Stanford University has used the single-cell gene expression capabilities of Fluidigm integrated fluidic circuits (IFCs) to identify the source of cancer stem-cells' resistance to radiation.
Researchers applied the properties of the Fluidigm chip to isolate individual molecules and help prove their hypothesis on the relative resistance of cancer stem-cells to radiation.
In a paper entitled 'Association of Reactive Oxygen Species Levels and Radioresistance in Cancer Stem-Cells', published in the 4 February 2009 issue of Nature Magazine, researchers found that there was a protective pathway that shielded the stem cells - even cancer stem-cells - from DNA damage.
When this pathway was blocked, the cells became more susceptible to radiation treatment.
In a Stanford University press release, Dr Robert Cho, a clinical instructor of pediatrics, said: 'Our ultimate goal is to come up with a therapy that knocks out the cancer stem-cells.' Cho and radiation oncologist and post-doctoral fellow Dr Maximilian Diehn, PhD, are co-first authors of the publication.
They collaborated with scientists at Stanford and City of Hope National Medical Center to conduct the research.
They studied breast epithelial stem-cells from humans and mice to unravel why cancer stem-cells are more resistant to radiation than other cancer cells.
Gajus Worthington, chief executive officer of Fluidigm, said: 'Fluidigm's Biomark system was used to identify one of the pathways that helped to explain the radio-resistance of single cancer stem-cells.
'The team was able to then show that by inhibiting this pathway, the resistance was reduced.' Unlike most cells in the body, which are relatively expendable, stem cells are difficult to kill.
When these researchers looked at gene expression levels, the human breast-cancer stem-cells were churning out much higher levels of antioxidant proteins than non stem-cells.
Dr Michael Clarke, the associate director of the Stanford Institute for Stem Cell and Regenerative Medicine, said: 'The resistance observed in the breast-cancer stem-cells seems to be a similar if not identical mechanism to that used by normal stem-cells.' Clarke, who discovered the first cancer stem-cells in a solid tumour, is a member of the Stanford Cancer Center and the senior author of the research.
He added: 'Although your body would normally eliminate cells with chromosomal damage, it also needs to spare those cells responsible for regenerating and maintaining the surrounding tissue: the stem cells.
'It's protective.' This protection backfires in the case of cancer, however.
Clarke added: 'Basically we need to figure out a way to inactivate that protective mechanism in cancer cells while sparing normal cells.' For many patients, it is a life-or-death question.
