The role of the p53 molecule is to prevent cells from becoming cancerous. However, in the neuroblastoma cells, Professor Latchman and his colleagues have discovered that another molecule, called Brn-3a, is involved. This molecule appears to activate the Bcl-2 gene, suggesting that it may be responsible for making these cells become cancerous. With support from AICR, Professor Latchman and his colleagues will be studying the way these two molecules control the Bcl-2 gene and how this influences the growth and division, or death, of these cancer cells. If we could find a way to tip the balance from molecules that activate oncogenes, to molecules that turn them off, we might be able to develop this into a new way to treat these cancers.
All cells have a complex internal mechanism which controls everything they do.
This same mechanism controls how rapidly the cells grow and divide and whether they die out or not. In other words, it controls whether the cells are cancerous or normal. This internal control mechanism is made up of many different genes, some of which control the activity of the cell and others which control the activity of the genes themselves.