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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In April, 1985, a 60-year-old Japanese male was diagnosed as having refractory anemia with an excess of blasts (RAEB). He thus was treated solely with blood transfusions until June, 1986, when a new diagnosis revealed that his illness had been transformed into acute myelogenous leukemia (M2). Chromosome analysis at the initial diagnosis had revealed a normal male karyotype. When the subsequent diagnosis of AML was made, however, a chromosomal abnormality [46, XY, -20, +der (20) t (?8;20) (q22;p13)] was detected. Myelodysplastic syndrome (MDS) in patients evidencing a karyotypic alteration from the initial karyotypic findings progresses in severity that includes overt leukemia, and results in a shorter survival than in patients who show no further karyotypic changes. Therefore, the prognosis of patients with MDS can be predicted more accurately by subsequently reanalyzing their chromosomes after the initial analysis, as well as by examining their peripheral blood/counts, and by monitoring bone marrow cytology.
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PMID:[Refractory anemia showing excess of blasts (BAEB) that transformed into acute myelogenous leukemia (AML-M2) with a t (?8;20) chromosomal abnormality]. 323 Jun 41

A case of T-cell acute lymphoblastic leukemia with a translocation between chromosomes #1 and #18 is described. The breakpoints were at bands 1q23 and 18q21. A single cell contained the translocation t(1;19)(q23;p13). The breakpoint on chromosome #1 was the same in both translocations, and the breakpoint on chromosome #18 was the same as that in t(14;18)(q32;q21) associated with follicular lymphoma. The possible relationship between chromosome bands 1q23 and 18q21 and the morphologic features of the leukemia cells is discussed.
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PMID:T-cell acute lymphoblastic leukemia with translocation (1;18). 325 56

The adhesion receptors Mac-1, LFA-1, and p150,95 are cell surface alpha/beta heterodimers that play a key role in leukocyte adhesion processes. The genes for Mac-1, LFA-1, and p150,95 alpha subunits have been located to chromosome 16 by means of Southern blot analysis using a series of somatic cell hybrids. Chromosomal in situ hybridization has demonstrated that the genes for the three alpha subunits map to the short arm of chromosome 16, between bands p11 and p13.1, defining a cluster of genes involved in leukocyte adhesion. The gene encoding the LFA-1/Mac-1/p150,95 beta subunit, and defective in leukocyte adhesion deficiency, has been located on chromosome 21, band q22. The leukocyte adhesion receptor alpha and beta subunits are mapped to chromosomal regions that have been shown to be involved in cytogenetic rearrangements in certain patients with acute myelomonocytic leukemia and the blast phase of chronic myelogenous leukemia, respectively.
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PMID:Chromosomal location of the genes encoding the leukocyte adhesion receptors LFA-1, Mac-1 and p150,95. Identification of a gene cluster involved in cell adhesion. 328 62

Two cases of childhood myelodysplastic syndrome with chromosome abnormalities involving band 11p15 are described. The first case, with inv(11)(p15q23), had a complex clinical course; the initial diagnosis was aplastic anemia, then refractory anemia with excess of blasts in transformation (RAEB-t), and finally, before death, chronic myelomonocytic leukemia with hematologic features similar to those of chronic myelogenous leukemia (CML). The second case, with t(4;11)(p13;p15), progressed from RAEB to acute myelogenous leukemia (M2). In the literature, we found 12 patients with nonlymphocytic leukemia and chromosome abnormalities involving band 11p15, including seven cases with t(7;11)(p13-p15;p15); four cases (including the present case 1) showed CML-like hematologic features. It is suggested that translocations involving 11p15 are a nonrandom chromosome abnormality in nonlymphocytic leukemia.
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PMID:Childhood myelodysplastic syndromes with 11p15 translocation. 329 71

