“Cancer is a disease as old as humankind,” writes Sue Armstrong in her new book, “p53: The Gene That Cracked the Cancer Code.’’ The earliest known reference to the malady in humans was in an Egyptian medical text dated around 1600 BC.
Cancer remains with us. It can even be said to have undergone a metastasis of its own, increasing with the aging of our population. Half of men and a third of women living today will receive a cancer diagnosis. Cancer is the second-leading cause of death in the United States after heart disease.
So the reader can be forgiven for finding the opening line of Armstrong’s chronicle of a breakthrough discovery in the battle against the disease to be something of a puzzler: “The question that’s obsessed me for the whole of my career is: Why is cancer so rare?” In posing this question, Gerard Evan, a professor of molecular biology at the University of California, San Francisco and Cambridge University in England, makes a particular point.
One cell, its regulatory and control mechanism on the blink, is all it takes to start the spiral of events that ends in malignancy. The cells in the human body number in the trillions, and they divide — some, like those in the skin and the digestive tract, more or less constantly. Considering this, it is remarkable that things don’t go awry more often.
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The reason is that our cells have evolved complex mechanisms to prevent it, to catch and correct glitches, halt cell division until the necessary repairs are made, and, if all else fails, engineer their own death — a fail-safe mechanism known as apoptosis.
And the primary responsibility for this cleanup and maintenance process lies with a protein called p53 — referring to the substance’s molecular weight of 53 kilodaltons. The gene responsible for encoding the protein, commonly referred to in scientific literature as TP53, may be the most studied gene in history.
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Among the most tantalizing pieces of information to emerge from decades of cancer research is that in the development of nearly all cancers there is a single, unifying factor: It happens only when p53 has been inactivated.
“p53: The Gene That Cracked The Cancer Code’’ is the story of the research that led to this understanding — less a long road than a meandering set of paths that crossed and doubled back and more often than not led to blind alleys and dead ends.
Armstrong, a British science journalist, has rendered, from what easily could have become a tangled web of complex science, a readable story of discovery. As in the best travel writing, it’s not the destination that’s important here, but the journey. This is not only a story about the gene on chromosome 17, nor only about the nature of cancer, but also about how science works.
“The history of science is strewn with groundbreaking discoveries which are only subsequently recognized as such,” Armstrong writes. “Often the circumstances are mundane — a scruffy laboratory with test tubes and microscope slides scattered among scientific papers . . . a white jacket over the back of a swivel chair.”
Armstrong’s accessible, if sometimes tending toward folksy, style and well-crafted explanations offer a glimpse of a world that too often seems off limits to the average person, poorly understood, frequently misconstrued, occasionally distrusted. Science is laborious and painstaking; it is long hours of lab work, the slow accumulation of data. It is also about unraveling mysteries, the puzzle of an unexpected result, the reward of patience, the joy of sudden insight, all adding up, over time, to progress.
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The journey of p53 is nowhere near over, Armstrong writes. Every answer inevitably invites new questions, and p53 will continue to be a protein of interest for years to come, particularly as investigators seek ways to put what they now know to therapeutic use in cancer treatment.
Ellen Bartlett is a writer living near Washington, D.C.