Do Broad Commonalities Exist in Cancer?

This is the age of biotechnology, and many believe that one of the crowning triumphs of the age will be the defeat of cancer. If we're going to greatly extend healthy human longevity, then the defeat of cancer certainly has to be achieved one way or another. I think that the one of the most exciting possibilities in modern cancer research is that a cure for cancer is in fact easy, but we don't yet know how to do it.

Let me explain what I mean by "easy." This is an era in which we can order cells around, identify cells by tiny differences in their surface biochemistry, construct viruses to order, and in which researchers are rapidly deciphering and manipulating the most fundamental mechanisms of our biology. In this sort of background, "easy" means that researchers find some common mechanism necessary to all (or even just most) cancers. Scientists will then pile in and develop a way of attacking cancer by disrupting or manipulating that mechanism, and there the story is done. We'll have a robust cancer therapy, and will reap the benefits thereof.

"Hard" on the other hand means that there is no common mechanism shared between more than a tiny fraction of cancers. They're all radically different, even from individual to individual, or between millions of different human genotypes. There can be no one therapy, widespread and constantly improved upon by research and development: curing cancer will mean a vast array of potential therapies for millions of different types of malfunctioning cells. It will be an unending war of attrition. Alternatively, perhaps a common mechanism exists, but getting at it is something researchers don't evisage attaining for decades yet. Aubrey de Grey's WILT or OncoSENS falls into the latter category, I think. In biology as in physics, if you dig down deep enough you're eventually going to find the right plug to pull out of the socket - for WILT it's the lengthening of telomeres required by all cancers. You should read up on WILT to see the biological engineering and remaining research required to make that happen, however; it's not trivial.

Right now, the dominant thinking in the cancer research community is that cancer is hard. Everyone would like to see a breakthrough that makes it easy, however. You can see some of this at work in cancer stem cell research in past years. Are these errant stem cells distinctive in any way across some or all cancers, and so a single type of therapy can be deployed for many cancers, or are they as varied as cancers are in all other ways? Are cancer stem cells a path to "easy" or are they just another facet of "hard?"

With all this in mind, my attention was directed today to a paper in which researchers outline a common immune system defect in several different types of cancer. Laypeople might prefer the press release to the paper itself:

Human immune cells communicate constantly with one another as they coordinate to fight off infection and other threats. Now researchers at Stanford University's School of Medicine have shown that muffling a key voice in this conversational patter is an early step in the progression of human cancers. Silencing an inter-cell signaling mechanism called the interferon pathway may be one way newly developing cancers gain the upper hand. It may also explain the immune dysfunctions seen in many cancer patients and why cancer immunotherapies are often ineffective.


Lee and his colleagues had previously shown that the interferon signaling pathway was compromised in melanoma patients. In the current study, the researchers investigated whether patients with two other types of cancer - breast and gastrointestinal - also showed the same defect.


They have a clear defect in the interferon signaling pathway," said Lee. When the researchers looked more closely at the lymphocytes from breast cancer patients, they found that the defect was equally severe in samples from people with early- and late-stage cancers - indicating that the problem must arise soon after the cancer begins to develop - and that it was present regardless of whether the patient had ever been treated with chemotherapy.


"It's now looking like the interferon pathway may harbor a general immune defect in many types of cancers."

One of the many roles of the immune system is to kill off cancerous cells that we all develop but never know about. A single immune system issue that is in fact the root cause of many types of cancer (or rather the root cause of those cancers surviving long enough to threaten their host) would be good news indeed, as it could in theory be detected and corrected early, long before issues arise.

There are questions of cause and effect here; is the cancer doing something to the immune system, or is the immune system defect what leads to cancer? The answer to that question is ultimately much less important than whether or not this applies to many other types of cancer. If it's specific to only a few cancers or patient populations, then it will remain one of a thousand similar modestly funded projects.

The down side to relying upon the immune system to do the heavy lifting for you in any cancer therapy is that our immune systems decay dramatically with advancing age. This is one of the reasons that cancer is an age-related condition: a faulty immune system less able to do its job. If the cancer research community keeps heading down the road of immunotherapy, as seems likely, I think that increasing resources will be directed towards restoring an aged immune system to youthful function. That is a necessary step to best using the immune system's capabilities to target and destroy specific unwanted cells, whether or not researchers are interested in engineering greater longevity.
Rebecca J. Critchley-Thorne, Diana L. Simons, Ning Yana, Andrea K. Miyahira, Frederick M. Dirbas, Denise L. Johnson, Susan M. Swetter, Robert W. Carlson, George A. Fisher, Albert Koong, Susan Holmes, & Peter P. Lee (2009). Impaired interferon signaling is a common immune defect in human cancer Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0901329106

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