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  • Proteins
  • The bcr-abl gene is constitutively active (meaning it does not require activation by other proteins), and sends signals to activate proteins and enzymes which speed up cellular division and can lead to the formation of abnormal white blood cells that proliferate to the point that they interfere with normal blood cell production, leading to leukemia. (oncolink.org)
  • treatment
  • For the treatment of chronic phase Ph+ CML in patients resistant or intolerant to prior therapy that included imatinib. (pdr.net)
  • For the treatment of newly diagnosed chronic phase Ph+ CML. (pdr.net)
  • Because both of these diseases express the BCR-ABL protein, this would render them potentially susceptible to treatment with ponatinib. (wikipedia.org)
  • Blast crisis is diagnosed if any of the following are present in a patient with CML: >20% myeloblasts or lymphoblasts in the blood or bone marrow Large clusters of blasts in the bone marrow on biopsy Development of a chloroma (solid focus of leukemia outside the bone marrow) The only curative treatment for CML is a bone marrow transplant or an allogeneic stem cell transplant. (wikipedia.org)
  • Other than this there are four major mainstays of treatment in CML: treatment with tyrosine kinase inhibitors, myelosuppressive or leukopheresis therapy (to counteract the leukocytosis during early treatment), splenectomy and interferon alfa-2b treatment. (wikipedia.org)
  • For treatment of progressive plexiform neurofibromas associated with neurofibromatosis type I, early research has shown potential for using the c-KIT tyrosine kinase blocking properties of imatinib. (wikipedia.org)