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)

Myeloid committed stem cells belong to a subpopulation of small nucleated cells, which are defined by their capacity to form colonies of mature myeloid cells in agar-medium. They are termed "Colony forming Unit, CFUC", and such cells are detectable in bone marrow and peripheral blood. Bone marrow cells from 15 control patients with regular myelopoiesis contained 86 +/- 46 CFUC/10(5) bone marrow cells and 23 +/- 14 CFUC/ml blood. In 10 patients with aplastic anemia, only 0-10, 5 CFUC/10(5) BM-cells were found and no CFUC were detectable in the peripheral blood. 17 patients with chronic myeloid leukaemia showed a moderate elevation of bone marrow CFUC (X = 105), while the circulating CFUC were markedly elevated (105-42.000/ml). The circulating CFUC were closely correlated with the number of leukocytes (p less than 0,001). In 12 patients with primary osteomyelofibrosis, the number of circulating CFUC was also (raised (325-22.199/ml) and again, a correlation with the number of leukocytes was observed (p less than 0,05). As, on the other hand, there was no difference in the leukocyte count between the control group and patients with osteomyelosclerosis, the simultaneous assessment of circulating leukocytes and CFUC proves a diagnostic tool. Pancytopenia with a hypercellular bone marrow results from either neoplastic or metabolic alterations of haemopoiesis; in pancytopenia with neoplastic infiltration or transformation, the number of CFUC was lowered, whereas it was slightly elevated in pancytopenia due to metabolic alterations. In patients with acute leukaemia, only a minority of cells was capable of proliferation in vitro. The growth of leukaemic cells in culture, their prolonged survival along with the expression of functional properties may be clinically used for a more subtle classification of blast populations. The data on patients with acute leukaemia indicate, that basic mechanisms of normal blood cell regulation operate in leukaemic haemopoiesis as well.
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PMID:[The determination of myeloid-committed stem cells in systemic disorders of myelopoiesis: implications for physiopathology, diagnosis and prognosis]. 694 36

Four cases of acute myelogenous leukemia and six cases of chronic myelogenous leukemia after treatment with azathioprine and prednisone for renal allotransplantation have been described in the literature. We report another two cases of acute leukemia 10 and 5 years after successful renal allotransplantation. Patient 1, a 29-year-old farmer, exhibited the signs of acute lymphatic leukemia resistent to treatment with cytostatic agens. Death was due to pneumonia. Patient 2, a 47-year-old salesman, developed pancytopenia together with splenomegaly. After splenectomy an atypical subacute myeloid leukemia became apparent which was not treated due to withdrawal of the patient. He died 2 months after diagnosis. Both patients received long-term immunosuppressive therapy with azathiopine and prednisone until the leukemia was diagnosed. A relationship between long-term immunosuppression and the occurrence of leukemia is postulated.
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PMID:[Acute leukemia after kidney allotransplantation (author's transl)]. 699 44

A patient with Philadelphia positive chronic granulocytic leukemia in clinical remission is described, who developed Shigella dysentery complicated by fatal toxic megacolon, pancytopenia and bone marrow aplasia. The difficulties of differential diagnosis between active ulcerative colitis and Shigella dysentery and problems relating to the management of these two disorders are discussed. Leukocyte function in chronic granulocytic leukemia and its role in infection in these patients is also briefly reviewed. The rare association of bone marrow aplasia and Shigellosis is stressed.
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PMID:Fatal Shigella dysentery complicated by toxic megacolon and bone marrow aplasia in a patient with chronic granulocytic leukemia in remission. 700 62

Acute myelofibrosis (AMF) was diagnosed in a 59-yr-old black male in September 1978, on the basis of pancytopenia, lack of hepatosplenomegaly, fibrosis of the marrow, and paucity of teardrop red blood cells in the peripheral blood. Since then the patient has demonstrated an unusually long survival of 36 mo with a changing cytogenetic course. His initial 46, XY normal karyotype changed in 20 mo to trisomy 8, followed 1 yr later by 1:4 translocation in peripheral blood. Simultaneously with these changes, the fibrosis in the bone marrow progressively decreased, ultimately terminating in chronic granulocytic leukemia-like presentation with reversal to 46, XY karyotype. Fibroblast culture failed to show any evidence of cytogenetic abnormalities. The disappearance of fibrosis confirmed by trichrome and reticulin stains and lack of cytogenetic abnormalities in fibroblasts confirms the secondary role of fibrosis.
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PMID:Karyotypic polymorphism in acute myelofibrosis. 711 54

