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)

Leukemic cells from seventy patients with various types of human leukemias were examined for expression of the WT1 gene, the Wilms' tumor gene located at chromosome 11p13. WT1 was expressed in 7 of 16 cases of acute lymphoblastic leukemia, 15 of 22 with acute myelogenous leukemia and 8 of 10 in blast crisis of chronic myelogenous leukemia. No detectable WT1 RNA was found in chronic leukemias, including chronic lymphocytic leukemia, plasma cell leukemia, hairy cell leukemia and chronic myelogenous leukemia in chronic phase. The expression pattern of WT1 in these human leukemia samples indicates the involvement of this gene in the early stage of hematological cell differentiation.
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PMID:Expression of the Wilms' tumor gene (WT1) in human leukemias. 131 88

We analyzed the rearrangement of T-cell receptor (TcR) delta chain gene in 196 cases of hematological malignancies. This rearranged band (s) was observed in 15% of the total cases investigated. All T-ALL patients and cell lines, except for P30/Okubo, had a new band (s) or deletion of J delta 1 gene locus, indicating the gamma delta T-cell type or the alpha beta T-cell type. In the other T-cell malignancies, the delta rearranged band (s) was recognized in 5% of T-cell lymphomas, 20% of AILD but not in ATL, Hodgkin's disease, T-CLL. Inappropriate delta rearrangement was frequently recognized in 63% of B-ALL and 50% of CML-BC but none or few (5% less) in B-CLL, B-lymphoma and AML. Southern blotting, using J delta 1 and V delta gene probes or Pst I enzyme digestion, indicated that the inappropriate delta rearranged band in B-ALL and CML-BC is V delta 2D or DD without a J delta locus. The rearranged band (s) involved J delta locus, was mostly recognized in 5/6 cases of CD7 (+) stem cell leukemia. Therefore, the TcR delta gene is useful in evaluating clonality for the most immature T-cell neoplasms, not showing rearrangement of the other TcR genes. Moreover, this delta gene may be a useful tool for distinguishing T-lineage from the other lineages, using the characteristic rearrangement pattern (V delta 2D as a inappropriate pattern, or (D) DJ and V (D) DJ as the T-lineage pattern (s)).
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PMID:[Analysis of T-cell receptor delta chain gene in hematological malignancies]. 132 69

Protein kinase C (PKC) activation and/or modulation of its isoenzyme expression play key roles in regulating the response of haematopoietic cells to both growth factors and non-physiological inducers of cell growth and differentiation. The level of PKC activities for both cytosol and particulate fractions of ALL and CLL cells are lower than those of AML type. Atypical AML blasts expressing T-cell associated CD2 and CD7 determinants have significantly lower PKC activities compared to typical AML blasts. Analyses of PKC isoforms (-alpha, -beta, and -gamma) show considerable variation with respect to leukaemic cell distributions and subcellular localisations. PKC-alpha and -beta are usually the major species in cytosolic fractions, whereas PKC-gamma is the predominant type in particulate fractions. All lymphoid cells express PKC-gamma in the cytosol, albeit as a minor component, while the occurrence of cytosol PKC-gamma in AML cells appears to be associated in particular with a typical lymphoid antigen expression.
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PMID:The expression and possible roles of protein kinase C in haematopoietic cells. 133 6

The expression and function of neural cell adhesion molecule (NCAM, CD56, Leu19) on leukaemic blasts was investigated. The expression of NCAM was frequent (64%) in 14 studied cases of acute myeloid leukaemia (AML) but not in chronic lymphocytic leukaemia (CLL: 1/3 cases positive) or immunocytoma (IC: no positivity). No correlation with the expression of other AM (intercellular adhesion molecule-1 (ICAM-1), leucocyte function antigen-1 (LFA-1). VLA beta chain) or with AML type, according to FAB classification, was observed. Blocking of NCAM with anti-Leu 19 MoAb on AML targets resulted in a significant decrease of their susceptibility to LAK killing and in inhibition of conjugate formation. In the case of B prolymphocytic leukaemia (B-PLL) which did not express ICAM-1 or LFA-1 but was NCAM+, a complete resistance to LAK activity and lack of conjugate formation was observed. Blocking of NCAM on LAK effectors did not decrease their cytotoxic activity. Our results suggest that NCAM, in the presence of other AM, may have a supportive role in adhesion of leukaemic targets to LAK effectors.
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PMID:A supportive role of neural cell adhesion molecule (NCAM) in adhesion between leukaemic blasts and cytotoxic lymphocytes. 137

