Researchers at St. Jude Children’s Research Hospital have discovered evidence that a series of genetic mutations work together to initiate most cases of an aggressive and often-fatal form of acute lymphoblastic leukemia (ALL).
These defects, known as “cooperating oncogenic lesions,” include the deletion of a gene, IKZF1, whose protein, Ikaros, normally helps guide the development of a blood stem cell into a lymphocyte. The researchers also found that loss of the same gene accompanied the transformation of chronic myelogenous leukemias (CMLs) to a life-threatening acute stage. … Continue Reading »
In a new study published in PLoS Medicine, William Evans of St Jude Children’s Research Hospital, Memphis, and colleagues provide new insight into resistance to the widely-used cancer drug methotrexate (MTX) in patients with acute lymphoblastic leukaemia (ALL), the most common cancer in children.
ALL accounts for a quarter of all new childhood cancer cases every year in the United States. Children with ALL cannot fight even simple infections because genetic changes in immature lymphocytes – the white blood cells essential to the immune system – result in these cells dividing uncontrollably and failing to mature. The proliferation of these abnormal cells reduces the ability of the bone marrow to produce healthy blood cells. Children with ALL therefore are at increased risk of infection, and bruise and bleed easily, because they do not have enough white blood cells, red blood cells and platelets important for the clotting process. … Continue Reading »
Leukaemia – cancer of blood or bone marrow – is caused by mutations that allow defective blood cells to accumulate and displace healthy blood. To devise effective therapies it is crucial to know which mutations cause leukaemia and which cell type gives rise to leukaemic cells. Researchers from the European Molecular Biology Laboratory (EMBL) in Italy, the EMBL-European Bioinformatics Institute, UK, and the Universities of Harvard, USA, and Lund, Sweden, have now used genetic engineering to introduce a mutation found in human leukaemia patients into mice. In the current issue of Cancer Cell they report that the mutation causes leukaemia by triggering innate genetic programmes that allow white blood cells to proliferate uncontrollably. The findings have implications for the way leukaemia should be treated. … Continue Reading »
Biology News reports that a research team at the Moores Cancer Center at University of California, San Diego (UCSD) have gotten a leukemia patient’s immune system to start attacking their leukemia cancer cells. To do this, the researchers modified cancer cells to make them more recognizable by the immune system. These immunity-recognizable cancer cells were then injected back into the patient so that their body could begin producing antibodies.
Basically: a vaccine for leukemia.
This works because the antibodies that are produced target a transmembrane receptor called ROR1, which is involved in the Wnt pathway. Normally our bodies destroy all immune cells that make antibodies that recognize self, which is anything that is naturally present in the body. However, this particular part of the Wnt pathway is only present early on in development, so all the ROR1 receptors are gone before the immune system develops.