” respond to the drug, “and some patients have responded for at least a year.”
Of course, as with most drugs under development, there are safety issues to be dealt with and hopefully, eventually eliminated or at least minimized. For example, the anti-PD-1 drug manufactured by Bristol-Myers-Squibb “caused three deaths from lung inflammation” as a side effect. Clearly, in this connection, “more studies are needed to show whether those receiving the antibodies live longer than they would on conventional treatments.”

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