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)

From 583 cases of acute lymphoblastic leukemia (ALL) and 181 cases of acute myeloid leukemia (AML) in childhood, seven patients were identified to have t(11;19) (q23;p13) by sequential cytogenetic analyses. The t(11;19) was associated with B-precursor ALL at diagnosis in three patients and at relapse in one patient. All four tested patients with B-precursor failed to express the CD10 antigen when the t(11;19) was detected, and one of three patients tested expressed myeloid-associated markers. In three other patients the translocation was detected either at lineage conversion from ALL to M5 AML (n = 2) or from AML to CD10- B-precursor ALL (n = 1). Leukemic blasts of four patients had an entirely different karyotype at the time of lineage conversion or loss of CD10 expression, suggesting an induction of a second neoplasm. Thus the t(11;19) can be found in de novo or secondary acute leukemia with lymphoid (CD10-) or myeloid (monoblastic) phenotype. Further investigation of the gene(s) involved in the 11q23 chromosomal region and the breakpoints in the 19p13 region is needed to understand the leukemogenesis of this apparently heterogeneous group of disorders.
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PMID:Childhood acute leukemia with t(11;19) (q23;p13). 177 55

Seven hundred and forty-four newly diagnosed patients with acute leukemias between 1978 and 1990 were classified on the basis of immunological phenotypes. The majority of the patients were enrolled in the Tokyo Children's Cancer Study Group (TCCSG) studies. The incidence of subclassification of acute leukemias in this study was as follows: 522 patients with ALL (70%), 139 patients with ANLL (18%), 29 patients with biphenotypic leukemia, 8 patients with Ph1-positive acute leukemia (Ph1-AL), and 45 patients with infant leukemia. ALLs were classified into common ALL (cALL, 77%), T-ALL (15%), B-ALL (4%), and unclassified ALL (3%). The incidence of ALL subtypes in this study reflected those of TCCSG. Biphenotypic leukemias were categorized into 4 groups as follows; 1) cALL with positive myelomonocytic antigen(s) (N = 11), 2) unclassified ALL with positive myelomonocytic antigen(s) (N = 5), 3) ANLL with positive B-lymphoid antigen(s) (N = 4), and 4) acute leukemia with positive T-lymphoid and myeloid antigen(s). Infant leukemias were classified into ALL type (N = 27) and ANLL type (N = 18). In this present study, clinical features and immunological phenotypes of the acute leukemias with a poor prognosis, i.e. biphenotypic leukemia, Ph1-AL, and infant leukemia are analyzed and discussed.
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PMID:Immunological classification of childhood acute lymphoblastic leukemia. 179 11

Expression of p53 oncogene in blast cells may have prognostic importance in acute leukemia. Simple and reliable methods which could detect enhanced p53 expression in leukemia cells would be important for follow-up studies of leukemia patients in remission. We used immunoperoxidase (IP) technique with an anti-p53 monoclonal antibody PAb421 to study the expression of p53 in leukemia cells. The expression of p53 was studied in 9 cell lines and 17 de novo acute leukemia (9 acute myeloid leukemia [AML], 8 acute lymphoblastic leukemia [ALL]) patients. The expression of p53 was demonstrated in non-T non-B cells and Burkitt's lymphoma cell lines, but neither in two myeloid leukemia cell lines nor in normal lymphoid cells after mitogenic stimulation. p53 expression was demonstrated in 7 cases (2 AML, 5 ALL) but only in ALL cases the percentage of positive of cells was over 20%. Bone marrow cells from patients were studied also after short-term culture (AML patients); in 1 case the number of PAb421-positive cells rose significantly after culture. These data suggest that IP staining with PAb421 can be used to demonstrate high p53 expression in B cell leukemias.
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PMID:Detection of p53 oncogene in acute-leukemia cells by immunoperoxidase technique. 185 83

We examined the levels of protein kinase C (PKC) activity and the expressions of its three major isozymes, designated types I (gamma), II (beta), and III (alpha), in the cytosol and particulate fractions of cells from patients with acute myelogenous leukemia (AML), acute lymphocytic leukemia (ALL), and chronic lymphocytic leukemia (CLL), in an attempt to elucidate the cell type- or lineage-specific expression of these isozymes. The levels of PKC activities in the cytosol and particulate fractions from AML cells were higher than those from ALL or CLL cells. The average PKC activities of AML cells, ALL cells, and CLL cells were 18.7, 12.2, and 11.3 pmol/min/10(8) cells, respectively, in the cytosol fractions and 4.4, 3.1, and 2.6 pmol/min/10(8) cells, respectively, in their particulate fractions. M1 cells (French-American-British classification) and AML cells with T-lymphocyte-associated surface antigens, such as CD2 and CD7, had significantly lower PKC activities among AML cells. Immunoblot analyses using monoclonal antibodies against each isozyme revealed that all three isozymes were broadly distributed on leukemic cells with considerable variability in the level of expression. All lymphoid leukemic cells expressed PKC-gamma in the cytosol fractions, albeit a minor component; however, this type was observed in cells from only half the number of AML patients. Those AML cells with cytosolic PKC-gamma usually expressed lymphoid surface antigens, such as CD2, CD7, and CD19. On the other hand, cytosolic PKC-beta and PKC-alpha were commonly observed in all types of leukemic cells. AML cells expressed these two types at almost equal levels, but in lymphoid cells, expressions of PKC-beta were usually more abundant than those of PKC-alpha. These data suggest that AML cells with lymphoid antigens might have a lower PKC activity but more predominant expression of cytosolic PKC-gamma than the usual AML cells.
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PMID:Expression of three major protein kinase C isozymes in various types of human leukemic cells. 186 47

