Stem cells give clues to understanding cancer and make breakthrough in childhood...( Scientists in Switzerland are uncove...),Health

Scientists in Switzerland are uncovering new clues about how cancer cells grow and how they can be killed by studying stem cells, blank cells that have the potential to develop into fully mature or differentiated cells and other scientists in UK have made a breakthrough in understanding the cause of the most common form of childhood cancer, acute lymphoblastic leukaemia (ALL). The research should lead to less aggressive treatment for the disease and could result in the development of new and more effective drugs, an international conference on stem cell biology was told last month.

The conference, organised by the European Science Foundations EuroSTELLS programme and held in Barcelona on January 10-13, heard that stem cells and cancer cells share many similar features. For example 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.

On one hand, Professor Ariel Ruiz i Altaba of the University of Geneva in Switzerland is studying key proteins in stem cells and cancer stem cells cancer cells that are later responsible for tumour growth, the recurrence of tumours and the spread of the cancer to other parts of the body[1]. Four such proteins, called Sonic Hedgehog (Shh) and Gli-1, Gli-2 and Gli-3 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 told the conference participants.

Professor Ruiz i Altabas team has been experimenting with samples of brain and other tumours from patients, treating tumour cells and their cancer stem cells the cells that continuously replenish the growing cancer in the laboratory with chemicals that inhibit the activity of the Shh pathway and lead to the inhibition of Gli-1. We t
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