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Biomedical subjects

F Falzetti

Publications and source records attributed to F Falzetti.

28 records · Page 2Linked to original sources
PubMed1990

Treatment of HL-60 cells with dimethyl sulphoxide inhibits the formation of beta-N-acetylhexosaminidase S.

beta-N-Acetylhexosaminidase of HL-60 cells was separated into two main forms, A and S, by chromatography on DEAE-cellulose. Analysis of developmental changes in the isoenzyme pattern was complicated by the fact that the specific activity of beta-N-acetylhexosaminidase underwent a 6-fold change during the normal growth cycle. Two other lysosomal enzymes, beta-galactosidase and alpha-mannosidase, behaved similarly. Induction of differentiation of HL-60 cells with dimethyl sulphoxide at a low cell density (3 x 10(5) cells/ml) had a greater effect on the abundance of alpha-subunits of beta-N-acetylhexosaminidase, measured with 4-methylumbelliferyl-beta-N-acetylglucosaminide 6-sulphate, than of beta-subunits, measured with 4-methylumbelliferyl-beta-N-acetylglucosamine, and resulted in an isoenzyme profile in which A and B were the major forms, with the levels of form S greatly decreased.

Cell Division↗
PubMed1990

Partial trisomy 1q in idiopathic myelofibrosis.

Three cases of idiopathic myelofibrosis with partial trisomy of the long arm of chromosome 1 are described. Partial trisomy 1q was the only karyotypic change detectable in unstimulated peripheral blood cell cultures of one and bone-marrow cultures of two patients at diagnosis. The extra segment from chromosome 1 was located on different karyotype sites, i.e. 1qter, 1p34 and 6p22-23; 1q21-32 was the shortest overlapping region and the only trisomic segment in one of the three patients. These findings suggest that partial trisomy 1q is a primary chromosome aberration in myelofibrosis relevant in the pathogenesis of this hematologic disorder.

Aged↗
PubMed1990

c-fms expression in acute leukemias with complex phenotypes.

The c-fms proto-oncogene product, which is the receptor for the macrophage colony-stimulating factor CSF-1, is always found expressed in acute myeloid leukemia cells, irrespective of their stage of differentiation according to the FAB classification (Dubreuil P, Torrès H, Courcoul M, Birg F, Mannoni P. Blood 1988;72:1081-1085). We have extended this study and looked for c-fms expression in poorly differentiated myeloid leukemias, in a series of acute leukemias of either T or B origin and in biphenotypic leukemias. We now report that expression of c-fms is still related to the myeloid origin of the leukemic proliferation, but that it can also be found in some acute leukemias presenting clonal rearrangements of the T cell receptor gene. Thus expression of the c-fms/CSF-1 receptor may not be exclusively a marker for myeloid proliferations.

Acute Disease↗
PubMed1989

Evolution of multiple cytogenetic clones and leukemic transformation in a case of myelodysplastic syndrome.

The cytogenetic follow-up of a case of refractory anemia with excess of blasts (RAEB) that rapidly evolved to acute myeloblastic leukemia (M1-FAB type) is described. Bone marrow analysis at presentation revealed two chromosomally abnormal clones that shared an interstitial deletion of the long arm of chromosome 5 (5q-) and a terminal deletion of the short arm of chromosome 12 (12p-), but that differed from one another in the localization of a very similar segment of chromosome 17 (i.e. 17q11-12qter) on two clearly distinct karyotypic sites: 2q37 and 17q25. Fourteen percent of the metaphases examined bore the 2q+ marker and 38% the 17q+ marker; the remaining cells had a normal karyotype. A second study carried out 4 months later, at onset of the acute phase, revealed that the clone with normal karyotype had almost completely disappeared and that there had been an inversion in the ratio of the two abnormal cell populations. In the final study, made 1 month before death, the cells with t(2;17) had totally effaced the other clone. These findings seem to indicate that, among the karyotypic changes that occurred in an original clone with 5q- and 12p-, only the t(2;17) could have played a crucial role in the final leukemic transformation.

Anemia, Refractory, with Excess of Blasts↗
PubMed1989

Antioxidant enzymes and proliferative activity of cell lines of different origin.

The effects of catalase treatment were studied in two in vitro passaged ascites tumour lines (ATP C+ and EAT) and in three in vitro established human myeloid leukemia cell lines (HL-60; KG-1; KG-1a) characterized by the arrest of cells at different stages of maturation. The results demonstrate that catalase treatment favoured proliferation in the in vitro passaged ascites tumour cells, but not in the in vitro established leukemia lines. Enzyme assays on five in vitro cell lines revealed that catalase was only present in HL-60. Although glutathione peroxidase activity was initially found in all five cell lines, it disappeared from two ascites tumour cells when they were transferred in culture. It is hypothesized that catalase treatment favours ascites tumour cell proliferation because it replaces glutathione peroxidase in eliminating H2O2.

Catalase↗
PubMed1986

t(4;21) (p16;q22) in blastic crisis of a chronic myeloid leukemia with variant Philadelphia translocation.

A chronic myeloid leukemia (CML) patient who had presented a t(2;9;22) translocation during the chronic phase developed an unusual t(4;21) (p16;q22) translocation during the M2 type FAB classification blastic crisis. The role of these two recombinant chromosomes in the genesis of the terminal phase is discussed, particularly as the breakpoint on chromosome 21 near to the ets-2 oncogene locus, seems to be the same as that described in the t(8;21) (q22;q22) translocation specific of type M2 AML.

