To understand better how cancer cells grow and how they can be killed, Swiss scientists are studying stem cells. In the mean time a UK research group has taken a step forward in understanding the cause of acute lymphoblastic leukaemia (ALL), the most common form of childhood cancer.
These facts were revealed during an international conference on stem cell biology, organised by the European Science Foundation's EuroSTELLS programme in Barcelona, last month.
The conference was also told that stem cells and cancer cells share many similar features. Those making presentation suggested that the cellular machinery that sends signals between stem cells to tell them when and how to develop is in many cases similar to the signalling mechanisms that operate between cancer cells.
Professor Ariel Ruiz i Altaba of the University of Geneva in Switzerland talked about four proteins — namely Sonic Hedgehog (Shh) and Gli-1, Gli-2 and Gli-3 — that act through a biochemical pathway to send important signals between cells.
"We have shown that interfering with Shh signalling decreases the size of tumours, which is proof of principle that the tumours require the pathway," Professor Ruiz i Altaba said.
"We take tumour samples and grow them in a variety of ways. When we treat them with inhibitors that block the Shh-Gli pathway, they all respond, demonstrating that every tumour we have tested requires this signalling pathway," the researcher added.
Meanwhile, Dr Manel Esteller of the Spanish National Cancer Research Centre (CNIO) in Madrid has been investigating the way that genes in cancer cells and stem cells are modified by a process called methylation, wherein some of the genes in a cell are rendered 'silent' by the attachment of chemical entities called methyl groups.
"We have seen that in some leukaemias there is a gene involved in differentiation that is methylated. In cultured cells we see that if we put the unmethylated gene back into the cell, we stop the growth of the cells in culture, and also in mouse models. This gene is acting as a tumour suppressor," Dr Esteller said.
The hope is that further investigation of factors such as DNA methylation could lead to potential new treatments for cancer.
Professor Tariq Enver of the Weatherall Institute for Molecular Medicine at the University of Oxford, who presented findings of his research on acute lymphoblastic leukaemia (ALL), said that his study had shown for the first time the existence of cancer stem cells in ALL.
Comparing the blood of three-year-old identical twins (one had the disease, while the other was healthy), the researchers found that both twins had genetically abnormal blood cells —'pre-leukaemic' stem cells that reside in the bone marrow.
It appears that these cells can either lay dormant or can somehow be triggered to develop into full-blown leukaemia stem cells. According to the researchers, these cells arise from an abnormal fusion of two genes during the mother's pregnancy.
Professor Enver said: "This research means that we can now test whether the treatment of acute lymphoblastic leukaemia in children can be correlated with either the disappearance or persistence of the leukaemia stem cell. Our next goal is to target both the pre-leukaemic stem cell and the cancer stem cell itself with new or existing drugs to cure leukaemia while avoiding the debilitating and often harmful side effects of current treatments."