Search PubMed⌕ Search

Biomedical subjects

T Vietti

Publications and source records attributed to T Vietti.

At least 37 records · Page 2Linked to original sources
PubMed1985

Comparison of cytotoxicity of single dose and infusion of alkylating agents.

Both cytotoxicity and host toxicity were examined for the alkylating agents HN2, BCNU and L-PAM administered intravenously (IV) either as a single bolus injection or a 24-hour infusion. The bolus injection was more effective than the infusion schedule at a given dose for BCNU and L-PAM. Unexpectedly, the HN2 infusion schedule was more effective than bolus injection at a given dose. When host survival was the endpoint, both HN2 and L-PAM were shown to be more effective by the infusion schedule.

Alkylating Agents↗
PubMed1984

Pre-B cell leukemia responds poorly to treatment: a pediatric oncology group study.

Seventy-eight of 362 children with acute lymphocytic leukemia (ALL) had leukemic cells similar in phenotype to normal pre-B cells. When the clinical and laboratory features of patients with pre-B and "null" cell phenotypes of ALL were compared, no significant differences were noted, except that the pre-B cell ALL phenotype had a higher percentage of black children. In contrast, patients with T cell ALL had a higher median age at diagnosis, frequent thymic involvement, and higher WBC counts. Patients with pre-B and "null" cell ALL were treated identically and patients with T cell ALL differently. Although no difference in remission induction rates was noted between patient groups with pre-B and "null" cell ALL, the remissions were of shorter duration for patients with pre-B cell ALL (p = 0.004). Similarly, overt leukemic involvement of both the central nervous system (CNS) and bone marrow was noted sooner in the patient group with pre-B cell ALL. Univariate and multivariate Cox life table regression analyses demonstrate the independent prognostic significance of the pre-B phenotype and illustrate that the prognostic influence of potential relapse risk factors, such as WBC, sex, and age, are specific for leukemia phenotype. These findings may have importance for the design and tailoring of therapy for children with acute leukemia.

B-Lymphocytes↗
PubMed1982

Properdin factor B and acute lymphocytic leukemia (ALL).

One hundred-sixty-four ALL patients were compared to 545 controls for differences in phenotype and gene frequencies at the Properdin factor B locus. In addition, 90 of the ALL patients were immune phenotyped. A significant association with the Bf F allele and ALL was found, resulting in an estimated relative risk of 3.62. There was no difference in the Bf S phenotype between ALL patients and controls. However, those homozygous for the Bf S allele are at a significantly low risk of 0.30 for developing ALL. ALL patients with a non-B/T cell type were 2.5 times more likely to be Bf SS homozygotes; in contrast, those patients with the pre-B cell type were 2.5 more likely to be Bf FF homozygotes. These data suggest association of the Bf locus with an ALL protection and/or susceptibility gene(s).

Alleles↗
PubMed1981

Combination chemotherapy study for remission maintenance in ALL: an evaluation of vincristine, cyclophosphamide and vincristine, cyclophosphamide, and BCNU: a Southwest Oncology Group Phase II Study.

Vincristine (VCR), cyclophosphamide (CP), and BCNU have antineoplastic activity in acute lymphocytic leukemia. In animal tumor systems, and in a clinical controlled study, vincristine and cyclophosphamide have been demonstrated to be more effective when given sequentially. In animal models, cyclophosphamide and BCNU have a synergistic effect if given simultaneously. In order to evaluate this potentially synergistic schedule in man, children with ALL in their second or greater remission were randomized to receive either a standard vincristine cyclophosphamide regimen (VCR 2 mg/m2 on day 1 and CP 450 mg/m2 on days 2 and 3) or this same regimen with the addition of 50 mg of BCNU given with the CP given on days 2 and 3. The standard two-drug regimen was given every 3 weeks and the potentially synergistic combination was given on a 4-week schedule. The median duration of remission (MDR) for the 18 children receiving the two-drug combination was 13.5 weeks, and for the 20 children receiving the potentially synergistic three-drug regimen combination, 15 weeks. With 95% confidence, the population MDR for the two-drug combination is from 63% to 125% of the population with the three-drug regimen. The toxicities of both regimens was tolerable. No statistically significant synergistic benefit was demonstrated in these patients with the addition of BCNU to cyclophosphamide.

