Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytogenetic studies of 91 consecutive patients with therapy-related myelodysplasia or overt acute nonlymphocytic leukemia disclosed characteristic defects of chromosome 7 in 48 cases and of chromosome 5 in 21 cases. The chromosome 5 abnormalities were consistently present in all abnormal mitoses at the time of diagnosis, as were the chromosome 7 abnormalities in 45 of the 48 patients. Various abnormalities, primarily of the short arm of chromosome 17, were observed in 13 cases, abnormalities of the long arm of chromosome 21 were observed in 12 cases, and rearrangements of 11q23 were seen in nine cases. Thirteen patients presented a normal karyotype. Previous therapy with alkylating agents, the presence of an initial myelodysplastic phase, and abnormalities of chromosome 7 or 5 were interdependent. Patients with 11q23 rearrangement typically developed overt leukemia of FAB types M4 or M5a without myelodysplasia and with a short latent period. Evaluated by Cox regression analysis, complete remission of the primary malignancy and a malignant lymphoma as primary tumor were the two most important and independent prognostic factors indicating a longer survival (P = .008). In addition, the platelet count at diagnosis was a significant prognostic factor (P = .01). For the subgroup of 62 patients with myelodysplasia, the number of chromosome aberrations, the percentage of blasts in the bone marrow, and the hemoglobin level were other significant and independent prognostic factors (P = .05, .05, and .004, respectively). The most important predictive factor for a favorable response to intensive antileukemic chemotherapy in overt leukemia was the absence of a preceding myelodysplastic phase (P = .0014).
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PMID:Chromosome aberrations and prognostic factors in therapy-related myelodysplasia and acute nonlymphocytic leukemia. 240 Aug 4

In four patients with trisomy 21 (three constitutional, one acquired) with a morphological undifferentiated leukemia, diagnosis of erythroid leukemia was established by both immunophenotyping and ultrastructural studies. Indeed, a majority of blasts from three patients expressed several erythroid markers such as carbonic anhydrase 1, spectrin beta chain, and glycophorin A. In addition, band 3 and hemoglobin were immunologically detected in a fraction of the blast cells from two cases. At ultrastructural level, a majority or all blast cells exhibited erythroid differentiation features such as theta granules and ferritin molecules. However, platelet glycoproteins GP Ib, GP IIb, and GP IIIa were also immunologically detected in a fraction (from 14-82%) of the blasts. Since the ultrastructural study indicated that some promegakaryoblasts were also present in three patients, double labeling between erythroid markers (glycophorin A or carbonic anhydrase I) and platelet glycoprotein (Ib or IIIa) was performed and showed a clear overlap between the two kinds of markers. A similar approach was performed at ultrastructural level and indicated that blast cells with ultrastructural erythroid features of differentiation may have three distinct phenotypes, i.e., presence of glycophorin A without platelet glycoproteins or, conversely, the presence of platelet glycoproteins without glycophorin A and coexpression of glycophorin A and platelet glycoproteins. Expression of glycophorin A correlated directly with the differentiation level of the erythroid blasts, whereas platelet glycoproteins were essentially expressed in the more primitive leukemic erythroid cells. The GP Ib synthesized by these blasts was subsequently studied. The GP Ib alpha mRNA analyzed by Northern blot from these erythroid cells was identical in size with that from megakaryocytic cells as was the molecular weight of the GP Ib molecule from both after immunoprecipitation by a monoclonal antibody. Therefore, "in vivo" erythroid leukemic cells may express the main platelet glycoproteins including GP Ib.
Leukemia 1989 Sep
PMID:Expression of platelet glycoproteins by erythroid blasts in four cases of trisomy 21. 252 26

A 26-year-old male was admitted to our hospital because of fever and leukocytosis. On admission, a white blood cell count was 28,300/microliters with 46.5% blast cells and 16.0% atypical monocytoid cells, a hemoglobin level 13.7 g/dl, and a platelet count 15.0 X 10(4)/microliters. Bone marrow contained 58.8% of peroxidase-negative blast cells. He was diagnosed as acute lymphoblastic leukemia (ALL L2) according to the FAB classification. Chromosome analysis revealed the marrow cells to contain 45, XY, -7, t(9; 22) (q34; q11). On surface marker analysis, the leukemic cells were positive for both lymphoid (CD10) and myeloid markers (CD13). Two color flow-cytometric analysis showed two distinct populations with CD10 and CD1 3, respectively. Rearrangements of both immunoglobulin heavy chain and T cell receptor beta-chain were observed. The "breakpoint cluster region" on chromosome 22 was not rearranged. On the basis of these findings, we thought this case being acute mixed leukemia. He was refractory to AdVP therapy and BHAC-DMP therapy. He is now under treatment with A-Triple-V therapy.
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PMID:[Philadelphia-positive acute mixed leukemia with monosomy 7]. 255 34