Aged↗
PubMedDate not supplied

Mesenchymal cells: a vehicle for gene therapy.

T cell-depleted allogeneic stem cell transplantation is associated with delayed immunological reconstitution. Bone marrow stroma and interleukin 7 (IL-7) regulate homeostasis of T lymphocytes. We engineered human stromal cells with a retroviral vector containing the IL-7 gene and studied in vitro effects on T cells. Human stromal cells were successfully transduced and generated a layer that was morphologically and phenotypically normal. IL-7-engineered stromal cells conserve the biological properties of unmanipulated stromal cells. Through their production of IL-7, they enhance survival and homeostatic proliferation of naive T cells. Because of this cytokine production, they might be an ideal vehicle for gene therapy aimed at supporting lymphopoiesis in the T cell-deficient host.

Bone Marrow Cells↗
PubMedDate not supplied

Results of a prospective study with high-dose etoposide, thiotepa and carboplatin and peripheral blood stem cell rescue for high-risk stage II-IIIA and selected stage IV breast cancer patients.

AIMS AND BACKGROUND: To investigate the safety and efficacy of a high-dose chemotherapy regimen with etoposide, carboplatin and thiotepa in high-risk stage II-IIIA breast cancer and in responsive metastatic patients. STUDY DESIGN: From April 1992 to December 1998, 24 patients with high-risk stage II-IIIA breast cancer (> or = 9 positive nodes) and 9 responsive metastatic patients were enrolled in the trial. After induction chemotherapy with an anthracycline-based regimen, peripheral blood stem cells were mobilized with cyclophosphamide (7 g/m2) and G-CSF (5-16 microg/kg/s.c./day). The high-dose chemotherapy regimen consisted of etoposide (1000 mg/m2), carboplatin (800 mg/m2) and thiotepa (500 mg/m2). At the end of the high-dose chemotherapy, all stage II-IIIA patients received radiotherapy to the breast or chest wall and draining nodes; stage IV patients were irradiated to sites of disease, if feasible. All ER+ and/or PgR+ patients were treated with hormone therapy. RESULTS: For stage II-IIIA high-risk patients, the median follow-up was 4.36 years (range, 1.93-6.94), and the Kaplan-Meier estimate at 5 years of disease-free survival and overall survival was 54.8 +/- 11% SE and 76.73 +/- 9.4% SE, respectively. For metastatic patients, the median follow-up was 4.93 years (range, 4.15-7.95), and the Kaplan-Meier estimate at 5 years of progression-free survival and overall survival was 22.2 +/- 13.9% SE and 76.2 +/- 14.8% SE, respectively. No treatment-related deaths were observed. CONCLUSIONS: Our results are comparable to those obtained in other high-dose chemotherapy trials but do not seem to be superior to conventional-dose therapy given to similar patients.

Adult↗
PubMedDate not supplied

beta-galactosidase transduced T lymphocytes: a comparison between stimulation by either PHA and IL-2 or a mixed lymphocyte reaction.

BACKGROUND: Retroviral-mediated gene transfer stably introduces exogenous genes into normal and neoplastic cells of the hematopoietic system. METHODS: We used two retroviral vectors [the first, FLac, expresses a chimeric protein (Sh-ble::LacZ) between the product of the phleomycin resistance gene (Sh-ble) and the bacterial beta-galactosidase encoded by the LacZ gene; the second, NuNL vector, contains a fusion sequence (LacZ::Neo) that expresses the LacZ and the neomycin resistance genes] to transduce T lymphocytes derived from the peripheral blood of healthy human donors. Two lymphocyte activation procedures were employed: a) phytohemagglutinin/interleukin-2 (PHA/IL-2) polyclonal stimulation; b) allogeneic stimulation in a mixed irradiated or non irradiated lymphocyte reaction, both supplemented with IL-2 (MLR/IL-2). Infection was achieved by co-cultivating activated T cells with the producing amphotropic cell line pretreated with mitomycin C for 96 hours. Infection and transduction efficiency were assayed by LacZ gene expression, which is detected as indigo blue staining with the chromogenic substrate 5-bromo-4-chloro-3-indolyl-beta-D-galactopyranoside (X..Gal). RESULTS: The highest percentage of transduced T cells was reached on the 3rd PHA/IL-2 and on 9th MLR/IL-2 activation days. In these conditions with FLac vector we obtained up to 80% X-Gal+ cells after PHA/IL-2 activation and 66% and 44%, respectively, with non irradiated and irradiated MLR/IL-2, respectively. Up to 40% X-Gal+ cells were obtained with NuNL vector after PHA/IL-2 stimulation, 40% with irradiated and 48% with non irradiated MLR/IL-2 activated cells. In term of transduction efficiency, large variability was observed among patients. There were no immunophenotypical differences between FLac or NuNL vector-transduced cells activated by either of the two techniques and the control cells. CONCLUSIONS: Our results indicate that: a) the use of FLac or NuNL vector retroviral-mediated gene transfer into T-lymphocytes derived from peripheral blood and stimulated by either PHA/IL-2 or a MLR produces a high percentage of transduced T cells; b) MLR is a good system for generating a transduced alloreactive lymphocyte population. The combination of high transduction efficiency and the capacity to obtain alloreactive transduced lymphocytes should open up the possibility of generating new in vitro and in vivo studies with selectable genes for in vivo therapeutic use.

Drug Resistance, Microbial↗