Background And Objective: Different therapeutic approaches are needed to restore apoptotic mechanisms in CLL cells, as present ones are not successful. We assessed the apoptotic effects of stable butyrate derivatives on CLL lymphocytes: in these molecules a mannose molecule is bound as ester to one-five butyrate moieties, conferring pharmacological stability to the pro-drugs which are able to induce apoptosis in primary AML blasts.
Design And Methods: Peripheral blood samples obtained from 17 patients with typical B-CLL were cultured in the presence of 0.
We report the onset of pure red cell aplasia (PRCA) in a patient with a history of polyglandular syndrome including Addison's disease, malabsorption syndrome, diabetes type I and gastric hyperplastic polyposis. An autoimmune origin for this complex disorder was not supported by the presence of organ specific antibodies, but T cells were found to be of polyclonal origin, as demonstrated by molecular analysis of T cell receptor (TCR) gene rearrangement. The pathophysiology of this case, based on laboratory findings and response to therapy, is discussed.
View Article and Find Full Text PDFBackground: Blast phase of chronic myeloid leukemia (CML) as well as the rare acute transformation of other chronic myeloproliferative disorders constitute forms of leukemia that are particularly refractory, even to aggressive chemotherapy. Many attempts have thus been made to identify new drugs that could be active in these diseases. We wanted to evaluate whether gemcitabine (dFdC), a pyrimidine analogue widely employed in lung cancer chemotherapy, was able to block in vitro proliferation of bcr/abl-positive and bcr/abl-negative blast cells in primary culture.
View Article and Find Full Text PDFBackground: Chronic myeloid leukemia (CML) is a disease characterized by the presence of a unique molecular marker, i.e. the fusion gene bcr-abl and its mRNA and protein products.
View Article and Find Full Text PDFThis study was designed to compare the effects of fludarabine and gemcitabine on cytosine arabinoside (Ara-C) uptake and retention, and their specific cytotoxicity on HL 60 human acute myeloid leukemia cells. The leukemic blasts were exposed to either drug at equimolar concentrations (10 microM) for 3 h and further incubated with Ara-C (5 microM), added immediately (day 0) or after an interval of 24 h in cells were kept in a drug free medium (day 1). On day 0, leukemic cells exposed to fludarabine 10 microM had a significant (P<0.
View Article and Find Full Text PDF