10 years ago today, at the 6th International Mutant p53 Workshop in Toronto, I first presented evidence to the world that p53 is not just a tumor suppressor, but that it is also a proto-oncogene (wild-type)! The p53 oncogene (mutated) was already well known but it was believed that, unlike all other oncogenes, the p53 oncogene originated directly from a tumor suppressor through neomorphic mutations (mutations by which the altered gene product acquires novel molecular functions). I showed that there is a proto-oncogene within p53 that is pro-oncogenic from the start, in its wild-type form, and that evolved with mammals for millions of years. I proposed that it is this product of evolution, this proto-oncogene, that becomes the mutated (over-activated) p53 oncogene in cancers and that we have to learn more about it so that we can target it to cure this disease. Part of our supporting data on the existence of a p53 proto-oncogene is now available via the servers at EMBO Reports, IJMS and BioRxiv (please consult the links below). MaRCU continues in its efforts to learn more about and to target this new proto-oncogene, which is possibly the most mutated proto-oncogene in cancer. (Contact areap53lab@gmail.com if you want to support our research.)

Our research about p53 proto-oncogene: 2016, 2022, 2023.

Continue reading “It’s been 10 years since (wt) p53 proto-oncogene was first presented to the world!” →

When the cell has a very important protein like Δ160p53 that can save its life under stress conditions, the cell wants to make sure the ribosome is not going to miss that start codon; so why not have two instead?

Read all the details in our new super exciting paper that is part of our also super exciting celebratory issue of the 40 years of p53 research. Click HERE!

Continue reading “Did you know that some proteins are translated from not one but two start codons?” →