A study conducted at MIT suggests that the late-stage restoration of protein p53 among patients may help slow the growth of lung cancer. These findings are based off of studies that involved lab mice that had been engineered to develop lung cancer.
Protein p53 has long been known to be a key protein in relation to cancer growth. Back in the 1980s, the protein was shown to be a critical factor in the process of turning healthy cells into cancerous cells. Through studies, p53 has been shown to directly block the reproduction process of cancerous mutations. This is because p53 is responsible for stopping cell division if DNA damage is detected.
Unfortunately, it has been shown that p53 functions are defective in approximately half of all patients who are diagnosed with cancer.
With this knowledge, there has been much research into the development of drugs that effectively switch on the function of p53. Now, MIT reports that such drugs may indeed help prevent the growth of aggressive metastasized lung cancers.
Surprisingly, the MIT researchers only saw a positive effect in p53 function when the protein was switched on later in a tumor’s progression. Initial attempts to switch on the p53 protein occurred when the mice had developed benign adenomas. At this point, it appears that a p53 switch-on results in no measurable effect on tumors.
However, subsequent tests that switched on the protein after tumors had become malignant showed more favorable results. Specifically, it was found that malignant cells were effectively cleared by p53, while non-malignant cells were not.
As a result of this unique happenstance, MIT researchers think p53 signaling pathways are only called to action when high levels of cancer genes occur. As such, the fewer DNA mutations present in benign tumor cells are not yet enough to result in the favorable actions of p53.
In response to the study, the MIT team is now looking into ways to effectively switch on p53 within human patients. Future studies will also look at how effective p53 is at fighting tumors that have already metastasized.