Detail of "64862-96-0"

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Growth of carcinoma of the esophagus and gastroesophageal junction in a human tumor cloning assay

Growth of carcinoma of the esophagus and gastroesophageal junction in a human tumor cloning assay. Harris, Gary J.; Turner, Judith N.; Von Hoff, Daniel D. (Health Sci. Cent. 60084-10-8 and 67699-40-5 are cas registry numbers. These chemicals are also mentioned in this article., Univ. Texas, San Antonio, TX 78284, USA). Cancer Drug Delivery, 3(4), 273-8 (English) 1986. CODEN: CDDED7. ISSN: 0732-9482. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The culturing of 23 specimens from 23 patients with squamous cell carcinoma of the esophagus and 15 specimens from 11 patients with adenocarcinoma of the gastroesophageal junction (GEJ) was attempted. Evaluable growth, defined as 320 tumor colonies per control plate, was achieved in 35% of the esophageal specimens and in 40% of the GEJ specimens. The specimens with evaluable growth yielded 20 evaluable drug tests for the esophageal group and 42 evaluable drug tests for the GEJ group. A pos. response to the chemotherapeutic agent, defined as ￡50% survival in drug treated plates relative to the control plates, was seen in 1 (5%) of the evaluable esophageal specimens and in 20 (47%) of the evaluable GEJ specimens. The only agent active in the esophageal group was cis-platinum [15663-27-1] (1 of 5 tests). Std. active agents in the GEJ group included: 5-fluorouracil [51-21-8] (1 of 1 test), vinblastine [865-21-4] (4 of 8 tests), vincristine [57-22-7] (1 of 1 test), and VP-16 [33419-42-0] (1 of 1 test). Active investigational agents included: methylglyoxalbisguanylhydrazone [459-86-9] (1 of 1 test), auranofin [34031-32-8] (3 of 3 tests), vinzolidine [67699-40-5] (4 of 6 tests), carbetimer [82230-03-3] (2 of 2 tests), and ametantrone [64862-96-0] (3 of 3 tests). The cloning results are consistent with the clin. observation that carcinoma of the esophagus and GEJ respond differently to chemotherapy. .

Ametantrone inhibits prostaglandin-mediated resorption in bone organ culture

Ametantrone inhibits prostaglandin-mediated resorption in bone organ culture. Warner, Margaret R.; Rappaport, Mark S.; Krieger, Nancy S.; Novak, Raymond F.; Stern, Paula H. (Med. Sch., Northwestern Univ., Chicago, IL 60611, USA). Prostaglandins, 28(4), 469-76 (English) 1984. CODEN: PRGLBA. ISSN: 0090-6980. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The ability of ametantrone (HAQ)(I) [64862-96-0], a prototypic anthracenedione, to inhibit prostaglandins (PG) synthesis and PG-mediated bone resorption was investigated using neonatal mouse calvaria in organ culture. Epidermal growth factor (EGF) stimulates bone resorption in this tissue by inducing PG synthesis. Consequently, if HAQ inhibits EGF-stimulated PG synthesis, it should also inhibit EGF-stimulated bone resorption. HAQ, at 10 mM, completely abolished EGF-stimulated PG synthesis and Ca release. Moreover, HAQ (1.0-30 mM) inhibition of EGF-stimulated PGE2 synthesis correlated with the inhibition of EGF-stimulated Ca release in a concn.-dependent manner. In contrast to EGF, parathyroid hormone stimulates resorption by a PG-independent pathway. HAQ at 10 mM had no effect on parathyroid hormone stimulated Ca release. HAQ inhibition of bone resorption appears to be primarily mediated by inhibition of PG biosynthesis.