Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023467 (acute myeloid leukemia)
35,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Short term clinical results of bone marrow transplantation on 66 patients conditioned with fractionated total body irradiation (12 Gy in 6 fractions and 3 days) are presented here. An acute toxic effects incident, similar to that obtained previously, a 27.6% interstitial pneumonitis associated with acute severe graft versus host disease in 77% of cases, 19.2% relapses, and 41% total crude survival with an actuarial probability of surviving for more than two years of 46% for ALL, 64% for AML and 28% for CML, are the results obtained since now.
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PMID:Fractionated total body irradiation for bone marrow transplantation: clinical results on 66 patients. 224 43

In May 1979, Memorial Sloan-Kettering embarked on a programme of hyperfractionated TBI (HFTBI), 1320 cGy in 11 fractions over 4 days with partial lung shielding (1 HVL), followed by cyclophosphamide (60 mg/kg/d x 2d) for cytoreduction prior to allogeneic bone marrow transplantation (BMT). Anterior and posterior chest wall electron "boosts" were given to the areas blocked (600 cGy in 2 fractions) on the last two days of treatment. Since then, we have treated over 600 patients with HFTBI, the majority for allogeneic BMT. Several modifications have occurred over the years. We have added a "boost" electron dose of 400 cGy to the testes in all male leukemic patients; this reduced testicular relapses from a rate of 14% (4/28) to 0%. In an attempt to increase engraftment of T-depleted BMTs, we added one additional fraction; since our present dose/fraction was also increased to 125 cGy, we now deliver a total dose of 1500 cGy in 12 fractions over 4 days for allogeneic transplants. Tolerance to HFTBI has been excellent relative to the single dose (SD) regimen utilised prior to May, 1979. The incidence of fatal interstitial pneumonitis (IP) decreased from 50% in the SD regimen to 18% after the introduction of HFTBI. In children, the incidence of IP was only 4% with HFTBI. With the introduction of T-depleted marrows, fatal IP in adults has decreased also, e.g. to less than 10% in CML patients. With conventional BMT after HFTBI, relapse at 5 years has been exceedingly low (e.g. in children, 13% for ALL, 2nd remission and 0% for AML, 1st remission) and engraftment has been 100%. With matched T-depleted BMT, rejections have occurred in 15% overall; the incidence of graft failure has not been reduced by the higher dose of HFTBI. Relapses in this setting are equivalent to relapses with conventional BMT for AML, but appear to be increased for ALL. Radiobiological findings related to HFTBI will also be discussed.
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PMID:Total body irradiation for bone marrow transplantation: the Memorial Sloan-Kettering Cancer Center experience. 224 51

During the stage of blast crisis, the increase in the population of peripheral blasts in one examined untreated CML patient, obeyed an exponential equation of growth that requires a maintained equal proportion of proliferating to quiescent blasts. A model of cell growth at CML blast crisis is presented, which interprets the required constancy of equal-size blast subcompartments in terms of regulation of the G0----G1 flow, the latter involving activation of one cell out of three interacting quiescent blasts in contact. This model is discussed in the light of evidence that G0 blast activation involves membrane-bound interacting sites interfering with growth-promoting pathways. The model-predicted proliferative index (f) value of 0.5 +/- 0.16 is found to be nearly identical to a reported estimate of the 3H-thymidine-labeling index of CML blasts at the crisis stage of the disease. It is also close to corresponding indexes of CML blood and marrow progenitor cells and to labeling indexes of AML and ALL large blasts.
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PMID:Cell growth in chronic myeloid leukemia at blast crisis. 228 42

