Targeted cancer treatment: new dual strategy halts cell division, study finds
The next step is to verify the concept in in vivo studies
A team of researchers at the MedUni Vienna in Austria has confirmed in a recent study a new concept for the targeted treatment of ovarian cancer. The concept is intended to better control the development of resistance and improve treatment outcomes. The strategy focuses on halting tumour growth by inhibiting two signal networks instead of just one.
The promising results were presented at the recent ECC2015 conference.
Targeted cancer treatment is designed to block the signalling networks used by tumour cells. This stops the malignant cells from receiving signals which lead, for example, to cell growth or cell death. Usually the structures involved are proteins, known as receptors, which are found in abundant numbers on the surface of the tumour cells or inside it and which pick up these signals and pass them on, ultimately causing degeneration of the cell.
Until now, the primary focus for treatment was the cell division signalling pathways, i.e. the mechanisms that prompt the cell to divide and grow.
Our idea was to block a second signalling system in order to improve the impact of the substance being used
Thomas Grunt from the University Department of Internal Medicine I, Head of the CCC Research Cluster Cell Signalling and Metabolism and leader of the new study, says: 'Unfortunately, malignant cells are very flexible and develop resistances to the new, targeted therapeutic agents we use. This is the biggest problem in oncology. Our idea was therefore to block a second signalling system in order to improve the impact of the substance being used.'
One such network involves metabolic pathways, which are also responsible for the establishment of the cell structure, energy gain and cell nutrition. Since malignant cells have a hyperactive fatty acid metabolism, the team of researchers took a closer look at this in their current study.
'We investigated how the two signalling pathways interact with each other at molecular level and we were able to identify an enzyme known as PI3K-mTORC1 kinase as the central interface for both systems,' says Grunt.
'Cell tests have shown that inhibiting this enzyme leads to cell death and reduces the rate of cell division.'
The next step is to test which of the substances that are already available for inhibiting PI3K-mTORC1 also work in humans.
