After a mixed-up start, it is now understood that most tumours exhibit dysfunction of the protein p53. Restoring its tumour-suppressing properties is no easy task.
But the truth was more complicated. As more researchers began to study p53, it became apparent that the tumour-causing versions of the gene were actually mutated. The unmutated, or wild-type, version of the gene, which was cloned from humans and mice in the 1980s, exerted the exact opposite effect: the gene acted as a potent inhibitor of tumorigenesis. Scientists had even got its size wrong; p53’s true molecular weight is closer to 44 kilodaltons.
In the three decades since researchers came to this realization, p53’s biological significance has become ever more apparent. The protein coordinates a wide range of essential cellular functions, and its evolutionary history dates back to some of the earliest multicellular life on Earth. Most of the time, p53 is kept in an inhibited state at low levels in the cell until it is required.
Some cellular crises might be minor, requiring a response focused on repair to restore cellular function. Catastrophic problems, however, might lead a cell to self-destruct to prevent further harm. These functions make p53 a crucial defence against biological and environmental insults that can give rise to cancer, leading some people to dub the protein ‘the guardian of the genome’. As demonstrated by those early studies of mutant forms of thegene, mutations that interfere with the function of p53 are well-known drivers of cancer.
Despite a formidable dossier of research into the function of p53 and its myriad mutants, there are still no approved drugs that can selectively target the p53 pathway in cancer. But there are some promising avenues of attack, including molecules that neutralize the disruptive effects of specific p53 mutations or that counteract the excessive inhibition of p53 seen in some tumours.
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