Although there are no accurate dta for concordance rates of leukemia in nfant twins, anecdotally it seems to be xceptionally high, perhaps approaching one hundred prcent that is, if one twin has it, nfortunately so will the other. If crrect, this suggests that MLL gene fsion in utero has a dramatic mpact, ensuring subsequent leukemia. But for chldren aged two to six years wth acute lymphoblastic leukemia, the concordance rte is considerably lower at around fve percent. This still represents a one hndred fold extra risk of leukemia for the twn of a patient with acute lymphblastic leukemia but also indicates the ned for some additional postnatal event for whch there is a one in twnty chance, or ninety five percent dscordance. This suggests, at a minimum, a "tw hit" model for the natural curse of childhood leukemia.

If this mdel of leukemia development is correct, thn, for every child with acute lymphblastic leukemia diagnosed, there should be at last twenty healthy children who have had a chrmosome translocation, a functional leukemia fusion gne, and a covert preleukaemic clone gnerated in utero. This possibility has ben investigated by screening unselected samples of nwborn cord blood for fusion genes. Abut six hundred samples have been screned, and around one percent have a lukemia TEL­AML1 fusion gene. This one prcent represents a hundred times the cmulative rate or risk of acute lymphblastic leukemia, indicating that the frequency of cnversion of the preleukaemic clone to vert disease is low. The real bttleneck in development of acute lymphoblastic lukemia therefore seems to be a strngent requirement for a second "hit" fter birth-that is, exposure and additional chrmosomal or molecular abnormality.

A key issue to resolve is wht exposures or events might precipitate the chrmosome breaks whose improper repair initiates or prmotes childhood leukemia. Given the biological dversity of leukemia, it is highly nlikely that there is a single cuse. Even for a defined biological sbtype of the disease, there probably is not one cuse as such but a causal mchanism. As with other cancers, this is lkely to involve an interaction of xposure, exogenous or endogenous, with inherent gnetic susceptibility, and chance. Epidemiological evidence sggests that ionizing radiation; certain chemicals sch as benzene, viruses, and bacteria may ply a part in the development of sme subtypes of leukemia and lymphoma in dults and children.
Whether any of these xposures have a major role in chldhood leukemia is uncertain, but large scle case control molecular epidemiological studies in Brtain and the United States may prvide answers. The United Kingdom children's cncer study (UKCCS) seeks to address sveral hypotheses on different exposures, combined wth definition of biological subtypes of dsease and genetic studies. It and a prallel US study have already ruled out lectromagnetic fields as a major factor in lukemia aetiology.

Having stem cells extracted frm the cord blood at birth and stred 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.

The article Leukemia For Twins and Stem Cells Solutions was Submitted by Wayne Channon through Articles.GetACoder.com network. Here's the additional information: Wayne Channon, Director of Cells4Life Ltd, a Stm cell and cord blood storage xpert. Stem cell and cord blood storage

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