Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 39-year-old Japanese female who had been followed as chronic myelogenous leukemia (CML) since 1984 was admitted to our hospital because of dizziness. On admission, platelet count markedly increased (245 X 10(4)/microliters) in spite of daily administration of busulfan 2 mg. She was diagnosed as accelerated phase CML with thrombocytosis. So we tried to use interferon alpha (IFN-alpha) finally given in a dose of 9 X 10(6) U daily by subcutaneous injection. After that, platelet count decreased to 70 X 10(4)/microliters and megakaryocyte count in bone marrow decreased from 887.5/microliters to 395.7/microliters. But we had to stop IFN-alpha because of severe side effects.
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PMID:[Thrombocytosis in chronic myelogenous leukemia (CML) controlled by interferon alpha (IFN-alpha)]. 276 64

A clinicopathological study was performed on 46 patients with chronic myeloproliferative diseases (CMPD) showing a thrombocythemia in excess of 1,000 x 10(9)/liter. When applying rigid diagnostic criteria only 23 patients were compatible with the initially suspected diagnosis of primary thrombocythemia (PTH). Comparison of PTH with the other entities of CMPD (CGL, 10, AMM, 6, and polycythemia, 7 cases) revealed a sustained elevation of the platelet count observable over a period of 2 to 8 years, no marked leukocytosis or abnormalities of the differential blood count, and a normal score of the leukocyte alkaline phosphatase. Episodes of hemorrhage and thrombosis as well as neurological symptoms (paresthesias, dizziness, headache), were encountered frequently as clinical manifestations in PTH. Survival time in PTH was significantly longer than in CGL with accompanying thrombocythemia. In a consecutively biopsied population of patients with CMPD, incidence of PTH was about 8%. In PTH the characteristic histopathology of the bone marrow consisted of an isolated (monolinear) proliferation of the megakaryocytes (density 127 +/- 47/mm2) without gross abnormalities of this cell lineage or a conspicuous increase in neutrophilic granulo- or erythrocytopoiesis. These lesions are significantly different from the morphological findings in the other CMPD with extreme thrombocytosis.
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PMID:Chronic myeloproliferative diseases with an elevated platelet count (in excess of 1,000,000/microliter): a clinicopathological study on 46 patients with special emphasis on primary (essential) thrombocythemia. 350 37

Imatinib mesylate targets the adenosine triphosphate (ATP)-binding sites of the protein tyrosine kinase domains associated with Bcr-abl, the platelet-derived growth factor (PDGF) and c-kit. In idiopathic myelofibrosis (IMF) PDGF is considered to be one of the growth factors responsible for the development of bone marrow fibrosis. Recently, it has been shown that imatinib has antifibrogenic effect on bone marrow fibrosis in chronic myelogenous leukemia. Treatment with imatinib alone in IMF has been associated with significant side effects. In this study, the safety and efficacy of imatinib therapy in IMF, either administered as a single agent or in combination with hydroxyurea (HU) and/or alpha-interferon (IFN-alpha) are evaluated. Eleven patients (median age, 63 years; range, 33-82 years) with IMF (n = 8) or postpolycythemic myelofibrosis (PPMF) (n = 3) were studied All patients had been treated with HU (n = 9) and/or IFN (n = 7) before study entry. In all but one patient, treatment with these agents was discontinued when imatinib therapy was instituted. One patient continued IFN when treatment with imatinib was started. Imatinib was given at a dose of 400 mg/day. Nine patients were in an advanced disease phase. The patients have been followed for a median period of 2 months (range, 0.5-12 months). Treatment with imatinib has been stopped in six patients (55%), because of overt side effects (n = 4), recurrence of transitory dizziness and visual defects owing to a rising platelet count (n = 1), or the occurrence of an acute subdural hemorrhage that was evacuated without neurological deficits (n = 1). In nine patients imatinib treatment was followed by a rise in leukocyte and platelet counts that required combination with HU or IFN. The combined treatment modalities were followed by a rapid decrease in cell counts and were well tolerated apart from IFN side effects. A beneficial effect of imatinib was documented in three patients. It is concluded that leukocytosis and thrombocytosis are seen in most patients with myelofibrosis during treatment with imatinib. Combination therapy with HU or IFN seems safe and well tolerated and followed by a decrease in disease activity. A subgroup of patients in an early disease phase might benefit from imatinib therapy alone.
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PMID:Imatinib mesylate in idiopathic and postpolycythemic myelofibrosis. 1463 3

