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benzaldehyde/sarcoma

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조항임상 시험특허
5 결과

Inhibition of experimental and spontaneous pulmonary metastasis of murine RCT (+) sarcoma by beta-cyclodextrin-benzaldehyde.

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The effect of beta-cyclodextrin-benzaldehyde (CDBA) on pulmonary metastasis in C3H/He mice was examined. In experimental metastasis that was induced by iv injection of 1 X 10(6) RCT (+) cells, the highest inhibition was observed in the mice that were treated daily with CDBA (5 mg/day) for 1 week

Anti-tumor evaluation of benzaldehyde in the dog and cat.

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Fourteen dogs and 11 cats with various malignant tumors were treated daily with benzaldehyde at a dosage rate of 10 mg/kg of body weight, orally, divided into 4 doses. Clinical signs of toxicosis were not observed. A partial response (greater than 50% regression) was observed in animals with an oral

Therapy of P388 leukemia with benzaldehyde.

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Optimal schedules of benzaldehyde (50-100 mg kg-1 intraperitoneally) on day 1 or on several days after inoculation of 10(5) P388 leukemia cells to DBA 2J mice increased survival by 70-100%. No significant prolongation of survival was observed between the various schedules of benzaldehyde treatment.

Augmentation of murine lymphokine-activated killer cell cytotoxicity by beta-cyclodextrin-benzaldehyde.

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We investigated the effect of beta-cyclodextrin-benzaldehyde (CDBA) on lymphokine-activated killer (LAK) cell activity of spleen cells from normal or RCT(+)H-2(+)-sarcoma-bearing C3H/He mice. CDBA augmented the induction of LAK cytotoxicity in vitro against RCT(+)H-2+ tumor cells by IL-2, whereas

Tumor cell heterogeneity: impact on mechanisms of therapeutic drug resistance.

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OBJECTIVE The aim of these studies was to determine whether chemotherapy-resistant tumor cell sublines derived from a single starting cell population with identical treatment protocols, have the same mechanism of resistance. METHODS Twelve cyclophosphamide-resistant sublines were derived from KHT-iv
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