To define the clinical and biologic significance of childhood acute mixed-lineage leukemia diagnosed by stringent criteria, we studied 25 cases of acute lymphoblastic leukemia expressing greater than or equal to 2 myeloid-associated antigens (My+ ALL), and 16 cases of acute myeloid leukemia expressing greater than or equal to 2 lymphoid associated antigens (Ly+ AML). These cases represented 6.1% of 410 newly diagnosed ALLs (two treatment protocols) and 16.8% of 95 AMLs (two protocols). T-lineage--associated antigens were identified in 9 of the My+ ALL cases and in 14 of those classified as Ly+ AML; all but 1 of the 19 cases that could be subclassified had an early thymocyte stage of differentiation. The My+ ALL cases had an increased frequency of French-American-British (FAB) L2 morphology (36%); the Ly+ AML cases were characterized by FAB M1 or M2 morphology, low levels of myeloperoxidase reactivity and combined populations of myeloperoxidase-positive large blasts and small blasts generally of hand-mirror morphology. Karyotypic abnormalities included t(9;22)(q34;q11) in three cases of My+ ALL, 11q23 translocations in two cases of My+ ALL, and 14q32 translocations in three My+ ALL and five Ly+ AML cases. Mixed-lineage expression lacked prognostic significance in either ALL or AML; however, the findings indicate that some patients with Ly+ AML may respond to prednisone, vincristine, and L-asparaginase after failing on protocols for myeloid leukemia. At relapse, two My+ ALLs had converted to AML and two Ly+ AMLs to ALL; one case in each group showed complete replacement of the original karyotype. Acute mixed-lineage leukemia does not adequately describe the heterogeneity of the cases identified in this study and should be replaced by a set of more restrictive terms that indicate the unique biologic features of these leukemias.
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PMID:Characterization of childhood acute leukemia with multiple myeloid and lymphoid markers at diagnosis and at relapse. 158 28

An increasing number of papers document cases of acute leukemia in which individual blast cells co-express markers normally restricted to a single cell lineage. Numerous terms are used to refer to cases with unscheduled expression of lineage-foreign proteins; the best defined categories were hybrid acute leukemia and acute mixed-lineage leukemia. The incidence of phenotypically variant acute leukemia varies with the quality and quantity of parameters used and the stringency of the criteria employed for its definition. Considerable interest has focused on acute lymphoblastic leukemia (ALL) cells expressing one or several myeloid lineage-associated antigens (My+ ALL), CD13, CD14, CD15, CD33, and CDw65. Owing to legitimate and cryptic expression on lymphoid cells, CD11b and CD15 reagents may not be considered as specific indicators of myeloid differentiation. The reported incidence ranged from 5 to 46% in 14 studies on My+ ALL, totalling 3817 patients. Several detailed reports documented a higher incidence of My+ ALL in adults (realistically in the range 10-20%) than in children (5-10%) and in B-lineage ALL as opposed to T-lineage ALL. My+ ALL cases are more likely to display unique cytogenetic [t(9;22), 11q23, 14q32] features than My-neg ALL. There appears to be no predominant expression of a single myeloid-associated antigen among those analyzed. As the morphological diagnosis of a leukemia subtype is often imprecise, some T-neg B-neg My+ ALL cases might actually contain FAB AML-M0 populations. While the expression of myeloid-associated antigens has no apparent prognostic significance in the majority of childhood ALL subtypes, in adults myeloid antigens seem to identify a high risk group of ALL patients with a poorer response to standard ALL therapy.
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PMID:Review of the incidence and clinical relevance of myeloid antigen-positive acute lymphoblastic leukemia. 188 19

Leukemic cells of patients with acute myeloid leukemia have recently been shown to spontaneously produce autostimulatory IL-1 and IL-6. In order to investigate the effects of systemic production of these cytokines on normal hematopoietic cells, mice were engrafted with bone marrow cells infected with high-titer retroviral vectors carrying the murine IL-1 alpha or IL-6 genes and the neomycin phosphotransferase gene. Sustained expression of the introduced IL-1 alpha and IL-6 genes was documented by Northern-blot analysis of RNA from G418-resistant mast cells and T cells, derived from bone marrow and spleen, respectively, of successfully reconstituted mice 6-10 months after transplantation. A single mouse engrafted with IL-1 alpha-infected cells which presented with a dramatic neutrophilic granulocytosis (54-fold elevation in circulating neutrophils) was sacrificed for health concerns 2 months post-transplant. Modest changes in peripheral leukocyte counts (at most a 2-fold rise) were observed in all of the other mice, and they remained healthy throughout the observation period. The majority displayed increased hematopoietic activity in bone marrow and spleen, predominantly granulopoiesis, with moderate lymphoid hyperplasia seen in the spleens of mice constitutively expressing IL-1 alpha. These mouse models provide the opportunity to evaluate the potential of persistent IL-1 alpha and IL-6 expression to contribute to leukemogenic transformation.
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PMID:Leukocytosis in mice following long-term reconstitution with genetically-modified bone marrow cells constitutively expressing interleukin 1 alpha or interleukin 6. 189 48

