Although there are no accurate data for concordance rates of leukemia in infant twins, anecdotally it seems to be exceptionally high, perhaps approaching one hundred percent that is, if one twin has it, unfortunately so will the other. If correct, this suggests that MLL gene fusion in utero has a dramatic impact, ensuring subsequent leukemia. But for children aged two to six years with acute lymphoblastic leukemia, the concordance rate is considerably lower at around five percent. This still represents a one hundred fold extra risk of leukemia for the twin of a patient with acute lymphoblastic leukemia but also indicates the need for some additional postnatal event for which there is a one in twenty chance, or ninety five percent discordance. This suggests, at a minimum, a "two hit" model for the natural course of childhood leukemia.
If this model of leukemia development is correct, then, for every child with acute lymphoblastic leukemia diagnosed, there should be at least twenty healthy children who have had a chromosome translocation, a functional leukemia fusion gene, and a covert preleukaemic clone generated in utero. This possibility has been investigated by screening unselected samples of newborn cord blood for fusion genes. About six hundred samples have been screened, and around one percent have a leukemia TELAML1 fusion gene. This one percent represents a hundred times the cumulative rate or risk of acute lymphoblastic leukemia, indicating that the frequency of conversion of the preleukaemic clone to overt disease is low. The real bottleneck in development of acute lymphoblastic leukemia therefore seems to be a stringent requirement for a second "hit" after birth-that is, exposure and additional chromosomal or molecular abnormality.
A key issue to resolve is what exposures or events might precipitate the chromosome breaks whose improper repair initiates or promotes childhood leukemia. Given the biological diversity of leukemia, it is highly unlikely that there is a single cause. Even for a defined biological subtype of the disease, there probably is not one cause as such but a causal mechanism. As with other cancers, this is likely to involve an interaction of exposure, exogenous or endogenous, with inherent genetic susceptibility, and chance. Epidemiological evidence suggests that ionizing radiation; certain chemicals such as benzene, viruses, and bacteria may play a part in the development of some subtypes of leukemia and lymphoma in adults and children.
Whether any of these exposures have a major role in childhood leukemia is uncertain, but large scale case control molecular epidemiological studies in Britain and the United States may provide answers. The United Kingdom children's cancer study (UKCCS) seeks to address several hypotheses on different exposures, combined with definition of biological subtypes of disease and genetic studies. It and a parallel US study have already ruled out electromagnetic fields as a major factor in leukemia aetiology.
Having stem cells extracted from the cord blood at birth and stored in a cord blood bank or a stem cells bank is a way to protect your child from future diseases.
It can be very useful as it contains hematopoietic stem cells, progenitor cells. The stem cells in the cord blood are mainly used to treat blood and immune system related genetic diseases, cancers and blood disorders like diabetes or leukemia.