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

In the present study we carried out allogeneic bone marrow transplantation (BMT) in 14 leukemia children with high risk prognostic factors. Six patients with acute nonlymphocytic leukemia (ANLL), four with acute lymphocytic leukemia (ALL), two with chronic myelogenous leukemia (CML), and two with myelodysplastic syndrome (MDS). Among these patients, six with ANLL, two with ALL, one with CML and one with MDS were alive in complete remission 8 to 58 months post-BMT. Four patients died of relapse (one with ALL, and one with MDS), and chronic GVHD (one with ALL and one with CML). In six patients recombinant granulocyte colony stimulating factor (rG-CSF) was used to shorten the period of granulocytopenia. The mean time of recovery to granulocyte count of 500/mm3 was 13.2 days in the rG-CSF+ group, being 15.9 days faster than that in the rG-CSF- group. In light of these results, allogeneic BMT is shown to be a choice of treatment for leukemia children with high risk prognostic factors and rG-CSF may be an effective reagent to prevent infectious episodes in BMT.
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PMID:Allogeneic bone marrow transplantation for malignant hematologic disorders in children. 128 58

A family with a high incidence of leukemia was investigated and followed up for 10 years. Up to now, 7 of 48 members in this family had acute nonlymphocytic leukemia. Chromosomal aberration was found in 3 healthy members, 2 of whom were found to have 47, XX, +5, -8, +Mar, del (7) (q22-qter) and 45, XO, -Y chromosomes and developed this disease 5 and 7 years later respectively. Pedigree analysis suggested that the hereditary defect in the family should rest on the maternal lineage. It is considered that hereditary factors play an important part in the pathogenesis of leukemia in the family.
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PMID:A study on a family with high incidence of leukemia. 129 Dec 2

Only in these latest years has been possible to consider Hodgkin disease (HD) as a neoplastic syndrome, thank of immunohistochemistry and cytogenetic techniques which have confirmed the monoclonal origin of typical cellular marker of disease: the Reed-Sternberg cell (R-S cell). Interesting associations have been observed between children suffering from HD and the positivity of EBV antigen above all in the socio-economically developed countries. The histopathologic classification of HD is divided in four sub-types, with different incidence in the pediatric age: the nodular sclerosis and the mixed cellularity are more rap-presented than the lymphocyte predominance and mostly the lymphocyte depletion. Histopathologic classification is essential for the prognosis and a correct therapeutic approach to disease. The management of HD is based on chemotherapy and radiotherapy associated; the results of treatment are more and more encouraging with a global survival over 95%. Sequelae of treatment are reduced in modern therapeutic trials: in particularly injury to somatic growth, cardiopulmonary system, gonadal and thyroid functionality is reduced by using low dose and involved fields for the early stage patients. The most important sequela in children treated for HD is the risk to developed a second malignant neoplasm; in particularly acute nonlymphocytic leukemia and non Hodgkin's lymphoma. In patients treated with radiotherapy alone increase the risk to develop solid tumors like sarcomas and carcinomas, which can appears several years after diagnosis.
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PMID:[Hodgkin's disease in childhood]. 130 82

The t(6;9) that characterizes a specific subtype of ANLL fuses the 3' part of a gene located on chromosome 9q34, CAN, to the 5' part of a gene located on chromosome 6p23, DEK. On the 6p- chromosome, the resulting DEK-CAN fusion gene is transcribed into a leukaemia-specific 5.5 kb chimaeric mRNA that encodes a putative DEK-CAN fusion protein. No transcription could be detected from the reciprocal CAN-DEK fusion on chromosome 9q+. Analysis of 17 t(6;9) ANLL cases showed that the translocation breakpoints occur in a single intron of 7.5 kb in the CAN gene (ICB9) and in a single intron of 9 kb in the DEK gene (ICB6). As a result, the presence of a t(6;9) in blood or bone marrow cells can be faithfully diagnosed by Southern blotting. Moreover, the result of the translocation is an invariable DEK-CAN transcript, which can be sensitively monitored by RNA-PCR. Surprisingly, a SET-CAN fusion gene was found in leukaemic cells from a patient with AUL. Like CAN, SET is located on chromosome 9q34, which explains the apparently normal karyotype of the leukaemic cells. The occurrence of a SET-CAN fusion gene indicates that CAN may be the relevant oncogene involved in leukaemogenesis, and that activation of CAN can be effectuated through fusion of its 3' part to either DEK or SET. As yet, the function of CAN, DEK or SET is unknown. None of the proteins shows consistent homology to any known protein sequences. However, preliminary localization data and analysis of sequence motifs suggested that DEK-CAN may have a role in transcription regulation. CAN contains several dimerization domains and a repeated motif that can function as an ancillary DNA-binding domain. DEK and SET are non-related proteins, but they share a stretch of acidic amino acids, which is also present in the fusion proteins.
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PMID:Translocation t(6;9) in acute non-lymphocytic leukaemia results in the formation of a DEK-CAN fusion gene. 130 67

