In the article below my comments are in bold within square brackets:
Conquering [huge overstatement] Cancer by Thwarting Tumor’s Immune Shield
by Jocelyn Kaiser on 2 June 2012, 12:00 AM|
A type of drug that helps the body’s immune system attack tumors is showing promise. In early clinical trials [meaningless] involving several hundred patients with various kinds of advanced cancer, up to one-quarter of those who received the treatment saw their tumors shrink, and some are still alive more than a year later.
[Trivial. This strategy has no promise of a cure. We need cures! We need practical preventives! Note the pathetic satisfaction with incremental gains. We demand way too little of our researchers.]
The results are the latest good news for so-called immunotherapy treatments that work by overcoming [too strong a word] a tumor’s ability to evade the immune system. One way cancer cells escape destruction is by producing a protein on their surface, known as programmed death ligand-1 (PD-L1), that locks onto a protein called PD-1 on T cells, a type of immune cell. When the two connect, that prevents T cells from detecting the tumor and signaling the immune system to attack. Researchers have hypothesized [more like wild speculation] that giving people with tumors an antibody (a protein) that blocks either PD-1 [blocking the T cell ligand is a bad idea – don’t interfere with the operation of NORMAL cells! This is sheer desperation. And won’t the antibody to the Tcell ligand block the shield of those normal cells who express this marker? Oncologists cannot target all tumor cells and only tumor cells because of the heterogeneity of tumors.] or PD-L1 would keep the proteins from engaging and switching off T cells—and a small initial [why are you even writing about it?] clinical trial of an anti-PD-1 drug confirmed that this strategy holds promise for treating cancer.
So do two larger, multicenter studies of this approach, which are being presented today at the annual meeting of the American Society of Clinical Oncology in Chicago. When a group of 296 patients with five types of advanced cancer received an infusion of an antibody targeting PD-1 every 2 weeks, tumors shrank 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. Many patients have responded to the drug for a year or longer. “These are very encouraging signals [Yeah, for getting more funding. Not encouraging for patients who need cures],” says melanoma researcher Suzanne Topalian of Johns Hopkins University in Baltimore, Maryland, a leader of the multicenter study.
In a separate study at Hopkins and elsewhere in which 207 cancer patients received an antibody that blocks PD-L1, 10% to 17% [not even as good as the other discouraging study] of those with one of three types of cancer have responded, and some patients have responded for at least a year.
As with most early drug studies, the trials were predominantly designed to test safety; more studies are needed to show whether those receiving the antibodies live longer than they would on conventional treatments. (Topalian says the 1-year survival results are encouraging, however. In other studies, advanced melanoma patients on standard treatment lived for 6 to 7 months on average.) And the drugs, both made by Bristol-Myers Squibb, can result in severe side effects: The anti-PD-1 drug caused three deaths from lung inflammation [Great! A faster way to die].
Still, the fact that both drugs seem to have a clinical impact “says that this combined [PD-1/PD-L1] pathway is important as a target for cancer therapy,” Topalian says. When researchers tested tumor samples from 42 of the patients receiving anti-PD-1, nine of 25 who responded had PD-L1 on their tumors, while none of those lacking PD-L1 on their cancer cells responded. That means a test for PD-L1 [no, the results of these tests are ambiguous – tumors are heterogeneous; some cells will have it. Some won’t] could potentially tell doctors which patients should get the drug, much as physicians now routinely test breast cancers to see if they should receive various hormone therapies.
The twotrials, whose results are also reported online today in The New England Journal of Medicine, have “broken the ceiling” of a 10% to 15% response rate for a similar strategy that targets a T-cell protein called CTLA-4, says oncologist Antoni Ribas of the University of California, Los Angeles, who wrote an accompanying commentary in the journal. A CTLA-4-blocking antibody called ipilimumab was approved for melanoma treatment by U.S. regulators last year. But it seems to cause more side effects than anti-PD-1 drugs, probably because CTLA-4 is present on T cells in more tissues of the body.
“The biggest feature of all these approaches is that it engages [an immune] memory response, so responses tend to be durable,” says Ribas. Still, one significant remaining challenge is to get more [no kidding] patients to respond to the growing number of these immunotherapy drugs. One way to do that may be to combine them with other treatments, Topalian says. [Great – multiple ineffective drugs, each with huge side effects, add up to one good drug, which by definition works for everyone and has negligible side effects. Strange math.]
[What if we networked all of this brainpower, focused it on the two needful things, under strong leadership, and set aggressive deadlines and tight budgets? The two needful things are 1. Practical prevention strategies: no vegan diets, please! And 2: Cures: no treatments, please! What could we not achieve?]