Multiple myeloma (MM) and chronic lymphocytic leukemia (CLL) are closely related B-cell cancers. Parallel and divergent features of these diseases are reviewed. In MM, expression of multiple hemopoietic lineage-associated antigens on the malignant cells and the substantial likelihood of progression to acute myelogenous leukemia suggest transformation of a pluripotent stem cell. In CLL, transformation more likely involves a committed B-cell progenitor. Another difference is that clonal evolution with associated cytogenetic progression is common in MM but not CLL. Other data, including studies of proto-oncogenes and tumor suppressor genes, suggest that MM results both from increased proliferation and accumulation of tumor cells, whereas tumor cell accumulation is the predominant feature of CLL. These differences may be reflected in the seemingly greater role of cytokine abnormalities in MM progression. For example, osteoclast-activating properties of some cytokines account for bone involvement in MM but not in CLL. MM and CLL share common features such as stage-dependent anemia and immune deficiency. Both diseases respond to alkylating agents but vary markedly in their sensitivity to fludarabine (CLL greater than MM) and glucocorticoids (MM greater than CLL). Differences between these diseases in progression-free interval and survival may reflect different definitions of premalignant and malignant phases rather than biologic differences. Detailed comparisons between MM and CLL may provide additional insights into these and related B-cell cancers.
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PMID:Multiple myeloma and chronic lymphocytic leukemia: parallels and contrasts. 141 9

The human leukemias are a group of hematologic neoplasms characterized by uncontrolled proliferation of cells concerned with blood cell production. The cause(s) of human leukemia remains unknown. Bone marrow (BM) is believed to be the site of origin of human leukemias, although the specific locus(i) and/or cell(s) from which it arises have not been definitively identified. Generally, human leukemias and related proliferative diseases are thought to be clonal in nature; affecting a single hematopoietic stem cell, which then proliferates and replaces the marrow of normal hematopoietic stem cell systems. The condition is believed to be malignant in nature. Results of our current morphologic studies on well-fixed, ideally-stained thin sections of plastic-embedded bone marrow biopsies (BMB) from a large number of acute (AML, ALL) and chronic (CGL, CLL) leukemia patients suggest that human leukemias may not be clonal diseases. Instead, a large population of other resident cells--'endosteal cells'--appears to become involved in the process and it is possible that all members of this group enter the activity simultaneously. This change (transformation) in the endosteal cell population might be due to an abnormality (qualitative or quantitative) of diffusable, humoral factors (yet to be identified) that are responsible for the growth and proliferation of these hematopoietic precursor cells. In this context, the human leukemias may be considered not as malignant, but rather the result of an aberration of factor(s) that control hematopoiesis. In this respect, the human leukemias, particularly AML, ALL and CML, might be analogous to pernicious anemia (megaloblastic anemia) as it was understood 40-50 years ago.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The origin and spread of human leukemia. 143 86

Exponentially growing K562 cells incubated with 1-beta-D-arabinofuranosylcytosine (ara-C) accumulate ara-C triphosphate (ara-CTP) at a higher rate and to a greater concentration after pretreatment with 9-beta-D-arabinofuranosyl-2-fluoroadenine (F-ara-A) than do cells treated with ara-C alone. Potentiation of ara-C metabolism is due in part to an indirect effect of F-ara-A triphosphate (F-ara-ATP)-mediated reduction in deoxynucleotide pools and consequent activation of deoxycytidine kinase. Because the levels of deoxynucleotide pools and the activity of deoxycytidine kinase are cell cycle-specific, we investigated the effect of cell cycle phases on the accumulation of ara-CTP and the influence of F-ara-A pretreatment on such accumulation. Exponentially growing K562 cells were fractionated into G1, S, and G2+M phase-enriched subpopulations (each enriched by > 60%) by centrifugal elutriation. The rate of ara-CTP accumulation was 22, 25, and 14 microM/h and the rate of F-ara-ATP accumulation was 38, 47, and 33 microM/h in the G1, S, and G2+M subpopulations, respectively. The rate of elimination of arabinosyl triphosphates was similar among the different phases of the cell cycle. After pretreatment with F-ara-A, the rate of ara-CTP accumulation in the G1, S, and G2+M phase-enriched subpopulations was 43, 37, and 26 microM/h, indicating a 1.7-, 1.5-, and 1.9-fold increase, respectively. These results suggest that a combination of F-ara-A and ara-C may effectively potentiate ara-CTP accumulation in all phases of the cell cycle. This observation is consistent with the results of studies on the modulation of ara-C metabolism by F-ara-A in lymphocytes and leukemia blasts obtained from patients with chronic lymphocytic leukemia and acute myelogenous leukemia, respectively.
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PMID:Cell cycle-specific metabolism of arabinosyl nucleosides in K562 human leukemia cells. 145 54

