Recurrent cotyledonoid dissecting leiomyoma of the uterus.

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.

In vivo and in vitro assessment of the action of SN 28049, a benzonaphthyridine derivative targeting topoisomerase II, on the murine Colon 38 carcinoma.

Aim: SN 28049 (N-[2-(dimethylamino)ethyl]-2,6-dimethyl-1-oxo-1,2-dihydrobenzo[b]-1,6-naphthyridine-4-carboxamide) is a new DNA binding drug that targets topoisomerase II. SN 28049 is curative against the murine Colon 38 adenocarcinoma (CT38) while etoposide, another topoisomerase II-directed drug, shows minimal activity; we investigated the basis for this difference in vivo and in vitro.

Methods: Colon 38 tumours were grown in C57Bl mice and in immunodeficient mice.

Antitumour action of 5,6-dimethylxanthenone-4-acetic acid in rats bearing chemically induced primary mammary tumours.

Purpose: To evaluate the antitumour activity of 5,6-dimethylxanthenone-4-acetic acid (DMXAA), a vascular disrupting agent currently under phase II clinical trials in combination with cancer chemotherapy, in rats bearing chemically induced primary mammary tumours.

Methods: Tumours were induced in female Wistar rats by injection of N-nitroso-N-methylurea at 100 mg/kg subcutaneously. A clinically relevant single dose of DMXAA (1,800 mg/m(2)) was given to animals when tumours were measurable.

Estimation of radiation-induced interphase cell death in cultures of human tumor material and in cell lines.

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 [3H]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 [3H]thymidine incorporation.