A 68-year-old man complained of dizziness and was referred to our hospital by his primary physician for evaluation of an elevated leukocyte count. In April 2002, soon after the chronic phase of chronic myeloid leukemia had been diagnosed, he was treated with imatinib. In March 2010, imatinib treatment was completed and the BCR/ABL fusion gene had become undetectable by real time quantitative PCR. Subsequently, leukocyte counts and the hematocrit gradually rose. In August 2012, a bone marrow aspirate showed hypercellular marrow with marked erythroid hyperplasia and the presence of the JAK2 gene V617F mutation. He was diagnosed with polycythemia vera. Phlebotomy and chemotherapy were started in addition to imatinib administration. Shortly thereafter complete blood counts returned to normal levels.
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PMID:[Polycythemia vera developed after a major molecular response to imatinib mesylate treatment in a patient with chronic myelogenous leukemia]. 2468 42

In the present study, a case of chronic myeloid leukemia (CML) with complete situs inversus in a 68-year-old female patient was reported. The patient presented with general weakness, abdominal distension and tenderness in the right hypochondrium. A chest X-ray revealed a right-sided heart. Ultrasonography revealed situs inversus totalis. A bone marrow smear demonstrated CML in the accelerated phase. Imatinib mesylate was subsequently administered; the patient stopped taking imatinib mesylate following discharge from the hospital. The patient presented with dizziness, fatigue, and abdominal distention and pain 1 year subsequently. A bone marrow smear demonstrated CML in the blast crisis phase; CML had progressed to acute myeloid leukemia (AML) M2a. The patient was treated with imatinib mesylate and cytarabine. After 5 days, the white blood cell count had decreased compared with that measured at the time of admission, and the previous relevant symptoms had disappeared. The patient succumbed to AML 3 months after discharge from the hospital. Situs inversus totalis is an uncommon congenital anomaly that often occurs concomitantly with other disorders. The present study documented, to the best of our knowledge, the second recorded case of CML in a patient with situs inversus totalis. Previous studies on the pathogenesis of situs inversus have suggested it is caused by embryonic cells failing to rotate normally during early embryonic development. Although there are case reports of situs inversus totalis in patients with cancer, there are few reports on the association between situs inversus totalis and cancer. The present study examined a case of CML with situs inversus totalis and assessed whether the latter may be associated with cancer.
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PMID:A patient with chronic myeloid leukemia and situs inversus totalis: A case report. 2934 83

Lineage switch is very rare in blastic crisis of chronic myeloid leukemia (CML-BC). Here, we report a case of CML-BC in which the blast lineage switched from myeloid to B-lymphoid. A 35-year-old male was initially admitted to our hospital because of abdominal distention for over a year and dizziness for one week. Prior to presentation at our hospital, he visited a local hospital because of abdominal distention where his white blood cell count and bone marrow (BM) smear indicated CML. Results from peripheral blood (PB) counts, bone marrow analysis, immunophenotyping by flow cytometry, and the detection of the Philadelphia chromosome were consistent with a diagnosis of myeloid blast crisis from CML. The patient received chemotherapy with imatinib for induction, which diminished the number of blasts. However, after three months, the blasts were increased in the PB and BM. The BM study and immunophenotyping by flow cytometry revealed B-lymphoblastic leukemia. In accordance with his first admission, a chromosome study revealed a karyotype of 46, XY, t(9; 22)(q34; q11) in all 20 cells analyzed, and B-lymphoblastic transformation from CML was diagnosed. Despite three months of treatment with DVCP (daunorubicin, vincristine, cyclophosphamide and prednisone) chemotherapy in combination with dasatinib, the patient did not achieve complete remission. The patient decided to stop treatment and was discharged from the hospital for financial reasons. This case implicates the Philadelphia chromosome with p210 BCR-ABL1 fusion proteins as a key molecule in CML-BC. Further research is needed to assess the frequency, treatment, and prognosis of CML-BC patients with lineage switch.
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PMID:Myeloid Blast Crisis of Chronic Myeloid Leukemia Followed by Lineage Switch to B-Lymphoblastic Leukemia: A Case Report. 3236 84