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Biomedical subjects

G Masera

Publications and source records attributed to G Masera.

At least 127 records · Page 7Linked to original sources
PubMed1990

Cytotoxicity and DNA damage caused by 4-demethoxydaunorubicin and its metabolite 4-demethoxy-13-hydroxydaunorubicin in human acute myeloid leukemia cells.

4-Demethoxydaunorubicin (4-DMDR) and its major metabolite 4-demethoxy-13-hydroxydaunorubicin (4-DMDRol) were investigated for their cytotoxicity and mode of action against human leukemic cells. The drug and its metabolite appeared to be equally potent as both inhibitors of cell proliferation and inducers of DNA double-strand breaks in the OCI AML-3 cell line and cells derived directly from patients with acute myeloid leukemia (AML). This suggests that 4-DMDRol plays an important role in the antileukemic activity of 4-DMDR.

Adult↗
PubMed1990

Social integration of the older thalassaemic patient.

Because social policy favours the fullest possible social integration of chronically ill patients, we have evaluated the facilities that are needed to achieve this for patients with beta thalassaemia major in the light of the therapeutic advances that now permit them to survive into adulthood. We have investigated the social integration of adolescent and young adult thalassaemic patients, 171 from Greece and 112 from Ferrara in Italy. Patients in both areas show a good level of social integration and favourable self image, indicating what may be achieved by providing psychosocial support as part of a comprehensive approach to treatment.

Adolescent↗
PubMed1989

Treating childhood acute lymphoblastic leukaemia (ALL): summary of ten years' experience in Italy. ALL Steering Committee of the Associazione Italiana Ematologia Oncologia Pediatrica (AIEOP).

Between 1976 and 1986, 2,093 children with ALL were enrolled in three consecutive generations of trials conducted by the Associazione Italiana Ematologia Oncologia Pediatrica (AIEOP). A 50% event-free survival at 5 years was achieved overall in this population, approximately accounting for more than 50% of the entire childhood ALL population in Italy. Participation in the group protocols increased from the original seven founding centers to the current 37 institutions. Results in the standard population (non-T immunophenotype, non-FAB L3, and less than 50,000 white blood cells (WBC/ml) were considerably better with more recent, more aggressive protocols. The two major results in this population (N = 540) were a relatively low incidence (8% at 5 years) of central nervous system (CNS) relapse in the "good"-risk population (less than 10,000 WBC, ages 3-6 years, and FAB L1), without the use of cranial irradiation, and a projected 4-year disease-free interval for bone-marrow relapse of 80% in the "average"-risk group, where a three-drug reinduction program was adopted after consolidation. Overall, the event-free survival of the most recent generation (protocol 82, median follow-up time of 38 months) is 66% at 4 years (95% confidence limits [CL] 61-71). Based on these 10 years of experience, the general strategy of the group for the 90s is outlined and discussed.

Adolescent↗
PubMed1989

Meetings with parents after the death of their child from leukemia.

There is a growing interest in the emotional status of parents and siblings after the death of a child with chronic disease. For the past 7 years physicians at our center have systematically contacted parents who lost a child because of leukemia within the first few months after the death. From this experience it appears that most parents needed to talk at least once with the physicians who took care of their child. As expected, some parents and siblings were found to have significant psychological problems and to need psychologic support. We suggest that the opportunity to talk with a physician of the attending staff should be provided routinely to parents shortly after the death of a child from leukemia.

Acute Disease↗
PubMed1989

[Periodontal conditions in growth age patients treated for leukemia with chemotherapy and radiation therapy protocols].

Patients affected by acute leukemia under radiotherapy and chemotherapy, less them 12 years ols were investigated about periodontal health. Patients were in total remission. Clinical and radiological X-Ray exams investigated soft deposits, calculus, intensive gingivitis, periodontal lesions and CPITN index. The Authors concluded that indices of these patients are better than in normal subjects.

Adolescent↗
PubMed1989

T-cell receptor delta gene rearrangement in childhood T-cell acute lymphoblastic leukemia.

During the development of functional T lymphocytes, a variety of genes involved in antigen recognition undergo somatic rearrangement. These include the alpha, beta, and gamma chain genes. Recently a fourth rearranging gene, the delta chain gene, embedded in the alpha chain locus, has been described. We have determined the structure of the beta, gamma, and delta chain genes in 15 cases of T-cell acute lymphoblastic leukemia (T-ALL) representing stage I (CD7+, CD1-, CD3-) and stage II (CD7+, CD1+, CD3-) of intrathymic T-cell development. The alpha-delta locus was rearranged in 14 of the 15 cases. In three cases the delta constant region was deleted on both chromosomes, suggesting biallelic V-J alpha rearrangement. A limited pattern of rearrangement of the delta locus was observed in the remaining 11 cases. When the alpha-delta region was rearranged, there was rearrangement of the beta and gamma TcR in all cases except two; in these cases the beta chain was in the germline configuration. These findings support the hypothesis that delta chain gene rearrangement is an early event in T-cell development, possibly contemporary to gamma gene rearrangement, and that the delta locus has a limited repertoire.

