On February 7, the journal Science Translational Medicine saw the publication of a new study stating that, as peculiar as this may sound, a small-molecule drug might hold the key for curing cancer.The scientists who investigated the TIC10 molecule and its effect on cancer cells explain that, as far as mice are concerned, said molecule is quite capable of setting the body's very own tumor-destroying systems in motion.
More precisely, this molecule calls into action a protein known to scientists as tumor-necrosis-factor-related apoptosis-inducing ligand (or TRAIL, for short).
Furthermore, it makes TRAIL go into overdrive, something which translates into the cancer cells' being made to self-destruct.
Nature quotes Wafik El-Deiry, the study's lead author and an oncologist currently working with the Pennsylvania State University in Hershey, who commented on the findings on this research as follows:
“TRAIL is a part of our immune system: all of us with functional immune systems use this molecule to keep tumors from forming or spreading, so boosting this will not be as toxic as chemotherapy.”
According to the same source, the experiments carried out by Wafik El-Deiry and his fellow researchers have shown that, apart from being quite efficient in treating more run-off-the-mill (so to speak) types of cancer, this new therapy can also successfully tackle hard-to-treat brain tumors.
In fact, as oncologist Wafik El-Deiry puts it, “We didn’t actually anticipate that this molecule would be able to treat brain tumors — that was a pleasant surprise.”
Interestingly enough, TIC10 triggers the TRAIL gene not just in cancerous cells, but also in healthy ones, which basically means that, courtesy of a so-called “bystander effect,” healthy cells can be made to contribute to the demise of the cancerous ones.
For the time being, experiments having to do with using the TIC10 molecule to treat cancer have only been carried out on mice.
Still, researchers believe that, soon enough, they will be able to debut clinical studies on human patients.