Cytogenetic analyses were performed on 12 adult patients with abnormal megakaryoblastic proliferation which was detected by ultrastructural cytochemical study (platelet peroxidase) and platelet-megakaryocytes-specific monoclonal antibodies (TP-80, Plt1, AN51, and KOR-77). The patients consisted of two patients with myelodysplastic syndromes (MDS), three with acute megakaryoblastic leukemia (AMKL), six with megakaryoblastic transformation in Philadelphia-positive chronic myelogenous leukemia (CML-meg-BC), and one case of chronic myeloproliferative disorder (CMPD). Among them, an inversion of the long arm of chromosome 3 [inv(3)(q21q26)] was found in one AMKL patient with a normal platelet count. Chromosome change at band 3q26 was also found in one MDS patient without thrombocythemia. Furthermore, the long arm of chromosome 13, where rearrangements in myelofibrosis are clustered (13q12----q22) was seen in one MDS patient. Trisomoy of chromosome 19 was found in one AMKL patient and three CML-meg-BC patients. These findings indicate that cytogenetic abnormalities involving 3q26, 13q, and trisomy 19 are associated with hematologic neoplasia with megakaryocytic lineage in adult patients, although these abnormalities were not related to the survival of the patients. During the period of this study, two acute myelogenous leukemia patients (AML-M2 and AML-M5b) with chromosome rearrangements at band 3q21 and thrombocythemia were found, indicating that chromosome abnormality at band 3q21 is related to quantitative platelet dysfunction, whereas that at 3q26 is related to hematologic malignancies with a proliferation of megakaryocytic lineage.
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PMID:Cytogenetic findings in adult acute leukemia and myeloproliferative disorders with an involvement of megakaryocyte lineage. 229 63

Eighty consecutive patients were transplanted with human leukocyte antigen (HLA)-identical sibling marrow for acute myelogenous leukemia (AML, N = 29), acute lymphoid leukemia (ALL, N = 23), or chronic myelogenous leukemia (CML, N = 28). Donor marrow was depleted of lymphocytes using counterflow centrifugation. Median age of the recipients was 31 years. Pretransplant conditioning consisted of cyclophosphamide and fractionated total body irradiation (TBI) with a low (4.1 +/- 0.3 cGy/min) or high (13.1 +/- 1.6 cGy/min) midline average dose rate. In 43 patients, cytosine-arabinoside or anthracyclines were added to the conditioning regimen. Immunoprophylaxis posttransplant consisted of methotrexate (MTX) alone, cyclosporine A (CsA) in combination with MTX, or CsA alone; two patients received no immunoprophylaxis at all. Graft failure occurred in 4 of 77 evaluable patients (5%). The probability of acute graft-versus-host disease (GVHD) greater than or equal to grade 2 at day 100 after transplantation was 15%. The projected 3-year estimate of extensive chronic GVHD was 12%. Only three patients died of cytomegalovirus-interstitial pneumonitis. The projected 3-year probability of relapse was 30% (95% confidence interval [CI], range 8% to 53%) in transplants for AML in first complete remission (CR1), 35% (95% CI, 1% to 69%) after transplantation for ALL in CR1, and 38% (95% CI, 2% to 74%) after transplantation for CML in first chronic phase (CP1). The projected 3-year probability of leukemia-free survival (LFS) was 56% (95% CI, 35% to 77%) after transplantation for AML-CR1, 42% (95% CI, 16% to 69%) in patients transplanted for ALL-CR1, and 49% (95% CI, 18% to 80%) after transplantation for CML-CP1. After transplantation for AML-CR1, ALL-CR1, or CML-CP1, the median follow-up time for leukemia-free survivors was 31+, 30+, and 21+ months, respectively. Probabilities of relapse, survival, and LFS in AML-CR1 and ALL-CR1 transplants were comparable with those reported in recipients of untreated grafts. In patients transplanted for CML-CP1, probability of relapse was higher and probability of LFS was lower than in recipients of untreated grafts. In transplants for leukemia in CR1 and CP1, preparative regimen and immunoprophylaxis posttransplant were not associated significantly with the probability of acute GVHD greater than or equal to grade 2, extensive chronic GVHD, relapse, survival, or LFS. In bone marrow transplantation for leukemia, counterflow centrifugation is a useful technique for the prevention of GVHD.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Allogeneic bone marrow transplantation for leukemia with marrow grafts depleted of lymphocytes by counterflow centrifugation. 231 Aug 32

