P53 Gene Suppression Inhibits Colorectal Cancer Growth


Under the supervision of Professor Ute Moll, a team of researchers from the Department of Pathology at Stony Brook University School of Medicine showed that ablating a certain protein could translate into reduced tumor growth with colorectal cancer (CRC).

Genetic manipulation is one of the procedures that are currently at the forefront in terms of cancer treatments. Designing targeted solutions that are more efficient and safer for patients is one of the methods that is hoped to significantly improve outcomes and general health in cancer cases.

In CRCs, the disease creates certain mutations, and approximately sixty percent of times it is linked with the p53 gene, creating an alteration for mutp53 R248Q by exchanging Arginine (R) for Glutamine (Q). Ablating the gene resulted in stopping tumor growth and reduced tumor invasiveness for about fifty percent of patients. The international team found that the treatment was, in fact, halting Stat3 activation, a known cancer marker.

Dr. Moll remarked that “We discovered that in p53-mediated colorectal cancer driven by the most common mutant form of p53, there is an exploitable tumor dependence on continued expression of the mutant protein for the tumors to thrive”.

Furthermore, the use of a molecular drug 17AAG on Hsp90, another enzyme that is associated with p53, displayed similar effects in inhibiting tumor progression.

The article concludes by saying: “data suggests that this and similar p53 mutants represent actionable drug targets responsive to treatment by removal, for example with Hsp90 inhibitors”.

These findings suggest that, in the near future, genetic treatments could be employed to stop cancer even before it has time to develop.

In the United States alone, more than 140.000 new CRC cases are discovered each year.