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Closer to a cure for cancer?
This past weekend’s WSJ had an excellent article on how recent, fascinating developments in targeted therapeutics and immunotherapy show great promise for the treatment of cancer. It’s a must-read for anyone interested in the topic – whether you’re a patient, family of a patient, or even an investor in the technologies that are used. (Full disclosure: as BPV is in MolecularMD, a molecular diagnostics company that develops custom companion diagnostic products and supports clinical trial services for targeted cancer therapies.)
Memorial Sloan Kettering Cancer Center CEO Dr. Craig Thompson explains why he’s optimistic about new therapies aimed at increasing the body’s own ability to fight cancer in The Future of Cancer – Closer to a Cure.
Most people don’t acquire a significantly higher risk of cancer from the genes that they inherit from their parents. Instead, cancer arises as a result of copying errors (mutations) in the inherited genes, as our bodies make new cells to maintain our various organs. A recent widely quoted publication suggested that these errors are an inevitable consequence of trying to copy three billion bits of information as a cell divides.
That may be true, but it doesn’t mean getting cancer is inevitable. The fastest and most extensive rates of cell division occur when we are developing as embryos. Billions upon billions of cells are produced each day, yet cancer in newborns is exceedingly rare. In contrast, cell division in each of our tissues slows as we grow older, while the incidence of cancer increases with age.
What accounts for this discrepancy? We damage ourselves through exposure to invading pathogens and other environmental threats, thereby “constantly damag(ing) our tissues, forcing restorative cell proliferation to occur in a war zone of damage.” But recent advances in targeted therapeutics and immunotherapy “can have stunning efficacy” in the right situation without the toxic side effects of traditional chemotherapy.
It is in this inhospitable environment that most cancers arise. We have known for some time that many of these environmental exposures damage DNA, making it harder to copy and resulting in more mutations as cells divide. Recently, we have come to appreciate that during regeneration of damaged tissue, the rest of the body pitches in to keep every cell in the damaged tissue alive. Not just the healthy cells, but also the ones that have acquired mutations that render them unfit. Our immune system, which usually detects and destroys cells with excess mutations, is turned off…
Patients whose cancer bears specific mutations are now more effectively treated with drugs designed to selectively reverse the effects of those mutations. Such drugs are termed targeted therapeutics. The downside of this class of drugs is that they usually don’t have any benefit in treating cancers that don’t carry that specific mutation. While we don’t yet have many therapies that target cancer-causing mutations, the results can be dramatic when such drugs are available…
Immunologists have found that our immune system has a built-in “off switch,” a checkpoint that shuts down an immune response a few weeks after it is initiated. A new and expanding class of cancer therapeutics have been developed that have the ability to block this normal shut-off switch and thus augment the ability to recognize and destroy cells carrying mutations… Some patients with widely metastatic cancer have been rendered cancer-free with therapies aimed at increasing the body’s own ability to fight cancer.
Dr. Thompson closes with optimism; an optimism we share, thanks to the great work done by the teams at companies like MMD.
Why is finding a cure for cancer taking so long? A major reason lies in the fact that cancer is not one disease, but many. Each tissue has its own unique progenitor cells, and each tissue uses only a subset of the genes we inherit from our parents; each tissue is exposed to environmental insults differently. We are just beginning to understand the interplay of all these factors in the origin of the many forms of cancer. Understanding these issues will ultimately allow us to optimize the treatment approach to each patient’s disease.
While we aren’t yet ready to put cancer on the extinction list along with “simpler” diseases like smallpox and polio, it is clear that with more science—the lessons learned from cancer research over the past two decades—we face the future with less fear.
Genomics vs. Genetics
On related note, the conversation about new targeted therapies includes two terms – genomics and genetics – that are mistakenly used interchangeably. Genetics is the study of single genes in isolation, while genomics is the study of all the genes in the genome and the interactions among them and their environment(s). Genome British Columbia has a useful explanation of the distinction:
If genomics is like a garden, genetics is like a single plant. If the plant isn’t flowering, you could study the plant itself (genetics) or look at the surroundings to see if it is too crowded or shady (genomics) – both approaches are probably needed to find out how to make your plant blossom…
In studying human disease, for example, genomics examines all the genetic information to determine biological markers predisposing an individual to disease, whereas genetics uses the information from one or two genes to explain a disease state. Many diseases due to single gene defects have been identified. Now, geneticists want to tackle multifactorial diseases caused by the complex interactions between multiple genes and the environment.