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Genetic tracking identifies cancer stem cells in human patients
Date:5/15/2014

The gene mutations driving cancer have been tracked for the first time in patients back to a distinct set of cells at the root of cancer cancer stem cells.

The international research team, led by scientists at the University of Oxford and the Karolinska Institutet in Sweden, studied a group of patients with myelodysplastic syndromes a malignant blood condition which frequently develops into acute myeloid leukaemia.

The researchers say their findings, reported in the journal Cancer Cell, offer conclusive evidence for the existence of cancer stem cells.

The concept of cancer stem cells has been a compelling but controversial idea for many years. It suggests that at the root of any cancer there is a small subset of cancer cells that are solely responsible for driving the growth and evolution of a patient's cancer. These cancer stem cells replenish themselves and produce the other types of cancer cells, as normal stem cells produce other normal tissues.

The concept is important, because it suggests that only by developing treatments that get rid of the cancer stem cells will you be able to eradicate the cancer. Likewise, if you could selectively eliminate these cancer stem cells, the other remaining cancer cells would not be able to sustain the cancer.

'It's like having dandelions in your lawn. You can pull out as many as you want, but if you don't get the roots they'll come back,' explains first author Dr Petter Woll of the MRC Weatherall Institute for Molecular Medicine at the University of Oxford.

The researchers, led by Professor Sten Eirik W Jacobsen at the MRC Molecular Haematology Unit and the Weatherall Institute for Molecular Medicine at the University of Oxford, investigated malignant cells in the bone marrow of patients with myelodysplastic syndrome (MDS) and followed them over time.

Using genetic tools to establish in which cells cancer-driving mutations originated and then pro
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Contact: University of Oxford
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Source:Eurekalert

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