This is yet another in compound that has been found to have anticancer properties in vitro. How many of these have we seen in the last few years on the Beacon? Quite a few.
The challenge is being able to follow through with studies needed to get to human clinical trials, which are lot more expensive and time consuming. I hope this is not the last we hear of oleocanthalidomide. It will be interesting to see if oleocanthal supplements start to appear on the market, or if this is something that will be seen by the FDA as a drug or a supplement. What is the toxicity, if any, of concentrated oleocanthal? Can it be IV administered?
In the meantime, though, I will make my olive oil extra virgin.
News Article:
"Olive Oil Compound Kills Cancer Cells In Less Than An Hour: All-Powerful Oleocanthal," Medical Daily, Feb 20, 2015 (link to article)
Excerpt:
"What they found was that oleocanthal was destroying the cancer cells’ waste centers, known as lysosomes, which are larger than healthy cells and also more fragile. “Once you open one of those things, all hell breaks loose,” Breslin said. They provide a necessary stabilizing function for the cell. After oleocanthal did its damage, critical functions began to suffer and the cell soon died. Plus, healthy cells stayed intact. After oleocanthal “put them to sleep” for a day, they rebounded as if nothing had happened."
Related journal article:
O LeGendre et al, ,"(-)-Oleocanthal rapidly and selectively induces cancer cell death via lysosomal membrane permeabilization (LMP)," Molecular & Cellular Oncology, Jan 23, 2015 (link to abstract)
Abstract:
(-)-Oleocanthal (OC), a phenolic compound in extra virgin olive oil (EVOO), has been implicated in the health benefits associated with diets rich in EVOO. We investigated the effect of OC on human cancer cell lines in culture.
Amazingly, OC induced cell death in all cancer cells examined – as rapidly as 30 minutes after treatment in the absence of serum. OC treatment of non-transformed cells suppressed proliferation, but did not cause cell death. OC induced both primary necrotic and apoptotic cell death via induction of lysosomal membrane permeabilization (LMP).
We provide evidence that OC promotes LMP by inhibiting acid sphingomyelinase (ASM) activity, which destabilizes the interaction between proteins necessary for lysosomal membrane stability.
The data presented here indicates that cancer cells having fragile lysosomal membranes – as compared to non-cancerous cells – are susceptible to lysosomotropic agent-induced cell death. Therefore, targeting lysosomal membrane stabiltiy represents a novel approach to induce cancer-specific cell death.