Adolescent↗
PubMed1980

Intergroup Ewing's Sarcoma Study: local control related to radiation dose, volume, and site of primary lesion in Ewing's sarcoma.

One hundred ninety-three patients with localized Ewing's sarcoma treated at participating instutitions of the Intergroup Ewing's Sarcoma Study form the basis for this report. All patients received radiation therapy to the primary lesion and were randomized to receive vincristine, actinomycin-D, and cyclophosphamide (VAC) plus adriamycin (Regimen I); VAC alone (Regimen II); or VAC and bilateral pulmonary irradiation (Regimen III). Local control was achieved in 96% of the patients in Regimen I, and 86% of the patients in both Regimens II and III. The median duration of follow up was 83 weeks and median survival time was 172 weeks. Incremental doses of irradiation did not result in significant changes in the rate of local control of primary lesions. The local control rate was the same (92%) for tumors treated by means of whole-bone irradiation or with at least 5 cm of free margin around the lesion. The local control rate decreased to 79% for lesions treated with less than 5-cm margin. Excellent control was obtained for lesions involving the skull or spine (100%), and distal bones (fibula, 96% and tibia, 91%). Less favorable control rates were noted for pelvic and humeral lesions (84% and 79%, respectively). Bilateral pulmonary irradiation for subclinical disease played a role in lowering the incidence of lung metastases from 38% to 20% for patients treated with VAC. Lung metastases were similarly decreased (10%) when adriamycin was added to VAC chemotherapy.

Bone Neoplasms↗
PubMed1980

Phase I evaluation of vindesine in children: a Southwest Oncology Group pilot study.

Twenty-one children (19 with leukemia) were given 34 courses of vindesine on a weekly or twice-weekly schedule in escalating doses. Thirty-three courses were fully or partially evaluable for response and/or toxicity. Granulocytopenia was the dose-limiting toxicity. Transient jaw, neck, or bone pain was common after each dose. Motor weakness, paresthesias, and constipation were neither frequent nor severe. In this Phase I study, vindesine had some antileukemia activity in children previously treated with vincristine and other drugs. Phase II studies are warranted and a starting does of 1.85% mg/m2 twice weekly appears tolerable.

Adolescent↗
PubMed1980

Cytotoxicity of adriamycin combined with methotrexate against L1210 leukemia in mice.

The combination of adriamycin and methotrexate was found in mice to be synergistic in cytotoxicity to L1210 leukemia cells for a range of time intervals between the two agents. Cytotoxicity for normal hematopoietic stem cells was less than additive. Spleen colony assays were used to quantitate both cell populations. Increase in life-span assays yielded similar results. Also, the extent of synergy was dependent on the dose of adriamycin only.

Animals↗
PubMed1980

Effect of dose fractionation of daunorubicin on survival of leukemic cells.

Mice bearing transplanted AKR leukemia received daunorubicin either as a single dose or as four equally divided doses (0.2 mg/mouse; four times) with the time interval between the divided doses varying from 12 to 36 hr; survival of leukemia colony-forming cells was then assayed. When daunorubicin was administered in any of the fractionated schedules, the dose-survival curve was exponential with a shoulder region demonstrable. As expected, there was significantly less cell killing for the fractionated schedule than for a comparable accumulated single dose; however, with administration of the fourth dose for any interval studied, the increment in cell killing was so large that it was quite similar to that resulting from a single 0.8-mg/mouse dose. We examined the time course of cell killing for the 24-hr fractionation schedule and found greater killing than expected after each subsequent dose with the most pronounced increase occurring after the fourth dose. Possible mechanisms for this effect are discussed.

