Cloned p53 and then spent a career on what it does. The field's first reading of his own 1984 result, that p53 was an oncogene, turned out to be wrong, and the correction is the better story.
Moshe Oren cloned the p53 gene at the start of the 1980s with David Givol and Arnold Levine, and his laboratory at the Weizmann Institute has worked on it ever since, with Varda Rotter's group alongside. The two groups published back to back in the same issue of Nature in 1984, on pages 646 and 649, showing that p53 cooperates with ras to transform cells, and both read it at the time as an oncogene. It took until the end of that decade for the field to re-read the result: the clones in hand were mutant, and wild-type p53 is a tumour suppressor. That reversal is worth stating plainly rather than tidying away, because what followed from it is the modern position that mutant p53 does not merely lose the old function but acquires new and harmful ones, which is why mutant-p53 reactivators and selective degraders are a drug class at all. Oren's recent work is on how p53 restrains stemness by controlling histone modifiers.
| Title | Journal | Year |
|---|---|---|
| Participation of p53 cellular tumour antigen in transformation of normal embryonic cells Eliyahu D, Raz A, Gruss P, Givol D, Oren M. Published back to back with Parada, Land, Weinberg, Wolf and Rotter on pages 646 and 649 of the same issue. | Nature | 1984 |
| Molecular cloning of a cDNA specific for the murine p53 cellular tumor antigen Oren M, Levine AJ. PMID 6296874. | Proceedings of the National Academy of Sciences | 1983 |
| p53 regulates the expression of histone modifiers to restrict stemness and maintain differentiation Department of Molecular Cell Biology, Weizmann Institute of Science; indexed on Europe PMC | 2025 |
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