Truly a remarkable call for action; A Cancer “moon shot.” It is worth about $2 Billion and purports to cure cancer. It has the faint echo from some thirty years and tries to mimic the “landing on the moon” challenge proposed by President Kennedy.
The difference between landing on the moon and the “cancer moon shot” is one of technology and biology. Whereas technology is based on referential absolutes of certain laws, aerodynamic and physics, biology has no such laws etched onto its book covers. Try as we might using arbitrary metrics of measurement and outcomes, the cancer moon shot terminology is one of jumping the shark.
Ok, I have to admit that even with the success of finding the right trajectory of the rocket to reach the moon based on the earth’s circulation and orbital path, a malfunction in the carbon dioxide scrubber can create spectacular drama. Other times a space travel can be cut short by the frozen “O” Rings (hazard) and the peeled away tiles (another hazard) off the space shuttles. Barring those events that have been understood and placed in the “Risk categories” the flight to ideas into space travel continues successfully. The travel to the Moon and Mars and flying weightlessness in space are a thing of the present with known knowns.
Now drifting off to the biology related issues, we are faced with a myriad of problems; the most certain being; indeterminate end points or outcomes. Let us take the cell as the primary focus of our attention for the moment. Each cell from each organ is faced with a diversity of external pressures. A stomach, for instance, learns to live with the Helicobacter Pylori bacterium causing peptic ulcers in some all the way through chronic inflammation and cancer of the stomach in others, but not in all. Not all humans are affected equally. The bacterium finds solace in some as a subdued accomplice (saprophyte) and in others as a deadly weaponized life-form? Why so?
The landscape of lung cancer is also changing as we speak. Squamous cell type lung cancer once in majority as a form of Non Small Cell Lung Cancer initiated by smoking and other external pollutants seems to have given way to an Adenocarcinoma NSCLC sub-type increasing from 8.9% to 19.5% over the past 6 years. Interestingly this form is increasing in women-never-smoker category. Why so? Is it the transposon function playing through the generations as the sperm and ovum date?
Or let us look at something called GUCY2C receptor anchored by the Guanylin hormone, which appears to protect humans from colon cancer. Obesity seems to stem the function of the GUCY2C receptors and thus the normal proliferation of the colon cells goes awry. The dysfunction of the GUCY2C receptor seems to correlate well with weight gain and obesity. But what happens in lean individuals who develop colon cancer? What is the trigger there? There are other mechanisms in play, for sure; including the Lynch Syndrome, Inflammatory diseases of the colon etc. So there are many paths that lead to cancer formation in the colon. The next question then is, is there a final common pathway where arrests can be made to prevent the unholy and tortuous realm of malignancy so that the “cancer moon shot” may find success? Maybe, but (groan) there are many upstream and downstream pathways within the cellular interior, teaming with cross-talks (between pathways) within cellular signaling in force, to offset any specific targetable site. And just so we understand that the final common pathway if successfully arrested, might also lead to normal cellular function.
Another disturbing point of view is the heterogeneity of the cancer itself. Recently shown in Multiple Myeloma, where sub clones of the Myeloma cells exist within the same patient. Each sub-clone has a different set of mutated genes, some subtle, some overt and others manipulated through the epigenetic realm. These sets create the same havoc from sheets of plasma cells that cause fractured bones, kidney failures and other assortment of maladies on us, humans.
You might be able to see this non-linear malady a bit clearer. It is truly a dilemma crafted from the inherent variability of the cellular function. The cellular functions are like a flower blowing in the wind, as it holds on to its petals only to be lost in a gale event. From the seeds scattered by the gale-force breezes, mutated seeds give rise to a multitude of colored flowers and each bush with its own might, beauty and future. The gales or hurricanes can come and go and be of any intensity but the effect is never the same. Each iteration of exposure to hardship lends itself to a newness in the genetic structure and signaling. Robust flowers are borne of harsh climates and delicate ones arise in moderate climes. The mutation goes on and the targets keep varying in expression. A cancer thus has many facets to its etiology even in the same organ and the delicate balance of norm is upset by factors inside as well as outside of its milieu.
“Moon Shot” the so-called precision shot to a known celestial body, where the trajectory and orbital paths are known is a cinematic presentation for the mind’s eye in trying to capture the imagination. A well-meaning concept that attempts to target a moving target. Given the gravitational pulls of the various heavenly bodies viewable by naked eye, curing cancer with the moon shot is more like a shot in the dark. And shooting in the dark where the dark matter has its own set of rules creates another blind eye’s dilemma.
The $2 Billion outlay added to the NIH budget, may and probably will find a few new oncogenes or epigenetic pathways, tumor suppressor genes or other epiphenomena and with those, tiny blind alleys in the process, but will they give us an atlas to the cure for cancer? I have doubts. But some progress in the oncology field will be made, of that I am certain. Progress, means more alleys and pathways down the rabbit hole.