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Mouse Models To Determine The Cause Of Aggressive Leukemia

According to the research conducted by the scientists at St. Jude Children’s Research Hospital it was found that mutation and loss of tumor suppressor gene resulted in aggressive leukemias.// Researchers have used mouse models to determine the reason behind aggressive nature and drug resistant nature of the acute lymphoblastic leukemia (ALL). The investigators found that the combination of a mutation called Bcr-Abl and the loss of both copies of the tumor suppressor gene Arf in bone marrow cells triggers an aggressive form of ALL. Loss or inactivation of both Arf genes resulted in the multiplication of leukemic cells. These cells later did not respond to the drug imatinib. Imatinib is used to treat chronic myelogenous leukemia (CML), another blood cell cancer caused by the Bcr-Abl mutation.

Hence the St. Jude study provided evidence that imatinib resistance in mouse models of ALL did not depend on the presence of Bcr-Abl and the loss of Arf genes in the cancer cells. But depends on the interaction of the tumor cells with specific growth-promoting factors produced in the mice. When the leukemic cells from mice that had failed imatinib therapy were removed JAK kinases, which inhibits enzymes restored the cells’ imatinib sensitivity. The study’s findings were published in the journal of Proceedings of the National Academy of Sciences. The Bcr-Abl oncogene is formed when a fragment of the Bcr gene from one chromosome switches over to fuse with a portion of the Abl gene from the other chromosome. Bcr-Abl encodes for an enzyme called a tyrosine Kinase. This causes the abnormal, uncontrolled multiplication of leukemic cells. It was also shown that by inhibiting the Bcr-Abl kinase with imatinib durable remissions of cancer with minimal side effects in patients with CML was possible.

But imatinib has proven less effective in treating ALL patients with the Bcr-Abl mutation, and the basis of drug resistance in this disease is not clearly understood. But C
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