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Meth A tumor growth

In normal mice, an intraperitoneal 250 mg/kg 5FU treatment is not lethal, but 100% mortality was observed within 2 weeks after the same dose of 5FU treatment in mice bearing Meth A tumors. The mean survival time of Meth A-inoculated, 5FU-treated mice (23.1 1.2 days) is significantly shorter than that of 5FU-untreated tumor-bearing mice (29.0 3.5 days). In CVS-administered tumor-bearing mice, the mean survival time is 48.5 8.7 or 37.6 6.2 days with or without 5FU treatment, respectively. With respect to the antitumor effect as determined by tumor growth, 5FU was... [Pg.449]

Fig. (13). Effect of a combination of CVS and 5FU on body weight (A) and tumor growth (B) in tumor bearing mice. All mice were inoculated s.c. with 5x10° Meth A tumor cells on day 0. CVS was injected s.c. near the tumor on day 1,3,6,8,11 and 13. 5FU was treated i.p. at a dose of 250 mg/kg on day 14. Solid line means 5FU-nontreated, and dotted line means 5FU-treated mice ( ) means CVS-noninjected and (o) means CVS-injected mice. Fig. (13). Effect of a combination of CVS and 5FU on body weight (A) and tumor growth (B) in tumor bearing mice. All mice were inoculated s.c. with 5x10° Meth A tumor cells on day 0. CVS was injected s.c. near the tumor on day 1,3,6,8,11 and 13. 5FU was treated i.p. at a dose of 250 mg/kg on day 14. Solid line means 5FU-nontreated, and dotted line means 5FU-treated mice ( ) means CVS-noninjected and (o) means CVS-injected mice.
The growth of transplantable Meth A tumor was significantly suppressed in an Ag-specific manner when CVE was administered by not only an i.p. route [30], but orally as well [31]. It has been demonstrated that glycoprotein-rich substance (CVS) from the culture supernatant of Chlorella vulgaris strain CK displayed antitumor effect against experimental metastasis induced by Meth A fibrosarcoma [32]. [Pg.776]

The increased expression of adhesion molecules by the endothelium may activate polymorphonuclear neutrophils (PMN) in rabbits [72], During endotoxic shock, activated PMNs release their granule content and secrete both proinflammatory and cytotoxic molecules. Pickaver et al. [73] were the first to show PMN cytotoxicity against tumor cells. We showed that PMNs are toxic for PROb colon tumor cells [74] in BDEX rats. In vivo, PMNs have been implicated in the Schwartzman reaction [75], and may be involved in LPS-induced tumor necrosis. PMNs, when activated by LPS, synthesize and release NO. The role of NO in tumor growth will be discussed later. The decrease in tumor growth after intradermal injections of LPS is attributed to the induction of TNF-a secretion by PMNs both in intradermal tumors (Meth A sarcoma in BALB/c mice, MH-134 hepatoma in C3H/He mice, Lewis Lung carcinomas in C57BL/6 mice) and pulmonary Meth A metastases [76,77],... [Pg.525]

Tokoro, A., Tatewaki, N., Suzuki, K., Mikami, T., Suzuki, S., and Suzuki, M. 1988. Growth inhibitory effect of hexa-A-acetyl chitohexaose and chitohexaose against Meth A solid tumor. Chem. Pharm. Bull. 36 784-790. [Pg.250]

Figure 5. Tumor growth curves and complete response ratios (CR) after a single dose of DE> 310 with Meth A solid tumor model (long-term assay). Figure 5. Tumor growth curves and complete response ratios (CR) after a single dose of DE> 310 with Meth A solid tumor model (long-term assay).
Tokoro, A Tatewakl, N Suzuki, K Mikami, T Suzuki, S Suzuki, M Growth inhibitory effect of hexa-N-acetylchitohexaose and chitohexaos and Meth-A soUd tumor. Chemical and Pharmaceutical Bulletin, 1998, 36, 784-790. [Pg.1192]


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See also in sourсe #XX -- [ Pg.453 ]

See also in sourсe #XX -- [ Pg.25 , Pg.453 ]




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