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"This body of research is a culmination of decades of work, and at last provides a credible explanation for how the major type of childhood leukemia develops.The research strongly suggests that ALL has a clear biological cause, and is triggered by a variety of infections in predisposed children whose immune systems have not been properly primed.The research in his lab at The Institute of Cancer Research (ICR) was largely funded by the charities Bloodwise and The Kay Kendall leukemia Fund.
The goal of this trial was to assess the toxicity and potential efficacy of high-dose topotecan, melphalan and cyclophosphamide as a preparative regimen for patients with multiple myeloma undergoing autologous stem cell transplantation....
more The goal of this trial was to assess the toxicity and potential efficacy of high-dose topotecan, melphalan and cyclophosphamide as a preparative regimen for patients with multiple myeloma undergoing autologous stem cell transplantation.
Professor Mel Greaves, Director of the Centre for Evolution and Cancer at The Institute of Cancer Research, London, said: "I have spent more than 40 years researching childhood leukemia, and over that time there has been huge progress in our understanding of its biology and its treatment -- so that today around 90 per cent of cases are cured.
But it has always struck me that something big was missing, a gap in our knowledge -- why or how otherwise healthy children develop leukemia and whether this cancer is preventable.
It also busts some persistent myths about the causes of leukemia, such as the damaging but unsubstantiated claims that the disease is commonly caused by exposure to electro-magnetic waves or pollution.
"I hope this research will have a real impact on the lives of children.
Professor Greaves is now investigating whether earlier exposure to harmless 'bugs' could prevent leukemia in mice -- with the possibility that it could be prevented in children through measures to expose them to common but benign microbes. Firstly, while patterns of exposure to common infections appear to be critical, the risk of childhood leukemia, like that of most common cancers, is also influenced by inherited genetic susceptibility and chance.
Secondly, infection as a cause applies to ALL specifically -- other rarer types including infant leukemia and acute myeloid leukemia probably have different causal mechanisms.
Instead, he presented strong evidence for a 'delayed infection' theory for the cause of ALL, in which early infection is beneficial to prime the immune system, but later infection in the absence of earlier priming can trigger leukemia.
Professor Greaves suggests that childhood leukemia, in common with type I diabetes, other autoimmune diseases and allergies, might be preventable if a child's immune system is properly 'primed' in the first year of life -- potentially sparing children the trauma and life-long consequences of chemotherapy.