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Biomedical subjects

S Frytak

Publications and source records attributed to S Frytak.

At least 91 records · Page 5Linked to original sources
PubMed1978

Phase II study of metronidazole therapy for advanced colorectal carcinoma.

Thirty-two patients with advanced carcinoma of the colon or rectum were given metronidazole orally at a dose of 500-1000 mg/m2 three times a day for 7 consecutive days every 6 weeks. The dose-limiting toxic effects consisted of severe nausea, vomiting, and major motor seizures. Mild peripheral neurotoxic effects were also noted. No objective responses were noted in any of the 32 patients treated. High-dose metronidazole would not seem to have any role in the treatment of advanced colorectal carcinoma and may cause serious neurotoxicity.

Adult↗
PubMed1978

Evaluation of a fixed alternating treatment in patients with advanced breast cancer.

A total of 128 patients were randomly assigned to two induction treatment programs: Adriamycin and L-PAM versus Cytoxan, 5-Fluorouracil, and Prednisone in an effort to assess their primary capacity for objective response. The two regimens appeared quite comparable in this respect. The 100 patients who had achieved clinical benefit following initial treatment were subsequently randomly allocated to reveive either a fixed alternate treatment program involving the two drug regimens or were continued on the treatment program responsible for their initial improvement. Although those patients who received the fixed alternate treatment shcedule had a somewhat longer progression-free interval compared to the two single-treatment programs (median duration of 16 months versus 12 months, respectively), the three treatment programs including the fixed alternate treatment schedules had comparable median survivals of 21-24 months with little difference noted in survival curves at any point thus far in the analysis. There were no differences noted in survival for the fixed alternating treatment group of patients, with respect to which induction regimen had been utilized to achieve initial response. The toxicity for these treatment programs was tolerable and compatible with outpatient administration. Myelosuppression occurred in the vast majority of patients on either regimen but in both regimens was relatively platelet sparing.

Antineoplastic Agents↗
PubMed1978

cis-Dichlorodiammineplatinum(II) alone followed by adriamycin plus cyclophosphamide at progression versus cis-dichlorodiammineplatinum(II), adriamycin, and cyclophosphamide in combination for adenocarcinoma of the lung.

Forty-one patients with proven metastatic adenocarcinoma of the lung were randomized into two comparable groups after stratification for performance status and presence of measurable or evaluable disease. Treatment 1 consisted of cis-dichlorodiammineplatinum(II) (P) at a dose of 15 mg/m2/day by iv push on Days 1--5 every 4 weeks. Upon progression or the onset of renal toxic effects, patients were crossed over to cyclophosphamide (C) at a dose of 400 mg/m2, and adriamycin (A) at a dose of 40 mg/m2, both given by iv push on Day 1 every 4 weeks. Treatment 2 (CAP-I) consisted of C-A in the same doses as above plus concurrent P, 40 mg/m2 by IV push on Day 1 every 4 weeks. Eight patients receiving P developed serum creatinine values greater than or equal to 1.5 mg/100 ml versus one patient receiving CAP-I (P = 0.05). Objective regressions occurred in two of 22 patients with P, five of 17 with C-A, and eight of 19 with CAP-I (P = 0.025; CAP-I versus P). There was a significant increase in the median duration of regression in patients responding to C-A following P (267 days) versus patients responding to CAP-I (95 days). The improved rate of response with CAP-I and the prolonged duration of response with C-A following P suggest a potentiating effect between P and C-A whether given simultaneously or sequentially.

Adenocarcinoma↗
PubMed1977

A phase II study of triazinate (NSC 139105) in advanced colorectal carcinoma.

Triazinate (Baker's Antifol, NSC 139105) was given to 28 patients as a single agent in the chemotherapy of advanced colerectal carcinoma. The dosage utilized was 250 mg/m2 intravenously, administered daily in three consecutive days. Patients were evaluated at three weeks, six weeks, and then monthly until progression was evident. Various immunologic determinants (i.e., DNCB sensitization, immunoglobulins, recall skin tests, lymphocyte blastogenesis, and circulating lymphocytes, T-cells and B-cells) were obtained prior to treatment and at each re-evaluation. The principal side effects were dermatitis, stomatitis, diarrhea, nausea, somnolence, and leukopenia. There was no discernable effect of Triazinate on the immunologic determinants tested. There was one complete response, and four partial responses, for an objective regression rate of 18%. This study suggests that Triazinate has a definite, though limited, effect on advanced colorectal carcinoma.

Adenocarcinoma↗
PubMed1976

A phase I study of cytembena.