Increased numbers of bone marrow mast cells were found in 45 (2.2%) of 2,000 bone marrow specimens obtained from patients who had hematologic disorders. Mast cells were most frequently seen in the marrows of patients who had preleukemic syndromes, lymphoproliferative disorders, and acute leukemia. The 16 patients who had preleukemic syndromes included those with refractory sideroblastic and megaloblastic anemia (with or without an excess of blasts), idiopathic pancytopenia or pure erythrocytic aplasia, paroxysmal nocturnal hemoglobinuria, idiopathic refractory neutropenia, agranulocytosis or thrombocytopenia, and persistent eosinophilia. Five of the seven patients who had acute leukemia had nonlymphoblastic leukemia; two had blastic crisis of chronic granulocytic leukemia. Of the 13 patients who had lymphoproliferative disorders, eight had chronic lymphocytic leukemia, three had macroglobulinemia, and two had non-Hodgkin's lymphoma. Three patients who had chronic renal failure associated with severe anemia and two who had chronic liver disease, splenomegaly, or hypersplenism were also encountered. In this study there appeared to be a consistent relationship between the presence of increased numbers of mast cells and the lymphocyte and plasma cell counts in the bone marrow. The significance of the presence of secondary mastocytosis in premalignant lesions, neoplasia, and, in particular, lympho- and myeloproliferative disorders, is still unclear.
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PMID:Increased bone marrow mast cells in preleukemic syndromes, acute leukemia, and lymphoproliferative disorders. 745 27

Interferons (INF) are glycoproteins with protean antiviral, immunomodulator, and antiproliferative actions. In Haematology, IFN-alpha is the most widely used. Diffusion into the spleen, bone marrow and liver is good. Hairy cell leukemia is probably the malignant blood disorder which responds best to IFN. At some time during their treatment, nearly 90% of the patients require IFN. Treatment initiation is indicated when pancytopenia (polynuclear neutrophils below 1 x 10(9)/L) develops or in case of a very voluminous spleen. IFN-alpha 2a, 2b and 2c are active (leukocyte IFN is used less often, as is IFN-beta; IFN-gamma is ineffective). The standard dose is 3 x 10(6) U, three times a week for 12 weeks. Smaller doses and maintenance treatment is sometimes proposed. Haematological remission occurs in almost all cases, if not a misdiagnosis must be considered (villous lymphocyte lymphoma). Relapse usually occurs at the end of treatment, but sensitivity to IFN is not altered and final survival is improved. Nearly 90% of the patients are alive at 4 years. Although IFN is active in chronic myeloid leukemia, research in this area continues. Clinical trials have reported haematologic relapse in 90% and complete cytogenetic response in 15 to 35% of the patients. The effect on Ph+ cells is not observed with classical chemotherapies. Initial dose is generally 5 x 10(6) U/m2/day. High doses are not always well tolerated, but cytogenetic response is only seen in patients in haematologic and cytopenic remission. IFN therapy improves survival over classical treatments (median 62 versus 39 months). Survival is better after good cytogenetic response or complete remission. Combined chemo-IFN therapy is currently under study in an attempt to improve cytogenetic response. In terms of the molecular biology however, residual disease is almost always present and relapse is frequent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Interferons. Treatment of malignant hemopathies with interferons]. 751 80

A 45-year-old female developed cytogenetic relapse of chronic myelogenous leukemia 4 years after allogeneic bone marrow transplantation. To induce a graft-versus-leukemia effect, peripheral blood buffy-coat cells were collected from the original marrow donor during 5 rounds of leukapheresis over 3 weeks, and 2.47 x 10(8) cells/kg were infused into the patient. Acute graft-versus-host disease (GVHD) did not develop even after an interval of 50 days from the last donor leukocyte transfusion (DLT). However, karyotypic analysis of bone marrow cells performed on the same day showed an apparent decrease in the proportion of Ph1 chromosome-positive cells (1/20) among all dividing cells, compared with the proportion (13/20) observed before DLT. At the same time, the proportion of red blood cells (RBCs) of donor origin among the peripheral RBCs of the patient, which was less than 10% before DLT, began to rise and reached 100% at 4 months after DLT. The karyotype of bone marrow cells obtained on day 90 after DLT was completely normal. Although chronic GVHD of the buccal mucosa and liver developed in association with pancytopenia on day 71 after DLT, this improved rapidly with oral administration of cyclosporine. The clinical course of this patient suggests that acute GVHD is not a prerequisite for elimination of Ph1-positive cells by DLT.
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PMID:[Successful treatment of recurrent chronic myelogenous leukemia in allogeneic marrow transplant recipient with the donor leukocyte transfusion, without induction of acute graft-versus-host disease]. 756 96