Cell cycle phases of bone marrow cells from 8 patients with iron deficiency anemia (IDA), 8 aplastic anemia (AA), 30 myelodysplastic syndrome (MDS), 41 acute leukemia (AL) before treatment, 8 acute leukemia in relapse, 17 acute leukemia in complete remission (CR), 12 chronic myelogenous leukemia (CML) and 4 chronic lymphocytic leukemia (CLL) were analysed with flow cytometry. The proportions of phases of S. G2 M in patients with IDA, refractory anemia, and refractory anemia with ring sideroblast were similar to these in normal controls (P > 0.05). However, they were significantly lower in patients with AA, refractory anemia with excess of blast (RAEB) and transformed RAEB than those in normal controls (P < 0.01, respectively), and CML patients than in normal controls (P < 0.05). The S G2M% was apparently higher in patients with CML than that in CLL (P < 0.01). But, there was no difference between in ALL and ANLL (P > 0.05). It was higher in patients with AL in CR and in relapse than AL before treatment (both P < 0.01). It was still lower in the former than that in normal controls. (P < 0.05). The clinical significance of cell cycle status was also discussed in this paper.
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PMID:[Flow cytometric analysis of bone marrow cell cycles in patients with hematologic diseases]. 147 30

A nationwide cooperative incidence survey of leukemia was carried out by the Institute of Hematology, CAMS, from 1986 to 1988. The cooperative survey network covered 46 investigating areas, involving 22 provinces, municipalities and autonomous regions. More than 60 million person-years were supervised and 1670 new cases identified. The annual incidence rate of leukemia was 2.76/10(5) and the 95% confidence interval of population rate ranged from 2.63/10(5) to 2.89/10(5). The incidence rates in oil fields and polluted areas were significantly higher than those in other areas. The incidence rate of ANLL was 1.62/10(5); ALL, 0.69/10(5); CML, 0.36/10(5); CLL, 0.05/10(5); and special types, 0.03/10(5). The incidence rate and constituent ratio of CLL were significantly lower than those in Europe and America. A peak of ALL incidence rate before age 10 was seen; this rate then declined with increasing age until 30. However, the incidence rates of other leukemia rose with age reaching peaks at old age (50-70). The leukemia rate in males was significantly higher than that in females, both in youth (10-29), caused by ALL, and at old age (greater than or equal to 60), mainly caused by ANLL. The incidence rates of ANLL subtypes (including M2b) are also reported.
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PMID:[Incidence survey of leukemia in China. Chinese Epidemiologic Study Group of Leukemia and Aplastic Anemia]. 153 78

The expression of c-myb mRNA and protein was analyzed in fresh leukemic cells by Northern-blot analyses and by immunofluorescent staining using monoclonal c-myb specific antibodies. Staining of the cells was evaluated by flow cytometry. The results demonstrate c-myb mRNA expression predominantly in acute lymphocytic leukemia (ALL, 4/4 cases), acute myeloic leukemia (AML, 17/17) and chronic myeloic leukemia (CML, 12/12) but rarely in chronic lymphocytic leukemia (CLL, 1/17). Immunofluorescent analyses revealed expression of c-myb protein in the nucleus of ALL (5/7) and AML (9/9) with a good correlation of c-myb-positive cells and with the number of proliferating (Ki67-positive) blast cells.
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PMID:Heterogeneous expression of c-myb protein in human leukemia detected by simultaneous two color flow cytometric analysis. 156 Jun 75


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