A cell line with immature blast cell morphology was isolated from HL-60 promyelocytic leukemia cell cultures and designated HL-T. This new cell type is biphenotypic, expressing terminal transferase (TdT) together with myelomonocytoid immunologic features. TdT enzymatic activity, undetectable in HL-60, was determined to be 140 to 180 units/10(8) HL-T cells by the dGTP-assay, approximately 20% of the activity found in lymphoblastoid cell lines. HL-T predominantly synthesize the known 58-kDa TdT-protein plus a minor 54/56-kDa doublet. The 58-kDa steady state form is nonglycosylated and is phosphorylated. Precursor antigens S3.13 and MY-10, absent on HL-60, are expressed by HL-T; however, the cells are negative for HLA-Dr. Southern blot analysis by hybridization with immunoglobulin heavy chain (JH) and T cell-receptor chain gene (T beta) probes shows JH to be in the germ-line configuration in both cell lines and the T beta gene to be in germ-line in HL-60 but to be rearranged in HL-T. Truncation of the gene encoding the granulocyte-macrophage-colony-stimulating factor (GM-CSF), as found in HL-60, is not observed in HL-T. HL-T are resistant to differentiation-induction by retinoic acid and 1,25-dihydroxyvitamin D3. Cytogenetically HL-T share with HL-60 a deletion of the short arm of chromosome 9 at breakpoint p13, an aberration frequently found in patients with T cell leukemia. In addition, HL-T display t(8;9)(p11;p24) and trisomy 20. Tetraploidy is observed in 80% of HL-T metaphases with aberrations identical to those in the diploid karyotype. Like HL-60, the new line shows some surface-antigenic-T cell characteristics. Despite an antigenic pattern most consistent with that of helper-inducer T cells (T4+, D44+/-, 4B4+, 2H4-, TQ1+/-), HL-T cells and their conditioned culture medium suppress antigen, mitogen, and mixed-leukocyte-culture-mediated lymphocyte proliferation.
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PMID:HL-T, a new cell line derived from HL-60 promyelocytic leukemia cell cultures expressing terminal transferase and secreting suppressor activity. 330 49

The karyotypic abnormalities and clinical data on three patients in whom acute leukemia was diagnosed within the first 6 months of life are presented. The four structural chromosomal rearrangements detected in the bone marrow from these patients, i.e., t(7;12)(q36;p13) and t(1;19)(q11;q11) in case 1, t(2;10;11;12)(q21q31;p13;q13;q24) in case 2, and t(11;19)(q23;p13) in case 3, have not previously been associated with congenital leukemia. Acquired chromosomal changes have until now been reported in only 31 leukemic infants in this age group. Of the total material, 18 patients had acute lymphoblastic leukemia and 16 had acute nonlymphocytic leukemia. The by far most frequently recorded cytogenetic aberration has been t(4q;11q), seen in 14 cases of lymphoblastic leukemia. Although t(4q;11q) has not been found in a single patient with acute nonlymphocytic leukemia, these leukemias have often had other rearrangements involving the same region of 11q. Hence, genetic material around 4q21 may be active in lymphocytic differentiation, whereas gene(s) in 11q23 may be important in the neoplastic process in a less cell-type specific manner and perhaps particularly vulnerable to neoplastic rearrangement in fetal life. The finding of four cases out of 34 with translocations between 11q23 and chromosome 19 indicates that this rearrangement might characterize a specific cytogenetic subgroup of leukemia in the very young.
Leukemia 1987 Jan
PMID:New structural chromosomal rearrangements in congenital leukemia. 331 30

