Disease relevance of Leukemia, Lymphocytic, Acute

• Ninety-seven children with either acute lymphoblastic leukemia (ALL) or acute myelogenous leukemia (AML) received HLA-identical bone marrow transplants from sibling donors, after preparation with 1320 cGy of hyperfractionated total-body irradiation and high-dose cyclophosphamide [1].
• Deletions of the long arm of chromosome 6 (6q-) are frequently found in hematopoietic neoplasms, including acute lymphoblastic leukemias, non-Hodgkin lymphomas and (less frequently) myeloid leukemias [2].
• Thirty studies that evaluated gonadal function after cyclophosphamide therapy for renal disease or combination chemotherapy for Hodgkin's disease or acute lymphocytic leukemia provided data for analysis [3].
• The tal-1 proto-oncogene encodes a helix-loop-helix DNA-binding protein that has been implicated in the formation of T cell acute lymphoblastic leukemia (T-ALL) [4].
• Approximately 50% of acute lymphoblastic leukemias (ALL) of non-T origin and 50% of chronic myelocytic leukemia in blast crisis were also anti-B1 reactive. moreover, 21 of 28 patients with the common ALL antigen (CALLA) positive form of ALL were anti-B1 positive, whereas 0 of 13 patients with CALLA negative ALL were reactive [5].

Psychiatry related information on Leukemia, Lymphocytic, Acute

• Members of the AF4/FMR2 family of nuclear proteins are involved in human diseases such as acute lymphoblastic leukemia and mental retardation [6].
• A monoclonal antibody to common acute lymphoblastic leukemia antigen (neutral endopeptidase) immunostains senile plaques in the brains of patients with Alzheimer's disease [7].
• BACKGROUND: Daily life motor skills of children with acute lymphoblastic leukemia (ALL) were studied during treatment using the Movement Assessment Battery for Children (Movement ABC) [8].
• Furthermore, we studied IGFBP-2 levels in 24 children with congenital GH deficiency (GHD), 26 with acute lymphoblastic leukemia (ALL), 75 obese children, and 60 girls with anorexia nervosa (AN) at diagnosis and during a follow-up period [9].
• The incidence and the degree of P300 abnormalities in relation to psychometric findings was assessed in two groups of long-term survivors of acute lymphoblastic leukemia (ALL) in childhood [10].

High impact information on Leukemia, Lymphocytic, Acute

• We propose that they constitute a distinct disease, denoted here as MLL, and show that the differences in gene expression are robust enough to classify leukemias correctly as MLL, acute lymphoblastic leukemia or acute myelogenous leukemia [11].
• METHODS: We stratified and randomly assigned 182 children with newly diagnosed acute lymphoblastic leukemia to postremission regimens that included high-dose methotrexate and teniposide plus cytarabine [12].
• We therefore assessed the cardiac status of 115 children who had been treated for acute lymphoblastic leukemia with doxorubicin 1 to 15 years earlier in whom the disease was in continuous remission [13].
• Pharmacokinetics of mercaptopurine in children with acute lymphocytic leukemia [14].
• Acute lymphoblastic leukemia with brilliant cresyl blue erythrocytic inclusions--acquired hemoglobin H [15]?

Chemical compound and disease context of Leukemia, Lymphocytic, Acute

• Clinical pharmacodynamics of high-dose methotrexate in acute lymphocytic leukemia. Identification of a relation between concentration and effect [16].
• Low systemic exposure to oral mercaptopurine during maintenance therapy for acute lymphocytic leukemia in childhood adversely affects prognosis [17].
• Fourteen boys with acute lymphoblastic leukemia who had been treated with combination chemotherapy (prednisone, vincristine, methotrexate, and 6-mercaptopurine) were followed prospectively to assess the effect of this regimen on gonadal function [18].
• Asialo GM1, as a cell-surface marker in acute lymphoblastic leukemia [19].
• Inhibition of human acute lymphoblastic leukemia cells by immunotoxins: potentiation by chloroquine [20].

