Subject(s)
Immunologic Deficiency Syndromes/complications , Immunologic Deficiency Syndromes/diagnosis , Lymphohistiocytosis, Hemophagocytic/complications , Lymphohistiocytosis, Hemophagocytic/diagnosis , Piebaldism/complications , Piebaldism/diagnosis , Female , Humans , Primary Immunodeficiency Diseases , Young AdultABSTRACT
Treatment options for chronic myeloid leukemia (CML) have changed dramatically during the last decades. Interferon-alpha treatment and stem cell transplantation (SCT) clearly improved survival over conventional chemotherapy and offered the possibility of complete and durable responses. With the advent of the small molecule inhibitor imatinib mesylate (Glivec((R)), Gleevectrade mark) targeting the causative Bcr-Abl oncoprotein, the era of molecular cancer therapy began with remarkable success especially in chronic phase patients. Today, imatinib is the first-line treatment for CML. However, imatinib does not appear to be capable to eliminate all leukemia cells in the patients and pre-existing as well as acquired resistance to the drug has been increasingly recognized. To overcome these problems, several strategies involving dose escalation, combinations with other agents, and novel Bcr-Abl inhibitors have been developed.