Gene Rearrangement, T-Lymphocyte↗
PubMed1989

Cranial computed tomography findings in children with acute lymphoblastic leukemia at diagnosis.

Forty children newly diagnosed with acute lymphoblastic leukemia (ALL) were examined by computed tomography (CT) of the central nervous system (CNS) on hospital admission before any medication was started. The results of the CT scans were defined as normal, borderline (slight or moderate dilatation of the ventricular system and/or basal cisterns and/or convolutional sulci), or pathologic (severe cerebral atrophy). The mean age of the patients was 5.8 years (range 1.7-15 years). Sixteen of the 40 patients (40%) had CT scan abnormalities with 14 patients having borderline scans and two patients pathologic scans. No child presented with neurologic symptoms or CNS leukemia. These data suggest that CT abnormalities of the brain are common in children with ALL at diagnosis and may represent clinically unsuspected lesions secondary to leukemia.

Adolescent↗
PubMed1988

Neuroblastoma during acute lymphoblastic leukemia in remission.

Neuroblastoma was diagnosed in a child after a 20-month remission of a pre-B acute lymphoblastic leukemia (ALL). Clumps of atypical cells suggestive of neuroblastoma were seen in the bone marrow. They were positive for monoclonal antibody (MoAb) UJ13A (neuroblastoma cells) and negative for MoAb T29/33 (anti-leucocyte common antigen CD45) with immunocytochemical staining. A right paravertebral mass displacing the kidney was demonstrated by abdominal echotomography, and serum vanilmandelic acid was slightly increased. Despite specific chemotherapy against neuroblastoma and after a transient clinical improvement, the patient died 7 months later of disseminated disease. Immunocytochemical staining on cells frozen at diagnosis of leukemia with MoAb UJ13A and T29/33 was unable to demonstrate neuroblastoma cells and showed the pattern usually observed in leukemia (UJ13A- and T29/33+).

Antibodies, Monoclonal↗
PubMed1988

Comparison of histone variant synthesis in human lymphocytic leukemia cells and in normal lymphocytes.

The synthesis of core histone variants and of histone H1 variants was determined in fresh leukemic cells of eight patients with leukemia [seven acute lymphoblastic (ALL) and one chronic lymphocytic (CLL)], in normal lymphocytes from healthy donors or from ALL patients in complete remission. Histone variant synthesis was evaluated by incubating cells with [14C]Lys and [3H]Arg in medium without Lys and Arg and then by two-dimensional polyacrylamide gel electrophoretic separations (acetic acid-urea-Triton x-100 acetic acid-urea-hexadecyltrimethylammonium bromide for core histone variants; sodium dodecyl sulfate/acetic acid-urea-hexadecyltrimethyl ammonium bromide for H1 variants). As previously reported, quiescent lymphocytes and lymphocytes stimulated with phytohaemagglutinin (PHA) showed clearcut changes in the proportions of synthesis of core histone variants and H1 variants. Leukemic lymphocytes freshly obtained from blood showed a pattern of core histone synthesis and H1 synthesis intermediate between that of quiescent and PHA-stimulated lymphocytes; this is probably due to the presence of a mixture of resting and growing cells. When leukemic cells were stimulated to grow by mitogens, the pattern of core histone and H1 variant synthesis was similar to that in mitogen-stimulated normal lymphocytes. Histone variants whose synthesis is associated with the S-phase were not synthesized in leukemic cells treated with the DNA synthesis inhibitors hydroxyurea and 1-beta-D-arabinofuranosylcytosine (Ara-C). The pattern of acetylation of histone H4 was also apparently similar in leukemic cells and normal lymphocytes. The radioactivity associated with the ubiquitinated forms of H2A increased in nongrowing lymphocytes and in leukemic cells treated with DNA synthesis inhibitors whereas they decreased after mitogenic stimulation. Variability was wide in the synthesis of ubiquitinated H2A in different cases of leukemia. The only clear-cut difference between leukemic cells and normal lymphocytes was that leukemic cells from ALL patients, but not lymphocytes from normal donors or from ALL patients in complete remission, synthesized appreciable amounts of H1 degrees, increasing after hydroxyurea/Ara-C treatment and decreasing after PHA-stimulation. In leukemic cells from a CLL patient H1 degrees synthesis was undetectable.

Acetylation↗