Using an enzyme linked immunosolvent assay kit supplied by Toyobo Co., erythropoietin (EPO) concentration in plasma was measured. Normal 100 samples showed a logarithmic distribution in EPO concentrations and normal range was between 5.4-32.5 mU/ml (mean +/- 2 SD). Coefficient variations (C.V.) of 3 samples continuously assayed were 3.8%, 6.5%, and 9.1% and C.V. of 3 samples assayed day by day were 3.6%, 7.2%, and 11.5%. Dilution test revealed that 3 samples diluted to 75%, 50%, and 25% were on each line which go through zero point. After the addition of 5.0, 15.0, and 35.0 mU/ml of EPO to the 3 samples, assay of EPO revealed 95.5 +/- 6.3% (mean +/- SD) of recovery. Assay of EPO in plasma from 19 patients with aplastic anemia revealed that all samples were higher than normal range and that 4 samples from the patients with severe aplastic anemia (less than 8.0 g/dl of hemoglobin) showed higher than 3,000 mU/ml. Furthermore, 67% (14/21) of samples from patients with leukemia showed higher than normal range in EPO concentration. EPO concentration in plasma from 17 patients with chronic renal failure were within normal range although the patients showed anemia.
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PMID:[Assay of erythropoietin in plasma by enzyme-linked immunosorbent assay]. 260 Oct 73

14C- 12-L-hydroxy-5, 8, 10-heptadecatrienoic acid was produced by incubating the 10,000 x g supernatant of rat basophilic leukemia -2H3 cells with 14C-arachidonic acid in the presence of isoproterenol and hemoglobin. The Vmax was 125 p mol/min/2 x 10(7) cells and its Km value was 1.28 n mol, indicating the low synthetic activity even though a sufficient amount of the substrate was available. The synthesis was dose-dependently decreased by the addition of calcium ions and inhibited by ETYA and indomethacin but not by imidazol, suggesting that the production might be non-enzymatic break-down from PGH2.
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PMID:[Characterization of 12-L-hydroxy 5, 8, 10-heptadecatrienoic acid produced by rat basophilic leukemia-2H3 cells]. 261 43

Tiazofurin (2-beta-D-ribofuranosylthiazole-4-carboxamide, NSC 286193) is a synthetic nucleoside inhibitor of inosine monophosphate dehydrogenase. This agent has recently been shown to induce differentiation of human leukemia cell lines. In the present study, we have monitored the effects of tiazofurin on differentiation and proto-oncogene expression in K562 erythroleukemia cells. Tiazofurin induced K562 cell hemoglobin production in a concentration-dependent manner. This induction of a differentiated phenotype was also associated with a loss of proliferative capacity. In contrast to the reversible effects of hemin on induction of K562 cell hemoglobin synthesis, the effects of tiazofurin were irreversible. Northern blot analysis of K562 cells treated with 10 microM tiazofurin demonstrated the accumulation of alpha- and gamma-globin mRNA. The results also demonstrate that there was little if any effect of tiazofurin on levels of c-myc, c-myb, or c-abl mRNA. Furthermore, there were no detectable changes in Ki-ras, Ha-ras or N-ras expression at the mRNA and protein levels in tiazofurin-treated K562 cells. These findings suggest that tiazofurin induces changes in levels of globin transcripts but has little if any effect on c-myc, c-myb, c-abl, or c-ras gene expression in K562 cells.
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PMID:Effects of tiazofurin on globin and proto-oncogene expression in K562 erythroleukemia cells. 263 29

Acquired chromosomal rearrangements in acute nonlymphocytic leukemia (ANLL) have been linked to specific clinicopathologic features that suggest new disease subtypes. In this collaborative study, we report five patients with ANLL and a t(3;5) in their leukemic cells. At diagnosis, four of the patients had a t(3;5) as their sole karyotypic anomaly; the remaining patient had additional structural and numerical abnormalities. Careful cytogenetic analysis indicated that the breakpoints of this rearrangement are 3q25.1 and 5q34, in contrast to the various breakpoints reported in earlier studies (3q21----3q25 and 5q31----5q35). The karyotypic, morphologic, and clinical characteristics of this group, as well as those of 14 previously reported patients with the t(3;5), were compared to identify any features that might warrant consideration of a specific syndrome. The available information indicates a worldwide distribution and a nearly equal male:female ratio for patients with this translocation. The median age of the group, 37 years, was younger than that of all patients with ANLL, 49 years. A preceding myelodysplastic syndrome was observed in three patients. The limited numbers of observations on leukocyte count, hemoglobin level, and platelet count precluded meaningful comparison with data for ANLL patients in general. Although each FAB morphologic subtype, except M3, occurred in patients with a t(3;5), the frequency of M6 was much greater than expected. Bone marrows from each of the five patients we report showed increased numbers of megakaryocytes; trilineage dysplasia was observed in the marrow of each of the four patients for whom it could be assessed. Taken together, these findings suggest that the t(3;5) may affect cells capable of differentiation into multiple lineages.
Leukemia 1989 Jan
PMID:Clinicopathologic manifestations and breakpoints of the t(3;5) in patients with acute nonlymphocytic leukemia. 264 76

