1,393 research outputs found

    Preferential expression of the transcription coactivator HTIF1alpha gene in acute myeloid leukemia and MDS-related AML

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    HTIF1α, a transcription coactivator which is able to mediate RARα activity and functionally interact with PML, is encoded by a gene on chromosome 7q32–34, which is a critical region in acute myeloid leukemias (AML). With the assumption that this gene may be related to AML, we investigated the HTIF1α DNA structure and RNA expression in leukemic cells from 36 M1–M5 AML patients (28 ‘de novo’ and eight ‘secondary’ to myelodysplastic syndrome (MDS)). Abnormal HTIF1α DNA fragments were never found, whereas loss of HTIF1α DNA was observed in the patients with chromosome 7q32 deletion and translocation, and in one case without detectable chromosome 7 abnormality. HTIF1α RNA was found in acute myelocytic leukemic blasts, and was almost undetectable in normal mononuclear cells. The expression varied among the patients: higher in M1 to M3 subtypes, with the highest values in M1; low levels were constantly observed in M4 and M5 AML. In addition, HTIF1α was significantly overexpressed in MDS-related AML (MDR-AML), but not in MDS. We also found that HTIF1α expression was high in myeloid cell lines. In myeloblastic HL60 and promyelocytic NB4 cells, induced to differentiate along the monocytic–macrophage pathway by TPA or vitamin D3, HTIF1α expression decreased, whereas it was maintained at high levels on induction to granulocytic differentiation by RA or DMSO. In K562 cells, HTIF1α RNA levels did not change after hemin-induced erythroid differentiation. These results suggest that HTIF1α could play a role in myeloid differentiation, being distinctly regulated in hematopoietic lineages

    Design of a Base-Board for arrays of closely-packed Multi-Anode Photo-Multipliers

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    We describe the design of a Base-Board to house Multi-Anode Photo-Multipliers for use in large-area arrays of light sensors. The goals, the design, the results of tests on the prototypes and future developments are presented.Comment: 16 pages, 5 figures, submitted to Nucl. Instrum. and Meth.

    Study of prognosis in acute myeloid leukemias (AML) by cluster analysis

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    BACKGROUND. Cluster analysis is particularly effective in detecting homogeneous subgroups among large series of observations. We applied this relatively uncommon approach to the study of prognosis in 137 patients affected by acute myeloid leukemia (AML). METHODS AND RESULTS. Employing simple presentation parameters (age, WBC, splenomegaly, hepatomegaly) we used cluster analysis to define 3 groups with different overall survival (p = 0.0019). This classification was obtained following a rescaling of the variables and principal component analysis. Validation was performed through random definition of a control group. With the same variables, univariate analysis demonstrated age was the only prognostic factor, while Cox's model was not significant. CONCLUSIONS. In our series cluster analysis allowed a better definition of prognosis than Cox's analysis. Since the 3 groups are well identifiable, each patient can be rapidly classified and his allocation confirmed by discriminant functions. For cluster 2 we were able to project a possible myelodysplastic evolution, while cluster 3 was more frequently associated with a monocytic blastic component. We think that cluster analysis deserves consideration as an alternative statistical approach in the analysis of large series of data; its usefulness lies in its power to define homogeneous prognostic or biologic subgroups and to elaborate further hypotheses for new studies

    Centroblastic lymphoma

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    Review on Centroblastic lymphoma, with data on clinics, and the genes involved

    Anaplastic B-cell lymphoma

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    Review on Anaplastic B-cell lymphoma, with data on clinics, and the genes involved

    Immunoblastic lymphoma

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    Review on Immunoblastic lymphoma, with data on clinics, and the genes involved

    T-cell/histiocyte-rich large B cell lymphoma

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    Review on T-cell/histiocyte-rich large B cell lymphoma, with data on clinics, and the genes involved
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