Biological context of Leukemia, Lymphocytic, Acute

• The t(1;19) translocation that characterizes 25% of pediatric pre-B cell acute lymphoblastic leukemias (pre-B ALL) produces a chimeric gene, joining 5' sequences that encode a transcriptional activator domain of E2A with 3' sequences that, in part, encode a homeo box domain of a new gene called pbx1 [21].
• Growth inhibition and apoptosis due to restoration of E2A activity in T cell acute lymphoblastic leukemia cells [22].
• The DNA obtained from the leukemia cells of an acute lymphoblastic leukemia (ALL, L3 type) with a pre-B-phenotype and a typical t(8;14) chromosomal translocation showed a rearrangement juxtaposing the c-myc gene and the immunoglobulin (Ig) heavy-chain gene enhancer [23].
• Immunoglobulin mu-chain gene rearrangement in a patient with T cell acute lymphoblastic leukemia [24].
• Samples donated by patients with T cell acute lymphoblastic leukemia (T-ALL) were screened for mutations of the p53 tumor suppressor gene [25].

Anatomical context of Leukemia, Lymphocytic, Acute

• Leukoencephalopathy and elevated levels of myelin basic protein in the cerebrospinal fluid of patients with acute lymphoblastic leukemia [26].
• Immunotoxins containing pokeweed antiviral protein and monoclonal antibodies against human T cells or human transferrin receptor efficiently killed acute lymphoblastic leukemia cells [20].
• A young man with acute lymphoblastic leukemia was treated with vincristine sulfate, prednisone, and intrathecally injected methotrexate sodium for central nervous system involvement [27].
• Cooperation between the stem cell leukemia (SCL) transcription factor and its nuclear partners LMO1 or LMO2 induces aggressive T cell acute lymphoblastic leukemia when inappropriately expressed in T cells [28].
• Monoclonal antibodies J5, VIL-A1, and BA-3, known to react with the common acute lymphoblastic leukemia antigen (CALLA) were found to specifically stain normal human polymorphonuclear neutrophils (PMN) [29].

Gene context of Leukemia, Lymphocytic, Acute

• The BCR-ABL1 kinase expressed in acute lymphoblastic leukemia (ALL) drives malignant transformation of human pre-B cells [30].
• Cytotoxic T cell response against the chimeric ETV6-AML1 protein in childhood acute lymphoblastic leukemia [31].
• We report the direct involvement of atypical PKC-zeta in SDF-1 signaling in immature human CD34(+)-enriched cells and in leukemic pre-B acute lymphocytic leukemia (ALL) G2 cells [32].
• We have demonstrated that IL-4 significantly inhibited spontaneous [3H]thymidine ([3H]-TdR) incorporation by leukemic blasts from some B lineage acute lymphoblastic leukemia (BCP-ALL) patients (8 of 14) [33].
• The basic helix-loop-helix transcription factor TAL1 (or SCL) is a critical regulator of hematopoietic and vascular development and is misexpressed in the majority of patients with T-cell acute lymphoblastic leukemia [34].

Analytical, diagnostic and therapeutic context of Leukemia, Lymphocytic, Acute

• The common acute lymphoblastic leukemia antigen (CALLA), as defined by J-5 murine monoclonal antibodies, was detected on renal tubular and glomerular cells from fetal and adult donors by an indirect immunoperoxidase technique [35].
• Twenty-four poor-risk patients with acute lymphoblastic leukemia received a modified regimen of carmustine, cytarabine, cyclophosphamide, and 6-thioguanine (BACT) followed by autologous bone marrow transplantation (ABMT) [36].
• The common acute lymphoblastic leukemia antigen (CALLA) has been detected in biological fluids using a radioimmunoassay based on the inhibition of binding of 125I-labeled monoclonal anti-CALLA antibody to glutaraldehyde-fixed NALM-1 cells [37].
• A similar decrease in receptor expression was observed in vivo in PBL from patients being treated daily with 5 X 10(6) units/m2 per d of IFN alpha 2 by subcutaneous injection, for acute lymphoblastic leukemia or papilloma virus infections [38].
• We have utilized two-dimensional polyacrylamide gel electrophoresis, coupled with ultrasensitive silver staining, to identify lineage-related polypeptide markers in lymphoblasts from children with acute lymphoblastic leukemia [39].

References