Between April 1982 and July 1990, 101 patients underwent allogeneic or syngeneic bone marrow transplantation at the Mayo Clinic. This patient population consisted of 30 with acute nonlymphocytic leukemia, 25 with acute lymphoblastic leukemia, 29 with chronic granulocytic leukemia, and 17 with other diseases (aplastic anemia in 7, myelodysplastic syndrome in 5, and lymphoma in 5). The results achieved in our patients who underwent transplantation in first complete remission of both acute nonlymphocytic leukemia and acute lymphoblastic leukemia compare favorably with previously reported results. Only 1 of 15 patients (7%) with acute nonlymphocytic leukemia and 2 of 8 patients (25%) with acute lymphoblastic leukemia who underwent transplantation in first complete remission had a relapse. Thus, we recommend early bone marrow transplantation during initial complete remission for patients with either of these disorders who have adverse prognostic factors. In contrast, of 12 patients with either acute nonlymphocytic leukemia or acute lymphoblastic leukemia who underwent transplantation during relapse, 11 died within 6 months. Therefore, such patients should be offered new experimental treatments. Our patients with chronic granulocytic leukemia fared better when they underwent transplantation early during the course of their disease rather than during the accelerated or blast phase. Prospective studies are needed to determine the best approach in these patients.
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PMID:Mayo Clinic experience with allogeneic and syngeneic bone marrow transplantation, 1982 through 1990. 154 82

Langerhans cells originate in bone marrow and probably belong to the monocyte-macrophage lineage. CD1 is a specific marker of Langerhans cells. By immunofluorescence and immunoelectron microscopy, CD1a antigen and myeloid markers (CD11, CD13, CD14, CD15, CD33, HLA-DR) were studied in 53 cases of acute myeloid leukemias (AML) and 3 acute lymphoblastic leukemias (ALL). The 11 ANLL without monocytic component were CD1a negative. 2/5 of acute myelomonocytic leukemias (AML4) and 9/37 of acute monocytic leukemias (AML5) were positive. All 3 ALL were negative. No correlation was found between CD1a and myeloid markers. CD1a+ AML did not differ from CD1a- AML with regard to cytogenetics or response to therapy. The CD1a positive cells may originate from an abnormal proliferation of CD1a positive cells which are present in bone marrow and which may differentiate into Langerhans cell precursors.
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PMID:CD1-reactive leukemic cells in bone marrow: presence of Langerhans cell marker on leukemic monocytic cells. 137 Apr 20

Six patients with recurrent and/or refractory acute nonlymphocytic leukemia (ANLL) were treated with recombinant human granulocyte colony-stimulating factor (G-CSF) and cytotoxic agents administered simultaneously. Neither of the two patients who received cytosine arabinoside (ara-C) in combination with G-CSF achieved complete remission. The other four patients, who received multi-drug combination therapy together with G-CSF, all achieved complete remission. No major side effects due to G-CSF were observed. These results demonstrated that the effects of G-CSF in enhancing the sensitivity of leukemic cells to cytotoxic agents and accelerating the recovery of leukocytes could lead to its possible use in the treatment of ANLL.
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PMID:Treatment of acute nonlymphocytic leukemia by combination of recombinant human granulocyte colony-stimulating factor and cytotoxic agents: a report of six cases. 137 44

In a series of 89 patients with acute leukemia, orbital granulocytic sarcomas were observed in 7. All these patients had acute nonlymphocytic leukemia, and they were all children. The orbital involvement usually was bilateral, and the patients had proptosis, conjunctival hemorrhage, and chemosis. Morphologic, cytochemical, and immunophenotypic analyses did not show a predilection for any particular myeloid cell type. Two patients had biphenotypic leukemias with myeloid components. The ocular manifestations responded well to chemotherapy irrespective of the hematologic response.
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PMID:Orbital granulocytic sarcomas (myeloid sarcomas) in acute nonlymphocytic leukemia. 139 59

We report a case of idic(X)(q13),r(X)(p22q13), and del(X)(:p11-->cen-->q11:) in a 71-year-old female patient with de novo acute nonlymphocytic leukemia (ANLL), FAB-M4. The abnormal X chromosomes of this patient were identified cytogenetically by G-banding technique and were further confirmed by fluorescence in situ hybridization (FISH) using an alpha-satellite probe to chromosome X centromere. The features of this are compared with other cases reported in the literature.
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PMID:Cytogenetic and FISH studies of abnormal X chromosomes in a patient with ANLL. 139 97

Two patients with acute nonlymphocytic leukemia (ANLL) and trisomy 4 as the only cytogenetic aberration are presented. Including the two, a total of 31 cases with this karyotype have been described till now. A review of the 31 cases shows that they fall into two distinct age groups, a younger group of 10 patients (5-34 years) and an older group of 21 patients (50-75 years). With four exceptions the diagnosis was ANLL in all cases, mostly FAB classes M2 and M4. At the time of diagnosis 18 had clinical signs of active infection. In 20 cases the peripheral leukocyte count was above 10 x 10(9)/L but not associated with presence/absence of infection. The median survival was 17 months from diagnosis. Independent prognostic factors were diagnosis (p = 0.01), peripheral leukocyte count (p = 0.03), and percentage of metaphases with trisomy 4 (p = 0.04). The two age groups as well as presence/absence of infection at the time of diagnosis were without significant prognostic consequences.
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PMID:Trisomy 4: clinical picture, hematology, and survival. Presentation of two cases and review of the literature. 142 44


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