Twenty-two patients were given progressively increasing doses of Cytembena to determine toxicity patterns and to establish a dosage which produces definite but clinically tolerable toxicity when the drug is given by intravenous injections in a 5-day intensive course. Toxicity consisted primarily of nausea, vomiting, arm pain, and transiently decreased renal function. At higher doses, an "autonomic-storm" phenomenon was observed consisting of hypertension, tachycardia, tachypnea, hyperperistalsis, frequent explosive defecation, facial flushing and paresthesias, and chest pain with accompanying ischemic EKG changes. There was no evidence of mucocutaneous, hepatic, or hematologic toxic effects. Toxicity was dose-related, first being recognized at a daily dose of 300 mg/m2 and becoming clinically intolerable at a daily dose of 475 mg/m2. No permanent damage was observed in any of the organ systems monitored. An acceptable treatment regimen for most patients is 400 mg/m2/day for 5 days. Patient discomfort can be reduced by dividing each day's dose into two intravenous injections given at an interval of at least 6 hours. Coronary artery disease and impaired renal function should be contraindications to Cytembena therapy, and caution should be employed in the patients with significant impairment of liver function. Two of 22 patients, both with far-advanced carcinoma and previous chemotherapy failures, showed a favorable objective response to Cytembena therapy. Phase II studies to assess the magnitude of the drug's antineoplastic activity seem warranted.

Acrylates↗
PubMed1976

Clinical comparison of adriamycin and a combination of methyl-CCNU and imidazole carboxamide in disseminated malignant melanoma.

The effects of adriamycin were compared to a combination program of methyl-CCNU and imidozole carboxamide (DTIC) in 44 patients with disseminated malignant melanoma. There were objective clinical responses in 6 of 21 patients with the combination of DTIC and methyl-CCNU who received this program as primary treatment and none in 23 patients receiving adriamycin as primary treatment. Secondary responses were not observed with either treatment regimen. Toxicity with the combination program included leukocyte depression (less than 3,000/cu mm) in 25% and platelet depression (less than 100,000/cu mm) in 40% compared to 52% leukocyte depression and 16% platelet depression after adriamycin. There were no responses after the combination treatment program in the absence of myelosuppression. There was nausea and vomiting in virtually all patients, which was moderately severe in one third of the patients receiving the combination and in only 10% of those receiving adriamycin. Alopecia developed in all who received adriamycin but in only 15% of the combination treatment group. The combination treatment response of 28% was of the same order as most response rates previously reported in this disease. This randomized controlled clinical trail found adriamycin without clinical benefit and not worthy of further trial in patients with disseminated malignant melanoma.

Adult↗
PubMedDate not supplied

Neuronal autoantibody titers in the course of small-cell lung carcinoma and platinum-associated neuropathy.

The aims of this study were to investigate, in patients with newly diagnosed small-cell lung carcinoma (SCLC), whether or not there may be a relationship between the presence, type or titer of circulating neuronal autoantibodies and (i) the extent of SCLC dissemination at presentation, (ii) the development of peripheral neuropathy during platinum chemotherapy, (iii) survival time. We studied stored serum from 58 patients with uncomplicated SCLC who had participated in two trials conducted by the North Central Cancer Treatment Group (NCCTG); 29 had extensive disease and 29 had limited disease. No patient had neuropathy or other neurological or paraneoplastic problems at the time of enrollment but each group included 14 or 15 patients respectively who developed peripheral neuropathy in the course of chemotherapy. We tested five consecutive serum specimens from each patient in blinded fashion by (i) an indirect immunofluorescence assay optimized to detect neuron-restricted nuclear and cytoplasmic antibodies (triple substrate of mouse cerebellum, gut and kidney), and (ii) immunoprecipitation assays to detect neuronal Ca2+-channel-binding antibodies (N-type and P/Q-type). Sera that were positive by immunofluorescence were analyzed further by Western blotting. Neuronal autoantibodies were significantly more frequent in patients who had limited SCLC at presentation (12/29 or 41% positive) than in those with extensive SCLC (5/29 or 17% positive, P = 0.02). Neuronal autoantibodies of nuclear or cytoplasmic specificity were found in 50% of the seropositive patients with limited SCLC (21% of the total group), but in no patient with extensive SCLC (P = 0.01). The frequency of neuronal autoantibodies did not differ significantly among patients who did and did not develop peripheral neuropathy. Titers fell progressively during chemotherapy and did not rise again when peripheral neuropathy became clinically evident. This argues against a synergism between drug toxicity and neuronal autoimmunity as the mechanism of platinum-associated peripheral neuropathy. Seropositivity for neuronal autoantibodies did not affect the survival of patients with either limited or extensive SCLC. It is conceivable that the immunosuppression attendant on combined cisplatin/etoposide therapy cancels a pre-existing protective antitumor immune response (presumably cytotoxic-T-cell-mediated) for which the nuclear and cytoplasmic paraneoplastic IgG autoantibodies serve as a surrogate marker. Testing of this hypothesis would require the survival of seropositive and seronegative patients to be compared in a larger trial, using a therapeutic modality that does not compromise immunocompetence.

Antineoplastic Agents↗