A patient with Ph-negative chronic myeloid leukemia showed active karyotypic evolution when he entered blast crisis. One cell line, which predominated briefly in an accelerated myeloid phase, was characterized by the t(11;19)(q23;p13). Chromosome in situ hybridization demonstrated movement of the oncogene c-ets-1 from the der (11q-) to the der (19p+). The breakpoint at 19p13 was in the vicinity of the human insulin receptor gene locus (INSR). No rearrangements of the c-ets and INSR genes were found in Southern blot analyses. Myeloid lineage was indicated by cell morphology and absence of immunoglobulin JH gene rearrangement and was supported by loss of the germ line bcr-3' gene. Chromosome rearrangements involving 11q23 and movement of c-ets-1 characterize monocytic and lymphoid leukemias and have not previously been reported in myeloid blast crisis of chronic myeloid leukemia.
Leukemia 1988 Feb
PMID:Transposition of the oncogene c-ets-1 in a t(11;19)(q23;p13) cell line transient during clonal evolution of blast crisis chronic myeloid leukemia. 342 1

This article reports six cases of acute nonlymphocytic leukemia (ANLL) and an abnormal chromosome #16. All had the same hematologic pattern at diagnosis, i.e., peripheral blood hyperleukocytosis with a high percentage of monocytes and blast cells. The bone marrow showed three different cell populations: (a) myeloblasts, (b) monocytes and promonocytes, and (c) abnormal eosinophils. In three cases, an ultrastructural study confirmed the cytologic data. In all six cases, the diagnosis was acute myelomonocytic leukemia with bone marrow eosinophilia (M4-Eo). All cases showed an abnormal chromosome #16 in the bone marrow cells; in four cases, well-banded chromosomes were obtained, showing a pericentric inversion inv(16)(p13;q22). One patient had a 4-year remission, and another is still in remission 14 months after diagnosis. Three patients relapsed 7, 9, and 20 months after diagnosis. The last patient died soon after diagnosis. Thus, we do not support the hypothesis that patients with M4-Eo ANLL and chromosome #16 abnormality have a favorable prognosis.
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PMID:Acute myeloid leukemia with marrow hypereosinophilia and chromosome 16 abnormality. 345 67

Biclonal leukemia was diagnosed in an 8 months old girl, combining lymphoblastic (FAB L1) and monoblastic (FAB M 5) phenotypes which were classified as O-ALL and AMol by immunological examination of surface-antigens. Chemotherapy for one cell type resulted in predominance or relapse of the other one. Chromosomal abnormalities diagnosed in the lymphoblastic clone consisted of translocation t(11;19)(q23;p13) and triple X. The breakpoint 11q23 neighbouring one well known oncogene (ets) is not strictly associated with special leukemic phenotypes. But it is often found in infants and usually correlated with a poor prognosis. The data of 18 patients with hybrid leukemias registered in the BFM studies strongly support the fatal course of the disease. 12 months after diagnosis approximately 1 out of 10 children is expected to survive disease-free.
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PMID:[Biclonal leukemia O-ALL/AMoL) with 11;19 translocation and trisomy X in an 8-month-old girl]. 345 33

The authors studied clinical and immunologic characteristics of six children with 1;19 translocation-associated acute lymphoblastic leukemia (ALL); two of the six had the balanced type, t(1;19)(q23;p13), three had the unbalanced type, -19,+der(19)t(1;19)(q23;p13) with a resultant partial 1q trisomy, and the other had a mosaicism of cells with the balanced type and those with the unbalanced one, t(1;19)/-19,+der(19)t(1;19). Leukemic cells of all three patients, in which intracytoplasmic immunoglobulin was determined, were proved to show pre-B phenotype. Of the six patients, three had an initial leukocyte count of greater than 50 X 10(9)/l, and were classified in the high-risk group. Three patients relapsed after a brief remission and died. The mosaicism observed suggested that at least in some patients the leukemic cells with -19,+der(19)t(1;19) might derive from those with t(1;19) as a step in the course of clonal evolution. Our data and a review of the literature indicate that there may be no differences in the clinical and immunologic characteristics between the patients with the balanced translocation and those with the unbalanced one, and that the leukemia with the 1;19 translocation may join with other translocation-associated ALLs, with which the patients are known to have poor prognosis.
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PMID:Balanced and unbalanced 1;19 translocation-associated acute lymphoblastic leukemias. 346 88


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