Seven cases of miliary tuberculosis in patients with hematologic disease were analyzed clinicopathologically. Mean age of the patients was 65 years, and the hematologic diseases were CML, AML, ALL, MDS and malignant lymphoma. Diabetes mellitus was present as a complication in three patients. Miliary tuberculosis was found in 5 cases during the first admission to our hospital owing to hematologic problems. In 4 of 6 cases, fever had started more than two months before admission, consequently, the tuberculosis probably began about that time. After admission, chemotherapy was administered in 5 cases, and steroid in 6 cases for hematologic disease. The mean total quantity of steroid administered was 2,134 mg of prednisolone and average treatment duration was 69 days. The chest roentgenographic shadow was so atypical that miliary tuberculosis was suspected in only one case. The initial chest roentgenogram showed hilar and mediastinal lymph node swelling as well as the shadow of pulmonary tuberculosis in two cases. It was thought that the hilar and mediastinal lymph node swelling could be explained by primary complex, although the patients were of advanced age, or by "secondary complex" reported by Terplan, K in 1940. The diagnosis of tuberculosis was made in two patients before their death by smear of aspirated fluid of cervical lymph node and by bone marrow cell block in one patients, and by pathological examination of mediastinal lymph node biopsy in the other patients. Tubercles were found from bone marrow cell block in 2 out of 5 patients and from bone marrow biopsy in 1 out of 3 patients, but the positive results were reported in 2 patients following death. Smears of sputum, gastric juice, urine, spinal fluid and pleural effusion were negative in all cases. One patient diagnosed as miliary tuberculosis also had pneumocystis carinii pneumonia. This case was treated with antituberculosis drugs for 20 days without improvement. Another patient diagnosed as miliary tuberculosis improved under treatment with antituberculosis drugs, but died of cytomegalovirus pneumonia. Autopsy in 5 cases revealed non-reactive miliary tuberculosis, and pulmonary hemorrhage probably due to DIC was present as a complication in two cases. In these cases, severe immunosuppression, which is a major precipitating factor of miliary tuberculosis, is thought to be induced by hematologic disease itself, chemotherapy, steroid or other underlying disease such as diabetes mellitus. Miliary tuberculosis in such compromised host is cryptic and progresses rapidly. Consequently, early diagnosis is very important. Retrospectively, the unexplained pyrexia was most important to suspect tuberculosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Clinicopathological study of miliary tuberculosis in patients with hematologic disease]. 237 32

It has been suggested that abnormalities of chromosome 3 at bands q21 and q26 are associated with the presence of increased numbers of abnormal megakaryocytes in patients with hematologic malignancies. The pretreatment bone marrows of 287 patients with leukemia (acute myeloid leukemia (AML), 225 patients; acute lymphocytic leukemia (ALL), 36 patients; or chronic myelogenous leukemia in blast crisis (CML-B), 26 patients) were reviewed to identify those with normal or increased numbers of megakaryocytes. Thirty-two patients with AML, one with ALL, and 10 with CML-B had normal or increased numbers of megakaryocytes. Of the 32 patients with AML, 19 patients had significant numbers of mononuclear or binuclear small megakaryocytes as well as megakaryocytes with separated nuclei ("micromegakaryocytes"). Cytogenetic analyses were obtained in 29 of 32 patients with AML and showed inv(3)(q21q26) (one patient); Ph1 (two patients); -5 and/or -7 (seven patients); normal karyotypes (10 patients). No patient with micromegakaryocytes had a chromosomal abnormality associated with a favorable prognosis. Overall, among 225 patients with AML, four had inv(3)(q21q26) or t(3;3)(q21;q26). Only one of these four patients had normal or increased numbers of megakaryocytes, although all four had micromegakaryocytes. One patient with CML-B had inv(3)(q21q26) but had decreased numbers of megakaryocytes and a platelet count of 24 x 10(3)/microliters. All five patients with abnormal chromosome 3 at bands q21 and q26 had additional cytogenetic abnormalities (Ph1 in two patients; -7 in three patients). Mean and median platelet counts were greater than 100,000/microliters for patients with marrow megakaryocytosis regardless of morphology, as well as for the patients with abnormalities involving 3q21 and 3q26. Abnormalities of megakaryocyte morphology, increases in the numbers of megakaryocytes, and normal to increased platelet counts are not uncommon in patients with acute leukemia and CML-B, and are not uniquely associated with changes involving chromosome 3.
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PMID:Clinical and cytogenetic correlations of abnormal megakaryocytopoiesis in patients with acute leukemia and chronic myelogenous leukemia in blast crisis. 238 80

