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Biomedical subjects

S Gundersen

Publications and source records attributed to S Gundersen.

At least 55 records · Page 3Linked to original sources
PubMed1988

Phase II study of iproplatin (CHIP, JM-9) in advanced testicular cancers progressing after prior chemotherapy.

Twenty-two patients with advanced testicular cancer received iproplatin at a dose of 180-240 mg/m2 every 4 weeks. All the patients progressed or recurred after chemotherapy including cisplatin. The most severe toxicity was thrombocytopenia with two toxic deaths after a first cycle of 240 and 180 mg/m2 respectively. Nausea and vomiting were almost universal but mild in intensity. One renal failure occurred 6 weeks after the first cycle while the tumor was progressing. No antitumor activity was observed in this heavily pretreated population of patients.

Adult↗
PubMed1988

Predictive chemosensitivity testing in malignant melanoma: reliable methodology--ineffective drugs.

A retrospective and a prospective trial were carried out in patients with malignant melanomas to investigate the predictive value of an in vitro chemosensitivity assay based on the Courtenay and Mills soft agar cultivation method. Evaluable in vitro chemosensitivity data for the three agents DTIC, CCNU, and vinblastine were obtained in 153 cases. In the retrospective study in which the patients received chemotherapy without prior knowledge of the test results, 50 in vitro/in vivo correlations (40 patients) were made, and in the prospective study, where patients received the single agent most active in vitro, 55 correlations (45 patients) were performed. In both studies the sensitivity of the test (the ability to identify patients who will respond to chemotherapy) was approximately 100% and the specificity (the ability to identify patients who will not respond) was 87-98%. Depending on whether 'no change' and 'mixed response' were classified as sensitivity or resistance, the predictive value of a negative test was approximately 100% and that of a positive test 37.5-87.5%. The response rate was low in both series, and although it was somewhat higher in the prospective than in the retrospective trial, the difference was not significant. The median survival time was not significantly different in the two treatment series. We conclude that the chemosensitivity assay here used is reliable and has predictive value, but that the chemotherapeutic agents currently available for treatment of melanoma are too ineffective to warrant routine use of the assay in this disease.

Dacarbazine↗
PubMed1987

The EORTC Early Clinical Trials Cooperative Group experience with 5-aza-2'-deoxycytidine (NSC 127716) in patients with colo-rectal, head and neck, renal carcinomas and malignant melanomas.

The Early Clinical Trials Cooperative Group of the EORTC conducted several phase II studies with a pyrimidine analogue of deoxycytidine, 5-aza-2'-deoxycytidine (DAC). The drug was given as three consecutive 1 h i.v. infusions of 75 mg/m2, separated by intervals of 7 h; courses were repeated every 5 weeks. A total of 101 eligible patients were studied: 42 with colo-rectal adenocarcinoma, 27 with squamous cell carcinoma of the head and neck, 18 with malignant melanoma and 14 with renal cell carcinoma. Drug-induced toxicities consisted of moderate myelosuppression, and nausea and vomiting. One single partial remission was seen in a patient with malignant melanoma. DAC given in this dose and schedule is devoid of antitumour activity in adult patients with these refractory types of carcinomas.

Adenocarcinoma↗
PubMed1987

Mitozolomide (NSC 353451), a new active drug in the treatment of malignant melanoma. Phase II trial in patients with advanced disease.

A phase II trial with mitozolomide was carried out in patients with malignant melanoma, since in preclinical studies this new imidazotetrazine had shown promising effects against human melanoma xenografts. Twenty-one evaluable patients with advanced malignant melanoma were treated with 115 mg m-2 of mitozolomide, given orally every 6 weeks. None of the patients had received prior chemotherapy. Two partial responses (10 and 7+ months) were observed. The responding patients had lung metastases, and one of them had, in addition, a huge (17 X 14 cm) lymph node metastasis in the groin. Also, one patient had a 48% tumour volume reduction of lung metastases. The dose limiting side effect of the treatment was bone marrow depression, with delayed leukopenia and thrombocytopenia. The median white blood cell counts and platelet nadirs were 2.5 X 10(9) 1(-1) (range 1.1-3.8) and 59 X 10(9) 1(-1) (range 14-95), respectively. Non-haematological adverse reactions were limited to mild or moderate nausea. It is concluded that orally administered mitozolomide is active against malignant melanoma and seems to have a response rate comparable to those of the most active established drugs.

Adult↗
PubMed1986

Phase II study of 5'-deoxy-5-fluorouridine (doxifluridine) in advanced malignant melanoma.

