Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of chronic myelogenous leukemia (CML) of 10-year survival in described. A 44-year old male was admitted to our hospital because of general malaise, abdominal fullness and fever in February, 1977. On physical examination, giant splenomegaly and hepatomegaly were detected. Peripheral blood examination revealed leukocytosis without hiatus leukemia , normochromic macrocytic anemia and thrombocytosis. NAP rate and score were 16% and 22. Cytogenetic analysis of PB without stimulator revealed 46, XY, Ph1. Then he was diagnosed as having a typical type of Ph1-positive CML. He had been successfully treated over 9 years by intermittent administration of busulfan. However, anemia suddenly progressed in February, 1986 followed by leukopenia and thrombocytopenia. Hemorrhage was not detected by the examination. Though he had been received blood transfusion, the anemia progressed rapidly. He was died of cachexia on 4th of August, 1987. The postmortem examination revealed bone marrow aplasia with no signs of blast crisis nor myelofibrosis. Secondary hemochromatosis was seen in the liver, spleen, pancreas and some other organs.
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PMID:[Bone marrow aplasia without blast crisis in a case of CML of 10-year survival]. 279 87

In May 2006, a 72-year-old man with acute myelogenous leukemia (M4Eo) was admitted to our hospital. He had been receiving antiandrogen treatment for prostate cancer (after an operation in 1998) and treatment for diabetes mellitus. He received chemotherapy according to the JALSG GML200 protocol, which led to complete remission; however, in January 2007, his leukemia recurred. CAG combination chemotherapy also resulted in complete remission by May 2007. In August 2007, he developed multiple liver tumors, abdominal pain, and fever. Contrast-enhanced computed tomography revealed hypovascular tumors in both early and delayed phases. Angiography showed ring-like tumor staining and a massive tumor, similar to those seen in metastatic hepatocellular carcinomas (HCCs). He eventually died because of aggressive enlargement of liver tumors during the following month accompanied by the simultaneous recurrence of leukemia and unsuccessful embolization of the hepatic artery. Autopsy specimens showed fibrosis and considerable iron deposition in the liver, suggested secondary hemochromatosis due to transfusion. We also detected multiple moderately differentiated primary HCCs. Secondary hemochromatosis, androgen imbalance, and humoral factors from leukemic cells were believed to be the causes of the rapid onset and development of HCCs.
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PMID:Multiple hepatocellular carcinomas developed 15 months after commencement of chemotherapy for elderly acute myelogenous leukemia. 2000 36