Scientists at the McGill University claim to have found a formerly unidentified series of communications between genes that are apparently in charge of whether cells may turn cancerous. The finding could result in a new generation of targeted therapies tuned to individual patients.
The study experts examined hereditarily engineered mice. These mice apparently do not have the capability to create the genes 4E-BP1 and 4E-BP2. Since these genes were thought to play a significant function in restraining cancer, the experts anticipated the 4E-BP ‘knockout’ mice to display extremely accelerated cancer development. But apparently it did not take place, much to the bewilderment of all the experts.
Dr. Emmanuel Petroulakis, a post-doctoral researcher at the Sonenberg Laboratory at McGill’s Faculty of Medicine and the study’s first author, commented, “We didn’t understand what was going on. We tried other experiments to try to promote the cells from these mice to become malignant, and they failed. We were shocked.”
Dr. Petroulakis is of the opinion that completely unidentified genetic pathways could be implicated, and the experts crossed their mice with a strain deficient of a different gene, p53, already identified to be a master ‘tumour suppressor.’
Dr. Petroulakis, mentioned, “Then we got what we expected. More than we expected. Mice with both the 4E-BP’s and p53 knocked out showed enhanced tumour growth, more than we’d see just knocking out p53 alone. This proves that the 4E-BPs are indeed tumour suppressors, but only in the context of this master tumour suppressor. That’s a whole new effect, a totally new concept in the literature.”
The connotation of the finding could clarify why a few cancer therapies function well in some patients and not at all in others.
Dr. Petroulakis remarked, “P53 is one of the most commonly mutated genes. So if it’s essentially absent or non-functional in about 50 percent of patients, therapies that target the 4E-BP activity such as what is called mTOR inhibitor drugs in those patients won’t work. Now we know that we’ve got to understand the p53 status of a tumour first, before beginning treatment with these inhibitors.”
He added by mentioning that things are moving towards personalized medicine. Using these techniques, if they understand the other molecular signatures operating at the same time, they can better design therapies tailored towards individual patients.
This study was published in the journal Cancer cell.