Eight patients with chronic myeloid leukemia relapse after allogeneic BMT were treated with IFN-alpha and buffy coat transfusions (BC) of the bone marrow donor. The antileukemic effect of this treatment was directly demonstrated in 4 patients by the disappearance of Philadelphia chromosome-positive metaphases or the loss of detectable BCR-ABL transcripts by polymerase chain reaction. In 2 patients in whom cytogenetic or polymerase chain reaction analysis was not performed, a change in hemopoietic chimerism with recurrence of donor-type hemopoiesis was demonstrated. Two patients, both treated in advanced stages of hematological relapse after BMT, did not respond. However, severe side effects of the treatment were observed: graft-versus-host disease (GVHD) occurred in 5 patients. Two of these patients progressed to severe chronic GVHD and 1 patient ultimately died of this complication. GVHD occurred in 5 of the 6 responding patients; one patient responded without developing clinical symptoms of GVHD. Six patients developed bone marrow hypoplasia after IFN/BC treatment, and pancytopenia occurred in 4 patients. None of these 4 patients recovered spontaneously and 2 patients died of complications of pancytopenia (cerebral bleeding, infection). Our results demonstrate that treatment of chronic myeloid leukemia relapse with IFN and BC transfusions is highly effective in patients with relapse in chronic phase. The occurrence of GVHD and pancytopenia, however, resulted in a high treatment-associated morbidity and mortality. Whereas a response to treatment was observed in 1 patient without GVHD, indicating that GVHD and a graft-versus-leukemia effect may be clinically separable, bone marrow hypoplasia occurred in all responding patients.
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PMID:Interferon-alpha and donor buffy coat transfusions for treatment of relapsed chronic myeloid leukemia after allogeneic bone marrow transplantation. 824 10

A significant proportion of patients relapse after allogeneic BMT for CML. These relapses have been treated by induction of a graft-versus-leukemia effect by transfusing donor leukocytes. We have treated a 27-year-old woman with interferon and donor leukocyte transfusion and a complete haematological and cytogenetic remission was obtained coincident with the onset of GVHD. Her course was complicated by prolonged and profound pancytopenia which was fully reversed by the administration of rGM-CSF. She remains in CR with mild dermatomyositis due to chronic GVHD 17 months after the procedure.
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PMID:Reinduction of remission of chronic myeloid leukemia by donor leukocyte transfusion following relapse after bone marrow transplantation: recovery complicated by initial pancytopenia and late dermatomyositis. 827 41

[Case 1] A 44-year-old female was referred to our hospital because of leukocytosis. The WBC count was 26400/microliters and NAP score 21. As Ph1 chromosome was detected, she was diagnosed as CML and treated with busulfan. Because of the rapid decrease of WBC, we stopped busulfan. Progressive pancytopenia and an increase of myeloblasts and promyeloblasts in the bone marrow was observed. We started vincristine and prednisolone therapy. Ph1 chromosome was not detectable and southern blot analysis did not show rearranged bands of M-bcr three years after the last therapy. [Case 2] A 74-year-old female was referred to our hospital by reason of leukocytosis and thrombocytosis. The WBC count was 22,500/microliters, the platelet 907,000/microliters, NAP score 53, and Ph1 chromosome was found. The diagnosis of CML was made, and she was treated with busulfan. The WBC rapidly fell to 1,900/microliters, when chromosome analysis revealed the presence of Ph1 negative clones (4/20). She was admitted due to thrombocytopenia and leukocytosis with the additional chromosome change of i (17q). Her peripheral blood and bone marrow pictures were consistent with blast crisis, and she died of cardiac tamponade. These two cases show the heterogeneity of CML patients, and also suggest the possibility that keeping the WBC count low may lead to a decrease of Ph1 positive clones.
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PMID:[Partial and complete disappearance of Ph1 chromosome in two patients with chronic myelogenous leukemia after conventional chemotherapy]. 836 76


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