The feasibility of ex vivo purging with long-term bone marrow cultures (LTBMC) for autologous transplantation in leukemia has been established. The procedure has been applied to patients with acute myeloid leukemia (in relapse or remission) and recently in one patient with chronic myeloid leukemia. The results in first remission AML are very encouraging with 4 out of 6 patients well and apparently disease free greater than 1 to 4 years post autograft. In patients transplanted with active disease, remissions of 6 to 8 months duration were seen in two patients transplanted in florid relapse. In a CML patient with 87% of his bone marrow cells Ph1 positive, there was a marked decline of karyotypically abnormal cells in culture. Reinfusion of the cultured cells into the patient resulted in engraftment with exclusively Ph1 negative cells. The therapeutic implications of LTBMC purging require further evaluation.
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PMID:The use of cultured bone marrow cells in autologous transplantation. 240 62

A murine monoclonal IgM erythrocyte antibody appeared to have anti-P (anti-globoside) specificity. The antibody was a relatively weak cold agglutinin, but a strong haemolysin and its reactivity with red cells was markedly enhanced by enzyme treatment. This antibody was used to study the cell and tissue distribution of globoside. Globoside was not only detectable on red cells and erythroblasts, but also on endothelial cells and on subsets of platelets, megakaryocytes and fibroblasts. It was not detectable on granulocytes, monocytes and most peripheral blood lymphocytes. Neither was it present on erythroblast precursors (CFU-E, BFU-E), pro-erythroblasts or on the cells of the pro-erythroblastic cell lines K562 and HEL. However, K562 cells expressed globoside when induced to mature into erythroblasts by sodium butyrate. Cells of patients with various leukaemias were also tested. A significant number of positively reacting cells was frequently (six out of 18) seen in cases with a CML blast crisis (CML-BC) and rarely in AML (four out of 37 cases). In CML-BC the P-positive cells were probably erythroblasts and/or megakaryoblasts. Thus, globoside appeared to be an interesting marker in CML-BC of the erythroblastic or mixed erythroblastic-megakaryoblastic type.
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PMID:A murine monoclonal IgM antibody specific for blood group P antigen (globoside) 242 10

We report on the characterization of four monoclonal antibodies which were prepared against membrane markers of human myeloid lineage. Fusion, isolation of hybridoma cells and their cloning and testing of the monoclonal antibodies by indirect immunofluorescence and FACS 440 analysis were performed by means of standard procedures. The results indicate that the monoclonal antibodies have a specificity against membrane markers of human myeloid lineage (exactly promyelo-granulocytes). These monoclonal antibodies do not react with human T and B lymphocytes, monocytes, erythrocytes and thrombocytes of peripheral blood. In normal bone marrow reactivity to matured myeloid cells was found to occur in promyelocytes and expressed on all granulocytes. These monoclonal antibodies also react with cells of myeloid cell lines and with other precursor cell lines represented by NALM-1, NALM-16, HEL, K-562, REH no reactivity was detected. The produced antibodies react with some leukaemic cells from patients with more mature myeloid cells (AML with promyelocytes, myelocytes and CML) they do not react with pathological cells from patients with CLL, AML (with myeloblasts), ALL, hairy cell leukaemia, erythroleukaemia and several types lymphoma. All antibodies have a IgM class and express granulocytotoxic and granuloagglutination activity. Using flow cytometry comparative analysis with other monoclonal antibodies was performed to detect the membrane structure (X-haptene) included in standard International classification as CD 15 group.
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PMID:Human leukocyte markers defined by monoclonal antibodies. I. Expression of X-hapten structure on cells of myeloid lineage. 246 63


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