An innovative chemical modification of an anti-cancer compound gives researchers the potential to seek out and kill cancer cells only, with little or no harm to normal, non-malignant cells.
Professor Jiri Neuzil from the School of Medical Science and GHI is leading a research team that has developed anti-cancer agents derived from vitamin E (VE), with the capacity to induce programmed cell death, a process known as apoptosis.
“This (chemical modification) potentially represents a new paradigm in efficient anti-cancer therapy. It has a very solid scientific basis because it sends the compounds where they matter most,” Professor Neuzil said.
“Thus, the process is much more efficient when the relevant drugs are targeted to mitochondria.”
He explained that mitochondria are organelles inside cells that contain their own DNA. While they are essential to supply the cells with energy, mitochondria also contain proteins needed to kill cells.
Working initially with Professor Smith from Otago University in New Zealand and recently with Associate Professor Marc Coster from Griffith’s Eskitis Institute, Professor Neuzil has successfully modified the VE-based drugs so that some 90 per cent of the agents localise to mitochondria, triggering the death of cancer cells much more efficiently than the non-targeted counterparts of the agents.
The process has been successfully tested on mice, focusing on breast and colorectal tumours.
“The new compounds don’t harm good cells. And they’re more efficient than (parental) compounds that don’t target mitochondria directly.
“Its potential is huge. We now want to test these agents in other types of tumours, preferably those that are hard to treat.”
Using this innovative approach, Professor Neuzil is attempting to ‘outwit’ cancer cells he describes as ‘bloody clever’.
“When cancer cells are exposed to certain agents, their genes mutate as they learn how to resist the drugs.”
However, by combining the vitamin E-derived agents with other therapeutic drugs, the cancer cell’s attention can be effectively ‘distracted’, reducing its capacity to mutate.
This combinatorial and, potentially, intermittent form of treatment also serves to reduce negative side-effects through the positive synergy of two or more drugs that exert their cancer cell-killing activity by different mechanisms.
Professor Neuzil’s pre-clinical research is also investigating if other recognised anti-cancer drugs are similarly effective in mitochondria when modified in a corresponding way.
To take the research to the important clinical stage, he is hoping to get the attentions and support of a benefactor.