It is well established that at its basis cancer is a genetic disease. For a cell to be truly cancerous, it must possess six traits as defined by Hanahan and Weinburg (2000): self-sufficiency in growth factors, insensitivity to anti-growth factors, evasion of apoptosis (controlled cell death), limitless replicative potential, sustained angiogenesis (blood vessel recruitment), and the ability to invade tissues and metastasize. No single cellular gene controls all six of these functions, so cancer is the end result of at least two, if not more, mutated tumor suppressor (loss-of-function mutations) and cell growth (gain-of-function mutations) genes.
Knowing the basics of how cancer arises, it is clear why curing cancer is such an enormous task. To illustrate this, let’s look at gene therapy, which has been often suggested as a promising therapy for cancer. In order to effectively treat a patient’s cancer with gene therapy, the mutated genes would first have to be identified and then a custom-tailored gene vector would have to be constructed in order to deliver the correct genes into every one of the tumor cells in order to restore normal function, or to induce the cells to undergo apoptosis. While this sounds relatively simple, gene therapy is still in its infancy. For example, while we currently know the gene mutations that cause cystic fibrosis and SCID (“bubble-boy” disease), we still lack the proper gene delivery vectors to safely and effectively treat either of this diseases. Add to that our lack of rapid and cost-effective patient genotyping and our current inability to cost-effectively make patient-tailored therapies, and it should be evident that treating cancer using this method is a sizeable and difficult undertaking which is still beyond our reach.
Yet with each advance in cell biology, biochemistry, and toxicology our understanding of how tumor suppressor and cell growth/proliferation genes affect the cell cycle grows, and we better understand the delicate and complex coordination between them; this gives us a better understanding of how cancer arises and what causes it, and enables us to better use our present therapies and design new ones to increase the rate of survival. Cancer is the ultimate disease; it is a patient’s own cells rebelling against them due to complex and still poorly-understood circumstances, and there is no penicillin for it, that is, no single panacea; the fact that it is the patient’s own cells at fault makes treatment especially difficult, since there is no surefire way to distinguish the transformed cells from normal cells in the absence of a tumor.
The goal of scientists working on cancer isn’t and should be to deliver a single “cure” to cancer, which by its nature isn’t a single disease, but instead to develop an ever-expanding and ever-improving array of therapies. Each of these therapies has its own strengths, to be used preferentially depending on the type of cancer in the patient; gene therapy could be considered the culmination of this approach, since it would deliver a near-infinite combination of custom-tailored therapies to target the distinct defects in a patients tumors. Equally if not more important than therapy, though, is prevention. If scientists can continue to identify risk factors for cancer, we have a much better chance of catching a patient’s cancer at an early and more treatable stage, increasing the survivability and quality of life.
The complex nature of cancer is why we are still without a cure for it, and it is arguable that we will never have a single “cure for cancer”. Yet with each breakthrough we better understand the disease and are opening new avenues for identification and treatment, so that hopefully someday treating cancer will be as routine and painless as having a mole removed.