Forty-two patients with malignant melanoma were treated with doxifluridine, 4000 mg/m2 daily X 5, repeated every 3 weeks. The daily dose was reduced to 3000 mg/m2 in patients who had experienced severe myelosuppression with prior chemotherapy. A total of 35 patients were evaluable for response, and 25 of these received two or more courses. Two responses were observed. Toxicity mainly took the form of nausea, vomiting, stomatitis, dizziness, ataxia, and fatigue. Mild leukopenia was frequent (43%). Nadir counts less than 1.5 X 10(9)/l leukocytes or 50 X 10(9)/l platelets were seen in 7% and 2% of the courses respectively. Doxifluridine has no useful activity against malignant melanoma.

Drug Evaluation↗
PubMed1986

Weekly adriamycin versus VAC in advanced breast cancer. A randomized trial.

In a prospective randomised study 128 patients with advanced breast cancer were treated either with Adriamycin (20 mg/week) or vincristine, Adriamycin and cyclophosphamide (VAC). An objective response was obtained in 31 and 35% of patients in the two groups. There was no significant difference with regard to duration of response or survival. Weekly low dose Adriamycin was well tolerated. When subjective side effects occurred, they were usually slight and transient. In approx. 40% of the patients no side-effects at all were observed. Eight per cent had alopecia requiring a wig. Only slight myelosuppression could be seen in a few patients and this had no practical implications. Most or all of VAC patients experienced severe toxicity with regard to nausea, vomiting and alopecia. Also myelosuppression was more pronounced among VAC patients. It is concluded that weekly doses of Adriamycin as single agent therapy for advanced breast cancer is as effective as the VAC combination delivered every third week, with considerably less toxicity.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1986

Radiation in combination with intra-arterial infusion therapy with dacarbazine for metastatic malignant melanoma localized to a lower extremity.

Fourteen patients with metastatic malignant melanoma localized to a lower extremity were treated with combined radiotherapy and intra-arterial infusion therapy with dacarbazine. All lesions that were included in radiation fields regressed completely. Two patients relapsed within radiation fields and six relapsed elsewhere. One patient had a serious intimal lesion caused by the catheter.

Aged↗
PubMed1985

Intra-arterial infusion of mitomycin C in treatment of breast cancer: occurrence of skin necrosis in irradiated patients.

Eight previously irradiated breast cancer patients with local recurrences were treated with intra-arterial infusions of 8 mg/m2 mitomycin C given at 3-week intervals. The mean time interval between radiotherapy and intra-arterial chemotherapy was 38 months (range 2-60). In five cases a temporary reduction in tumour size was observed. However, in 3 of the 8 patients severe local pain, starting immediately after the third course of treatment, was followed 4 weeks later by the development of deep necrotic ulcers of the chest wall. These cases are reported here and discussed in relation to the results of previous studies.

Adult↗
PubMed1985

The QRS complex during transient myocardial ischemia: studies in patients with variant angina pectoris and in a canine preparation.

We made continuous electrocardiographic recordings on magnetic tape during 15 episodes of ischemia in five patients with variant angina to determine the characteristics of the QRS changes. Orthogonal leads were used and the electrocardiograms were analyzed visually and by digital computer. Changes were quantified by subtracting baseline electrocardiograms from those obtained during ischemia. Large changes in the QRS occurred during ischemia but the waveform quickly returned to baseline when the episode subsided. In all patients there was prolongation of the QRS duration and an increase in QRS voltage during the terminal 40 msec of the waveform in the lead(s) showing the most marked ST displacement. The increase in the terminal QRS could be represented by a vector directed toward the ischemic zone. In a given patient the amplitude of ST displacement varied between episodes, presumably because of variation in the intensity of ischemia, but the QRS changes were directionally similar in each episode. In two patients there was also a smaller change involving the initial 40 msec of the QRS that could be represented by a vector directed away from the ischemic zone. To determine the possible mechanism for the electrocardiographic changes, ischemic episodes of 120 to 150 sec were produced in seven dogs and electrocardiographic recording and analysis techniques similar to those used in patients were employed. Myocardial conduction velocity was measured in three directions in the ischemic zone and was correlated with simultaneous electrocardiographic recordings from the body surface. The electrocardiographic changes in the dog preparation were virtually identical to those in the patients and strongly correlated with a fall in myocardial conduction velocity. We conclude that the QRS changes during variant angina result from the altered excitation pattern produced by conduction delay in the ischemic zone. The probable cause for the increase in terminal QRS voltage is delayed (and uncancelled) activation of the ischemic zone.

Angina Pectoris, Variant↗