Animals↗
PubMed1977

Combined treatment modalities of rhabdomyosarcoma in children.

Thirty-nine previously untreated children with rhabdomyosarcoma were managed by a coordinated program of surgery, radiation therapy, and chemotherapy during the years 1960 to 1973. The primary tumor was located in the head and neck (24), chest wall (1), abdomen (1), pelvis (10), and lower extremity (3). Radiation therapy consisted of tumor doses of 5000 to 6000 rads delivered in five to six weeks. Combination chemotherapy with actinomyctin-D, vincristine and cyclophosphamide was used after 1968. Seventeen of 25 cases (68%) treated after 1968 are alive two to five years following treatment. Only four of 14 cases (29%) who received less radical therapy before 1968 are alive. A relatively high incidence of local failure (23%) was noted in spite of adequate doses of radiotherapy. None of the four cases with metastatic disease at the time of diagnosis survived. Major complications were mainly noted in patients with orbital rhabdomyosarcoma. Correlation of absolute survival with dose of irradiation, primary site, extent of disease and histologic subtypes of the tumor are discussed.

Adolescent↗
PubMed1977

Cellular quantitation of in vivo effects of 1-beta-D-arabinofuranosylcytosine on leukemia L1210.

We derived a cellular model for the use of the cytidine analogue 1-beta-D-arabinofuranosylcytosine (ara-C) against L1210 leukemia in vivo from dose- and time-survival studies. We employed a quantitative assay for leukemia colony-forming cells to construct dose- and time-survival curves for single, divided, and infused doses of ara-C. Time-survival curves for a large dose range of ara-C indicated not only cell killing but also progression delay effects in vivo. Divided dose studies showed the extent of cell killing (optimum effect) to be dependent upon both the dose and the interval of time between administration of the drugs. When the drug was given as an infusion, the extent of cell killing was as great as that produced by the best fractionation schedule, an effect which was verified in terms of therapeutic efficacy in leukemic mice.

Animals↗
PubMed1976

Combined effect of cytosine arabinoside and thiopurines.

Dose and time survival for leukemic colony-forming units (LCFU) and normal hematopoietic colony-forming units (NCFU) were obtained after the administration of either 6-mercaptopurine (6-MP) or 6-thioguanine (TG). Survival decreased to a plateau level with increasing doses as expected with phase-specific agents. Time survival curves demonstrated increased killing of LCFU after administration of 2 mg of 6-MP/mouse or 0.1 mg of TG/mouse reaching a minimum by 3-8 hours with repopulation therafter. Cytosine arabinoside (Ara-C) (1 mg/mouse) was combined with each agent, and the effects of sequence and interval were examined in terms of LCFU and NCFU survival. When Ara-C and either thiopurine were administered together, fractional survival was less than additive. However, as the interval was increased for either sequence and for both combinations, survival decreased to synergistic levels. Variation in dose of Ara-C and TG showed an inhibitory effect to be dependent upon the Ara-C dose. A correlation between results from the colony assay for for LCFU and survival of treated tumor-bearing mice was demonstrated for Ara-C plus TG. The results of these experiments are interpreted in terms of the proliferation kinetics of L1210 and the cellular effects of the agents; their clinical implications are discussed.

Animals↗
PubMed1975

The enhanced cytotoxicity of combinations of 1-beta-D-arabinofuranosylcytosine and methotrexate.

Although both 1-beta-D-arabinofuranosylcytosine (ara-C) and methotrexate are presumed to be toxic as a result of their interference with DNA synthesis, results obtained with L1210 cells in vivo suggest that the combination of ara-C and methotrexate is capable of killing cells by a mechanism not related simply to DNA synthesis inhibition. Simultaneous administration of ara-C and methotrexate, or administration of these two agents within a 10-hr interval, independent of order, produces a synergistic cell kill of L1210 cells but a less than additive effect on normal hematopoietic stem cells. The extent of synergy seems dependent upon the dose of ara-C.

Animals↗