Introduction: Structural rearrangements of chromosome 3q have been described in approximately 2% of patients with acute myeloid leukemia. Breakpoints are mainly located in the 3q21 and 3q26 regions but may occur elsewhere on chromosome 3. To determine the relationship between these breakpoints and the hematological parameters, including outcome of these patients, we analysed data from newly diagnosed adult AML patients with 3q rearrangements referred to our institution over a 15-year period.
View Article and Find Full Text PDFBackground: Ischemia-reperfusion (IR) involves adhesion of leukocytes to the activated endothelium, leading to tissue damage. CD11/CD18 beta(2) integrins interact with their ligands on endothelial cells and may therefore represent a therapeutic target for the prevention of IR. We investigated the effects of three monoclonal antibodies (mAbs) that recognize epitopes of heavy or light chain of the beta(2) integrins on IR in kidneys.
View Article and Find Full Text PDFWith the aim of determining the ability of all-trans retinoic acid (ATRA) to improve prognosis in refractory and relapsed acute promyelocytic leukemia (APL), the data of 45 patients resistant to previous conventional chemotherapy or in first relapse were retrospectively reviewed. Thirty-seven patients presented with typical M3, five with variant form (M3v), and three with intermediate form. Seven patients died before any chemotherapy could be given.
View Article and Find Full Text PDFWe describe a patient with AML with a monocytic component who developed a T-lymphoblastic lymphoma. Lymphoma was diagnosed 9 months following AML diagnosis. To our knowledge, this is the first report of phenotypically documented T-cell lymphoma following AML.
View Article and Find Full Text PDFSurface markers were studied at first relapse in 66 cases of acute myeloid leukaemia (AML), using a panel of five monoclonal antibodies directed to CD13, CD14, CD15, CD33 and CD34 antigens. At time of relapse, there was increased expression of CD33 (P = 0.002) and CD34 (P = 0.
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