I just lost a friend to cancer.  One who was supposedly in remission.  Until we found out her “stroke” was a cacophony of tumors in her brain- and the rest of her body.  My father succumbed to three different cancers, simultaneously, and relatively quickly.

How is that possible?  Why did their immune systems fail them?  Is there some sort of autoimmunity disease that is related to cancer?  (My mother died from an autoimmune disease of unknown etiology.)  After all, our white blood cells are supposed to attack and kill invaders.  Why are they not effective against these diseases?

Well, there may finally be some answers to this query.  Because we now know that carcinoma uncannily develop a coat of armor- a protective shield that stops our white cells and the various (lethal) chemicals we inject into our bodies to destroy these cells- from being effective.

When that shield is pierced, our immune systems and our anti-cancer drugs work.  They can shrink cancers, stop them from growing amuck.  These immunotherapeutic drugs make sure that our immune systems do their “stuff”. Which is far better than using a drug to attack a specific gene- since it seems that, like bacteria which become antibiotic resistant, cancers can also become resistant to certain drugs.

Many of our problem cancers have developed specialized molecules that fool our immune systems.  They employ PD-L1 or PD-L2 to coat their surfaces, rendering the attack by T-cells totally ineffective. This is not to say that there are not other proteins cancer cells have found to mask them from our immune systems; it’s just that these are the two we have found so far.

So, we are developing drugs that coat these proteins- either on the cancer cells or on our white blood cells, affording our immune system the ability to attack and destroy the carcinoma.

One such drug is ipilimumab, which is one discussed in this review of small-cell lung cancers.  The initial studies with Yervoy [Bristol-Meyers Squibb’s version of the drug]  were presented in 2010 at the Annual Meeting of the American Society of Clinical Oncology.   That report described that 82 patients were treated; the average life span was 10 months with the treatment vs. 6 months without- and 23% survived two or more years versus 14% without the drug.

Unfortunately, there is a problem with the drug, as well.  Since the immune system acts in an elevated fashion, it occasionally attacks normal cells.  But, the concept is being pursued by several drug companies, because of it’s promise.

There is another approach being studied, as well.  We can modify our white blood cells (ex-vivo) to attack the carcinoma directly.  But, it is my guess that this very specialized approach will only be used for those cases where the simpler, first process fails to achieve its objectives.

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