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Biomedical subjects

L Begin

Publications and source records attributed to L Begin.

5 recordsLinked to original sources
PubMed1990

Mitomycin C and mitoxantrone chemotherapy for advanced breast cancer: efficacy with minimal gastrointestinal toxicity and alopecia.

In an attempt to examine the possibility of decreased toxicity in patients with advanced breast cancer who had not previously received chemotherapy, 33 women were given combination chemotherapy consisting of mitomycin C (10 mg/m2) every 6 weeks and mitoxantrone (6 mg/m2) every 3 weeks. The patients had predominantly visceral disease and received a median of two cycles of therapy. Of the 32 evaluable subjects, 15 (47%) achieved a partial response lasting a median of 7 months. Hematological toxicity was generally mild, although there were two episodes of sepsis. One patient developed hemolytic-uremic syndrome, and one subject developed pulmonary fibrosis, both presumably attributable to treatment with mitomycin C. Another patient died of hepatic failure (hepar lobatum). Thus, there were five patients who sustained life-threatening toxicities; this may have been due to the poor performance status and advanced age of some of the patients. Gastrointestinal toxicity and alopecia were minimal. Patient acceptance was high and there was an improvement in symptomatology in the majority of patients. In conclusion, mitomycin C and mitoxantrone chemotherapy is an active drug combination for the treatment of advanced breast cancer that seldom causes significant distressing gastrointestinal side effects or alopecia; however, the duration of response to this regimen appears to be shorter than that obtained with either cyclophosphamide - methotrexate - 5-fluorouracil (CMF) or cyclophosphamide - Adriamycin - 5-fluorouracil (CAF) combination chemotherapy.

Alkylating Agents↗
PubMed1983

Treatment of established spinal injury-induced gastric erosions in rats with cimetidine and 16,16-dimethyl prostaglandin E2.

Most research on the beneficial effects of pharmacologic agents on stress-induced acute gastric erosions in animals is directed at prevention. It is only the rare study that has been concerned with treatment of established erosions. A treatment model has been created using cervical cord-injured male Sprague-Dawley rats which consistently developed extensive linear erosions of the glandular portions of the stomach within 12 hr. A group of spinal rats was sacrificed after 12 hr to serve as a base of pretreatment ulcer severity. Treatment of established erosions with cimetidine 25 mg/kg every 2 hr in one group and 16,16-dimethyl prostaglandin E2 (16,16-dmPGE2) 5 micrograms/kg every 2 hr in a second group was compared to saline-treated controls. All drugs were administered by intraperitoneal route. Treatment began 12 hr after the cord transection and continued for another 12 hr at which time the rats were sacrificed. Both cimetidine and 16,16-dmPGE2 significantly inhibited the degree of erosion progression after 12 hr compared to saline controls (P less than 0.05). Acid output studies were carried out on a second set of rats subjected to the same experimental conditions with the addition of pyloric ligation 6 hr prior to sacrifice. A significant decrease in acid output (P less than 0.05) occurred only in the cimetidine group compared to control. It is concluded that both cimetidine and 16,16-dmPGE2 can arrest the progression of erosive changes in the stomach after cervical cord injury in rats. This is likely related to acid reduction by cimetidine and cytoprotection by prostaglandin.

16,16-Dimethylprostaglandin E2↗