Twenty-six cases of acute myeloid leukemia (AML) with cytochemical and immunophenotypic data were studied prospectively for immunoglobulin and T-cell receptor gene rearrangement. Dysmyelopoiesis was seen in 100% and Auer rods in 18%. Sudan black B was positive in 83% of the cases, peroxidase in 76%, nonspecific esterase in 74% (fluoride-inhibited in 82%), chloroacetate in 70%, acid phosphatase and PAS in 100%, and immunoperoxidase stains for platelet glycoprotein IIIa and factor VIII in 0% of the cases studied. Flow cytometry revealed myeloid phenotype in 19 of 20 cases. In four cases 5-86% of cells were TdT positive. Heavy-chain gene rearrangement was demonstrated in three cases (12%) and kappa light chain gene rearrangement in one; clinically significant rearrangement of the T-cell receptor gene was not found. Rearrangements of immunoglobulin genes are found occasionally in AML; these may represent nonspecific findings or coexistent lymphoid differentiation in AML.
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PMID:Prospective gene rearrangement studies and multiparameter analysis of acute myeloid leukemia. 190 18

A 19 year follow up study was conducted to explore the association between occupations expected to be exposed to electromagnetic fields and the occurrence of leukaemia and brain tumours. Incidence of cancer between 1961-79 was calculated and the standardised morbidity ratio (SMR) with a 95% confidence interval (95% CI) was related to that of all Swedish working men. For all the selected "electrical occupations" the SMRs for total leukaemia and brain tumours were near unity. Increased risks were noted for all leukaemia among electrical/electronic engineers and technicians, (SMR 1.3; 95% CI 1.0-1.7) as well as in the sub-groups of telegraph/telephone (2.1; 1.1-3.6) and machine (2.6; 1.0-5.8) industries. Risk for chronic lymphoid leukaemia was increased in the same occupational category (1.7; 1.1-2.5) and in the sub-group of machine industry (4.8; 1.0-14.0), as well as for all linesmen (2.0; 1.0-3.5) and power linesmen (2.8; 1.1-5.7). Risk for acute myeloid leukaemia was increased among all miners (2.2; 1.0-4.1) and miners working in iron/ore mines (5.7; 2.1-12.4). Increased risk for all brain tumours (2.9; 1.2-5.9) and glioblastomas (3.4; 1.1-8.0) appeared among assemblers and repairmen in radio and TV industry. Raised risk for all brain tumours was seen for all welders (1.3; 1.0-1.7) and welders in iron/steel works (3.2; 1.0-7.4) and risk for glioblastomas was also increased for all welders (1.5; 1.1-2.1). No major changes in relative risk estimates were noted after the exclusion of persons who were over 65 at the time of diagnosis. Although a homogeneous pattern of increased risks of leukaemia or brain tumour was not noted, the hypothesis that magnetic fields might play a part in the origin of cancer cannot be rejected.
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PMID:Incidence of leukaemia and brain tumours in some "electrical occupations". 159 76

Surface phenotyping by flow cytometry and cytochemical study were used to identify 15 adult patients with acute leukemia displaying ambiguous phenotypes. Differences were found in the blast cell karyotype and immunoglobulin gene rearrangements of terminal deoxynucleotidyl transferase (TdT)-positive acute myelogenous leukemia (AML) and biphenotypic leukemia expressing B lymphoid and myeloid markers. The karyotypic abnormalities, t(9;22) and t(4;11), were noticed in acute biphenotypic leukemia, and were consistently associated with rearrangement at the immunoglobulin locus. Furthermore, coexpression of CD19/CD20 and either myeloperoxidase or myeloid surface markers were predictive of finding the t(9;22) or t(4;11) karyotype. Patients with TdT-positive AML, on the other hand, were less likely to show rearrangement at the immunoglobulin locus, and did not have the t(9;22) or t(4;11). Instead, a variety of nonrandom karyotypic abnormalities were seen, including trisomy 13. Unlike common AML, the majority of TdT-positive cases demonstrated an abnormal karyotype with duplications and/or deletions present in all cases. In no instance was trisomy 8, t(8;21), t(15;17), or any other isolated translocation identified. The authors therefore suggest that immunophenotyping, when combined with cytochemical analysis of TdT and myeloperoxidase or Sudan black B, may aid in the characterization of subgroups of atypical acute leukemia, such that alternate approaches to therapy can be evaluated.
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PMID:Surface marker analysis and karyotype distinguish acute biphenotypic leukemia from acute myelogenous leukemia expressing terminal deoxynucleotidyl transferase. 191 54


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