Researchers at the B.C. Cancer Agency have made a critical breakthrough in understanding how the most malignant type of ovarian cancer spreads. Four out of five women with this form of the disease die.
The new discovery shows pathways that ovarian cancer follows when it invades neighbouring organs. And it offers a fundamental new insight into how ovarian cancer cells are structured internally. If this isn’t quite Nobel territory, it’s close.
The study does not offer a cure, nor does it define a new approach to treatment. But it does point the way for other researchers and pharmaceutical companies to follow.
What also emerges from this project is the fearsome complexity of the malady we call cancer. Every cell in a woman’s ovarian tumour can have a different genetic profile. How do we mount an attack on such a many-headed hydra?
The researchers used computer modelling to sift the endless variations and find patterns that would have eluded the microscope. And yet as hopeful as that is, the sheer scope of the challenge is daunting.
It took 13 years to map the 20,000 genes in the human genome. To map every mutation in the 50 most common cancers would be 10,000 times more complex.
The Greek myth of Cassandra, the princess of Troy who was fated to foresee the future but powerless to prevent it, comes to mind. There are millions of possible combinations. Using even the most powerful computers, can science ever enumerate them all, and devise the means to interrupt each one?
Moreover, it is unfortunately the case that progress in the treatment of cancer has been painfully slow. Atossa, the wife of Persian king Darius, had a Greek slave cut off her breast when she noticed a lump. More than 2,500 years later, mastectomy is still employed.
And many of the chemotherapy drugs in use today were discovered 50 or more years ago. They are the bluntest of instruments, killing indiscriminately any cell that grows faster than normal. Hair cells grow quickly, hence they too are killed, along with other innocent (and sometimes essential) bodily functions.
And that, in turn, points to a further difficulty. Unlike most maladies, the majority of cancer types are not caused by an external disease agent such as a germ, virus or parasite.
They are generated by a malfunction within the cell structures that themselves make up the human body. How do you kill something that builds within the same foundations we rely upon?
That is the case for pessimism. The case for optimism is stronger.
While it’s true only a handful of drugs have been developed to date that attack specific cancer mutations, 20 or more are in clinical trials. Some, like the breast-cancer drug Herceptin, have shown remarkable results.
And despite the vast number of mutations that cancers display, it is possible they share common vulnerabilities. The internal genetic stages through which cancer cells progress are not endless; they might be limited to as few as a dozen or so. That opens the door for targeted therapies that block these routes and stop the cancer in its tracks.
Lastly, gene-sequencing technology and computing power have expanded far beyond the human genome project, and might be on the brink of a further leap forward.
It has been estimated that quantum computers now under development could perform, in an instant, as many calculations as there are atoms in the universe. If this promise is realized, it might hasten the end of a monster that has pursued humans down the ages.
We can at least fervently hope so. The war on cancer is not over. But we do at last have the tools to win it.
