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

We report on eight patients who were 35 to 77 years old with an isochromosome 17q as the sole structural chromosomal anomaly. Additional numerical chromosomal changes were a trisomy 8 or 17 in two cases each and a trisomy 19 in one case. Five patients had myelodysplastic syndrome (MDS) diagnosed according to the FAB nomenclature as chronic myelomonocytic leukemia (CMML) in two cases, refractory anemia with excess of blasts in transformation (RAEBt) in two cases, and refractory anemia with excess of blasts (RAEB) in one case. One patient suffered from a myeloproliferative disorder (MPS). All cases progressed to acute nonlymphocytic leukemia (ANLL) type M1, M2, or M4 in a period of 2 to 30 months after initial diagnosis, except one patient with RAEBt who died within 2 months. Two patients presented with ANLL-M2 at time of diagnosis. Treatment during the chronic phase of disease consisted of mild cytoreduction and/or substitution of platelets or red blood cells. One patient with CMML received an allogeneic bone marrow graft and relapsed after 33 months with ANLL-M1. Treatment results for overt leukemia were poor, and survival was short, lasting from 1 to 4 months. Overall survival was 1 to 37 months (median duration, 6.5 months). Molecular studies in two cases revealed neither a BCR rearrangement nor a translocation of the ABL protooncogene, as observed in Ph1-positive chronic myeloid leukemia (CML). Thus, an i(17q) anomaly seems to identify a distinct subgroup of mostly myelodysplastic and, less frequently, myeloproliferative disorders that progress rapidly to ANLL, respond poorly to chemotherapy, and are associated with short survival after transformation.
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PMID:Isochromosome 17q in Ph1-negative leukemia: a clinical, cytogenetic, and molecular study. 222 38

A 57-year-old man complains of a reduced exercise tolerance and bone pain for years. There is a past medical history of hyperuricemia and anemia of unknown etiology. In a routine examination a leukocytosis of 64,000 per ml, increased number of thrombocytes and an elevated level of lactic dehydrogenase is found. The suspected diagnosis of myeloproliferative disorder, in the present case of chronic myelogenous leukemia, is confirmed by a diminished neutrophil alkaline phosphatase activity, bone marrow biopsy and the demonstration of the Ph1 (Philadelphia) chromosome. Magnetic resonance imaging reveals an infiltration of the bone marrow. After the initial treatment with busulfan the white cell count is lowered.
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PMID:[Weakness, bone pain]. 236 65

Marrow fibroblast colony formation was studied in patients with myeloproliferative disorders, using human serum or platelet-derived growth factor plus plasma-derived serum as growth-stimulating factors. Colony numbers negatively correlated with the patient's age, but were not different from those of controls. However, both maximum and average cell numbers per colony were significantly increased in patients with chronic myelocytic leukemia (CML) as compared to controls. These results suggest that fibroblast colony-forming cells with high sensitivity to human serum mitogen(s) exist in a CML bone marrow. These may possibly be involved in one of the mechanism concerned with promoting fibrosis in this disease.
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PMID:Fibroblast colony-forming cells with high sensitivity to serum mitogen(s) exist in bone marrow of patients with chronic myelocytic leukemia. 236 40

The DNA content of bone marrow megakaryocytes was analyzed in 24 patients with myeloproliferative disorders, 23 patients with secondary thrombocytosis and 15 normal volunteers using 2-color flow cytometry. Compared with normal controls, the majority of patients with secondary thrombocytosis, polycythemia vera and essential thrombocytosis exhibited a relative increase in higher ploidy (greater than 16N) cells. In contrast, patients with chronic myelogenous leukemia exhibited an increase in lower ploidy cells (less than 16N), with a modal DNA content of 8N. Patients with myeloproliferative disorders tended to show a decrease in the 16N megakaryocyte population compared with patients with secondary thrombocytosis. No correlation between ploidy distribution and platelet count was observed.
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PMID:Analysis of megakaryocyte ploidy in patients with thrombocytosis. 240 6

In the clinical phase studies, ranimustine showed very excellent responses against chronic myelogenous leukemia, polycythemia vera and thrombocythemia, and moderate responses against lymphoma or myeloma. The feature of response was the long duration. In cases with CML, CR rate was 82% and maintained for 2-18 months by single administration. In a randomized controlled study, the efficacy of ranimustine was compared with that of busulfan in 77 evaluable previously untreated patients with CML. These included 40 patients for an MCNU group (M) and 37 for busulfan group (B). No difference was seen in the remission rate, crisis rate and survival. A significant difference was observed only in the period of CR. Ranimustine showed almost equal efficacy to that of busulfan but was superior to busulfan in patients who needed rapid responses. The side effects were mild and transient. Despite of its administration by intravenous injection, use of ranimustine seemed convenient, considering the long interval between treatments, being comparable in this respect with oral busulfan. Ranimustine, therefore, seems a very effective drug for myeloproliferative disorders.
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PMID:[Ranimustine]. 240 79

