In the early 1970s, still a few years before molecular biology and genetics would revolutionize cancer research, scientists assumed that some general change in surface chemistry must occur on tumor cells to distinguish them from normal cells. Find that one difference, they reasoned, and oncologists would gain a foolproof marker to diagnose cancer. Thirty years ago this past November in the Proceedings of the National Academy of Sciences, a then 28-year-old English postdoc named Richard Hynes, Ph.D., reported that he may have found that foolproof marker. It was a hitherto unknown structural protein positioned on the surface of normal cells, but which was rare or conspicuously absent on tumor cells. Although Hynes would not directly speculate in his paper, it was tempting to imagine that tumor cells might cleave this seemingly growth-promoting surface protein as an essential step in metastasis. Hynes’ discovery and work in other laboratories set in motion a rush to characterize this mysterious “cancer” protein. Although the cancer breakthrough soon proved to be a false alarm, research on this new structural protein, called fibronectin, would catalyze a string of seminal studies, including the first molecular investigations of cellular adhesion proteins and their receptors, today two hot areas in cancer research.
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R. Longtin (2004) studied this question.