This study shows for the first time that DMXAA has significant in vivo antitumour activity against non-transplanted autochthonous tumours and in a host species other than the mouse.
Cotyledonoid dissecting leiomyoma is a benign smooth muscle neoplasm with an unusual growth pattern that is characterized by intramural dissection within the uterine corpus and often a placental-like appearance macroscopically in its extrauterine component that may be alarming to the surgeon. All cases reported to date have been nonaggressive. We report a case in a 33-yr-old woman who had a history of prolonged uterine bleeding. She was operated upon for uterine leiomyomas, and the diagnosis of cotyledonoid dissecting leiomyoma was made at the time of intraoperative consultation. To maintain fertility, the intrauterine tumor was resected by myomectomy and the extrauterine tumor by excision. However, persistent uterine bleeding that eventually became intractable and continued growth of the neoplasm in the uterus necessitated hysterectomy 5 yr later. She was living and well 2.5 yr after hysterectomy with no evidence of disease.
Our histological study of the ductus arteriosus compared 12 infants who were treated with E-type prostaglandins with 12 control infants matched as closely as possible for age and diagnosis. Distinguishing histological features were seen in five of the treated cases and in none of the untreated cases. These features were intimal tears in two and hemorrhage into the media in five. Medial edema, mural thrombosis, and interruption of the internal elastic lamina at sites not beneath intimal cushions occurred both in treated and untreated infants and therefore were not distinguishing features. The gross anatomical features of the ductus arteriosus were assessed in these 24 and in another 85 cases. Significant differences in the ductus arteriosus were noted between cases with pulmonary atresia or aortic atresia and normals, but not between those treated with E-type prostaglandins and controls.
A short-term assay method able to estimate the radiation response of human cancer tissue samples would be of great advantage to the individualization of radiotherapy in cancer patients. However, the effect of radiation on [ 3 H]thymidine incorporation by proliferating cells reflects a composite of cell cycle arrest and induced cell death pathways. Here we consider whether it is feasible to correct for cell cycle effects based on comparison of the effects of radiation and the mitotic inhibitor paclitaxel on [ 3 H]thymidine incorporation. Sixty-two short-term (7-day) cultures of human tumor tissue from 61 patients with melanoma, gynecological cancer, brain cancer, and head and neck cancer, as well as 18 5-day cultures of low passage human tumor cell lines, were irradiated at doses from 2 to 9 Gy, or exposed to paclitaxel (200 nM). [ 3 H]Thymidine incorporation was measured at the end of the incubation. Cell cycle times could be estimated from the paclitaxel data and were 2.7 to 18.6 days for melanomas, 2.5 to >40 days for carcinomas, 3.9 to 39 days for brain tumors, and 1.1 to 3.8 days for cell lines. The effects of radiation on [ 3 H]thymidine incorporation varied widely (0-97% and 0-99% inhibition for 2 and 9 Gy, respectively), and in 23 of the clinical samples, but in none of the cell lines, radiation caused significantly greater inhibition of 3 H]thymidine incorporation than paclitaxel (p < 0.05). We argue that that these differences reflect radiation-induced cell loss from G 1 phase and/or S phase. Responses of short-term cultures of clinical tumor material to radiation, with appropriate correction for cell cycle effects, might have the potential to provide information on radiation-induced cell death in individual patients.
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