hello darkness, my old friend
Here’s a cheery little thought of the day for you: As the population ages, the question is not if we will encounter cancer in our lives, but when.
Even though the term cancer is a catch-all, it is not one disease and there are more than 100 different forms. However, in all cases the fundamental starting point is the same: cancer originates in a cell that cannot stop dividing. The obvious irony is that it is this same cell growth and division amongst healthy cells that provides to us the ability to live. Normal cells will proliferate over a lifetime, gearing up to full speed following an accident or emergency, but as old-age approaches their capacity to keep dividing eventually ceases. Cancer cells don’t stop dividing. Ever. They grow faster, they adapt better: they are more perfect versions of ourselves. They are immortal.
In terms of cell type the daddy of all is the stem cell. Whilst we only possess a tiny number of these cells, they are the ones which are capable of our complete regeneration. As an example, our entire blood stream can arise from a single stem cell usually found inside the bone marrow. When required to do so by the body, this cell kicks into action and provides millions and millions of red blood cells in double quick time. And then, just as quickly, it can put itself back into hibernation. It stands to reason that if these uber strong stem qualities exist in healthy cells then they invariably exist in cancerous ones. It’s these that lead to relapse and the one big difference is that it appears they cannot be lulled back into a dormant sleep-like state. Cancer, then, is quite literally trying to emulate the regeneration of itself, its quest for immortality continues.
What causes any normal cell to lose control, to break down and to begin to grow uncontrollably? Genes control the growth of cells and it is thought that a rogue, or retrovirus gene, attaches itself to the cell’s DNA and delivers a genetic signal to alter its structure and growth characteristics. Carcinogens, such as tar, soot and smoke, are also capable of activating such gene and DNA mutation. Thus lung cancer occurs when a chemical carcinogen in cigarette smoke mutates a gene that controls the growth and development of a lung cell. This cell then grows uncontrollably. The more you smoke the more likely the carcinogens are to cause a reaction and mutation. And irrespective of any carcinogens, the older we become the more these mutations are likely to occur and the more they accumulate. The older we get the more the odds shorten.
Lung cancer has long been associated with smoking. Liver cancer has been long associated with inflammation and repair in liver cells caused by hep B & C, which in turn can be attributed to the booze and diet. Cervical cancer is often caused by the sexually transmitted virus, papilloma. These cancers do not arise accidentally or ‘naturally’ but can be caused by particular actions or behaviours, exposures which can be modified or changed. But for many other cancers, there is no identifiable and hence, modifiable risk. Aside from age that is. It would appear that the older we live the more susceptible we are to certain cancers such as breast or prostrate. Taken to its logical extreme, if the genes which unleash many forms of cancer are already present in every cell, stitched into our very DNA, then the older we get the more likely we are to experience cell mutation. As life expectancy has increased over the last century, from late-40s in 1900 to the current mid-70s, so the incidence of cancer has grown. In 2010 one in two men and one in three women will be diagnosed with cancer in the US, and there’s no reason to think the rest of the western world is any different. It’s when we are going to meet cancer, not if.
There is some good news though, of a sort: The way we imagine cancer is changing and it’s not the death-sentence it once was. In the past you battled it, you took it on and fought it tooth and nail. To the death. But for many forms of the disease this black-and-white outcome no longer has any relevance. Today’s treatments, usually centred around surgery, chemo and radiation are now often complemented by long-term drug use and a course of treatments can last five, ten years, or even a generation, or two. It is not unheard of for cancer patients to have a life expectancy equal to that of their age-related counterparts. The cat-and-mouse game of diagnosis, treatment, resistance, recurrence and more treatment is being stretched further and further.
Cancer, by its inherent genome nature, perhaps defines the outer limits of our survival but I for one am not prepared to rule out our own imagination and our capacity to out-think the wee beastie. As the English epidemiologist Richard Doll used to say that “death in old age is inevitable, but death before old age is not.”