Fetal hemoglobin (Hb F) may increase in patients receiving chemotherapeutic drugs, a result of potential use in patients with symptomatic hemoglobinopathies. We examined Hb F in 13 patients with myeloproliferative disease (six polycythemia vera, five polycythemia vera with myeloid metaplasia, one agnogenic myeloid metaplasia, and one chronic myelogenous leukemia) who were treated with hydroxyurea. Four patients showed an increase in Hb F from less than 1% to between 5% and greater than 8% while on hydroxyurea, and a decline to less than 1% when the drug was discontinued. This group of "responders" received a higher average daily dose of hydroxyurea, which was administered continuously rather than intermittently, when compared to the "nonresponders." Mean corpuscular volumes (MCVs) rose in most patients, and i antigen remained elevated or decreased; neither parameter correlated with Hb F levels. Both responders and nonresponders had therapeutically desirable suppression of WBCs and platelets, and almost all had no depression of reticulocytes or Hb.
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PMID:The effect of hydroxyurea on hemoglobin F in patients with myeloproliferative syndromes. 241 68

Bone marrow and peripheral blood cells from a patient with chronic myelogenous leukemia in erythroblastic transformation were studied by flow cytometry and for hemopoietic colony growth. Results demonstrated that this disorder had greatly expanded bone marrow erythroid colony (CFU-E) and myeloid colony (CFU-GM) progenitor compartments that were totally dependent upon erythropoietin and colony-stimulating factor. DNA, RNA and cell cycle analysis revealed that the bone marrow cells were diploid, had a high percentage of S phase cells (17%), and a unique bimodal RNA index of 5 and 13.8. Results are discussed and contrasted with other myeloproliferative disorders.
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PMID:Humoral-dependent hemopoiesis and flow cytometric analysis of chronic myelogenous leukemia in erythroblastic transformation. 244 Feb 21

Platelet-derived growth factor (PDGF) is thought to take part in the genesis of bone marrow fibrosis that can be found in patients with myeloproliferative diseases. We evaluated platelet mitogenic activity as the difference between serum and plasma activity in 8 patients with myeloproliferative disease. We observed a trend of lower values in 2 cases of polycythemia vera and 2 cases of essential thrombocythemia, as seen by other authors. Two patients suffering from chronic myeloid leukemia were within the normal range. In contrast, our 2 cases of idiopathic myelofibrosis showed increased levels. If confirmed by further studies, this could suggest a pathogenetic relationship between increased levels of PDGF and bone marrow fibrosis, and give differential diagnostic significance to the PDGF mitogenic assay in myeloproliferative diseases.
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PMID:Changes in the mitogenic activity of platelet-derived growth factor(s) in patients with myeloproliferative disease. 249 60

Two further cases of acquired isodicentric (X)(q13) chromosome in patients with myeloproliferative disorders are reported. One patient had a primary myelofibrosis and the other a chronic myelogenous leukemia. DNA replication study demonstrated that both abnormal X chromosomes were late replicating in all cells examined. The inactive condition of idic(X)(q13) seems to be indicative of a selective advantage for a cell carrying this alteration.
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PMID:Isodicentric X chromosome in myeloproliferative disorders. 249 63

The number of bone marrow-derived fibroblastoid colony-forming cells (CFU-F) and the production of colony-stimulating activity (CSA) by bone marrow stromal cells were studied in 71 patients with myeloproliferative disorders (MPD). The numbers of CFU-F in chronic-phase chronic myelogenous leukemia (CML), polycythemia vera (PV) and essential thrombocythemia (ET) were not different from those in normal subjects. However, the number of CFU-F in acute-phase CML was markedly decreased. Bone marrow adipocyte colony-forming capacity (adipo-CFC), which was previously shown to reflect both the number of preadipocytes and the stromal cell function in vivo, was increased in patients with chronic-phase CML, PV and ET, but was absent in acute-phase CML patients. The production of CSA by marrow stromal cells of MPD patients, however, was not different from that of normal subjects. These results suggest that the characteristics of marrow stromal and its precursor cells of chronic-phase MPD patients were not different from those of normal subjects, however, they became changed in acute-phase CML patients.
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PMID:Bone marrow stromal cells in myeloproliferative disorders. 250 72


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