Cancer development and the cellular environment

For the serious student of the biological sciences, the idea that the immediate, internal, biological environment can profoundly impact the ability of any type of cell to grow and evolve is hardly new. However, for those who are less accustomed to reading the scientific literature, the importance of the biological enviroment in the development of one or two early cancer cells into an an actual tumor, with the ability to metastasize, is not necessarily as apparent.

There is a helpful article on the front page of today’s New York Times that addresses how far we have come over the past 50 years in understanding this issue. Indeed, cancer researchers are now increasingly focused on the so-called “microenvironment” of cancer cells as a means to understand what can be done to prevent initial mutant cells from dividing and growing at the earliest possible stages. This can depend on the specific levels of a wide range of cellular factors and their precursors, since the growth or death of specific cells can be very highly dependent on the levels of specific proteins, enzymes, hormones, and other factors.

In the past we tended to believe that “cancer” was clinically inevitable once cancer cells started to grow in the body. We now know that this is not inevitable. There have been many experiments clearly showing that cancer cells do not necessarily grow if they do not have the right environment in which to develop, just as children do not grow to their full stature if they don’t get the right nourishment and exercise.

One problem, of course, is that we still don’t know enough about biological microenvironments to be able to manipulate them in the clinic with great accuracy. Another problem is that all too often we still make the mistake of thinking that “cancer” is one big disease. It isn’t. The various forms of cancer are as different as the forms of infectious disease caused by different types of bacteria and viruses. The common cold (caused by a common virus) has only one absolute similarity to the plague (caused by the bacterium Yersinia pestis): they are both “transmissable” diseases, with well-understood routes of transmission and time-frames within which an affected person is capable of passing  the infection on to another individual. Otherwise, these two diseases have very little in common at all.

In the case of “cancer” we see the same degree of variation between forms of this category of disease: indolent, low-risk prostate cancer (which occurs in some 30 percent of all prostate cancer patients) is a very different disorder to aggressive, high-risk, Gleason 8-10 prostate cancer, which is itself a slow-growing form of cancer when you compare it to something like acute myelogenous leukemia.

We are only going to be able to take really big steps in the effective managment of prostate cancer at any stage when we understand much more about why specific types of prostate cancer cells do and don’t grow in specific cellular environments. When we know that, we may well be able to target specific treatments to the specific cell in the specific environment, as opposed to the current forms of treatment for localized disease — pretty much all of which are akin to banging on the prostate with a hammer until the organ is no more in the hope that if there is no viable prostate there can be no viable prostate cancer.

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