We analyzed specimens from 268 patients with small lymphocytic lymphoma (SL) to identify prognostic factors significant for survival. These patients were staged and treated according to the protocols of the Cancer and Leukemia Group B, Eastern Cooperative Oncology Group, Southeastern Cancer Study Group, and the Southwest Oncology Group. Univariate analysis showed that a large-cell grade greater than I, WBC greater than 10,000/microL, hemoglobin (Hgb) less than 11 g/dL, age greater than or equal to 55 years, and failure to respond to treatment were all poor prognostic factors. Multivariate analysis showed that large-cell grade, age, degree of capsular invasion, and symptom type were independently associated with survival. Separate analyses of cases with and without leukocytosis indicated differences in survival. In patients without leukocytosis, age, presence or absence of anemia, and treatment response were significant prognostic variables; in patients with leukocytosis, large-cell grade, presence or absence of anemia, symptom type, and treatment response were significantly related to survival. Multivariate analysis showed that age was the only significant independent prognostic variable in patients without leukocytosis; in patients with leukocytosis, symptom type, large-cell grade, and bone marrow involvement were independently associated with survival. We conclude that several parameters, both clinical and pathologic, should be assessed at the initial diagnosis of SL to predict prognosis better.
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PMID:Small lymphocytic lymphoma: a clinicopathologic analysis of 268 cases. 264 79

The authors performed membrane antigen phenotyping on 75 patients with acute nonlymphocytic leukemia with a panel of myeloid-associated monoclonal antibodies. The 34 patients (45%) with CD34-positive leukemia were not significantly different from the 41 with CD34-negative leukemia with respect to age, hemoglobin, white blood cell count, or platelet count at presentation, but their blasts were more likely to lack the CD15 or CD33 antigens and to have FAB M1 or M2 morphologic characteristics. CD34-positive leukemia was more likely to arise after chemotherapy. Patients with CD34-positive leukemia were less likely to enter a complete remission even when analysis was limited to those patients receiving a high-dose induction-type chemotherapy regimen. Giemsa-banding karyotyping studies were obtained in 55 of the cases. In 30 of these cases (56%) clonal karyotypic abnormalities were demonstrated. Although the karyotypic abnormalities and phenotypes were varied, there was a high degree of association between the karyotypic abnormalities monosomy 7/del (7q) and the CD34-positive phenotype; this antigen was expressed on blasts from eight of the nine patients displaying this abnormality. Monoclonal antibody phenotyping of myeloid leukemia with reagents such as anti-CD34 may help to define biologically interesting subsets of ANLL with distinct clinicopathologic expression.
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PMID:Clinicopathologic and cytogenic features of CD34 (My 10)-positive acute nonlymphocytic leukemia. 264 3

The decrease in c-myc mRNA expression occurring in leukemia cell lines induced to differentiate is supposed to be an early event of the commitment to the differentiation program. Alternatively, the decrease in c-myc mRNA expression could be simply a consequence of loss of the self-renewal capability characteristic of the terminal differentiated phenotypes. In an attempt to clarify these hypotheses, we analysed comparatively the kinetics of variations in c-myc mRNA expression, hemoglobin synthesis, DNA and RNA syntheses, cell cycle kinetics and self-renewal capability in normal and hemin-treated K562 leukemia cells exposed for different periods of time to the antitumoral antibiotic doxorubicin. Times of exposure to doxorubicin were either 2 h, which resulted in reversible induction of hemoglobin synthesis without significant cytostatic effects, or continuously for more than 5 days, which resulted in an irreversible induction of hemoglobin synthesis and in the complete and irreversible loss of self-renewal activity. Comparative analysis of the experimental data indicated that the decrease in c-myc mRNA expression correlated with the loss of replicative activity, possibly due to an irreversible cytostatic effect of the long exposure to doxorubicin, but not with the commitment to the differentiation programs.
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PMID:In K562 leukemia cells treated with doxorubicin and hemin, a decrease in c-myc mRNA expression correlates with loss of self-renewal capability but not with erythroid differentiation. 265 92


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