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Tumor growth delay

Fig. 8. Combined effect of fractionated NS-398 and radiotherapy on the tumor growth delay of H460 (A) and HCT-116 (B) human tumor xenografts in nude mice. Day 0 is defined as the first day of treatment. Tumors were treated with vehicle (DMSO) or 36 mg/kg NS-398 on d 1 through 7. Radiation fractions (2 Gy) were given 2 h after drug administration starting d 2, for 5 consecutive days. Error bars represent the SE from 8-9 mice. (O), vehicle treatment alone ( ), NS-398 treatment alone ( ), radiation plus vehicle treatment ( ), radiation plus NS-398 treatment. Fig. 8. Combined effect of fractionated NS-398 and radiotherapy on the tumor growth delay of H460 (A) and HCT-116 (B) human tumor xenografts in nude mice. Day 0 is defined as the first day of treatment. Tumors were treated with vehicle (DMSO) or 36 mg/kg NS-398 on d 1 through 7. Radiation fractions (2 Gy) were given 2 h after drug administration starting d 2, for 5 consecutive days. Error bars represent the SE from 8-9 mice. (O), vehicle treatment alone ( ), NS-398 treatment alone ( ), radiation plus vehicle treatment ( ), radiation plus NS-398 treatment.
Squalamine has been tested in mammary, ovary, and lung cancer xenograft mouse models [20,23-26]. Results sho ved that squalamine alone had a modest effect on tumor growth delay and in some cases it resulted in decreased number of lung metastases. However, in most studies, squalamine treatment was more efficacious when combined with previously established anticancer agents such as cyclophosphamide, cisplatin, carboplatin, paclitaxel, 5-fluorouracil, or genestein, or with radiation therapy. [Pg.239]

Animal-Model, Tumoe-to-Noemal Tissue Ratios, Lasee Light Dose, Blood Cleaeance Kinetics, and Tumor Growth Delays to... [Pg.227]

Sensitizer Animal, tumor Tumor/skin Tumor/muscle Light dose (J/cm ) Clearance half-life (h) Tumor growth delay (days)... [Pg.227]

Albert JM, et al. Inhibition of poly(ADP-ribose) polymerase enhances cell death and improves tumor growth delay in irradiated 164. lung cancer models. Clin. Cancer Res. 2007 13 3033-3042. [Pg.183]

Using rat flank and intracranial 9L gliosarcoma models, Tamargo et al. (70) initially compared the efficacy of polymer and systemically based BCNU. EVAc polymer delivery in the flank model produced significant tumor growth delay relative to systemic administration (15.3 vs. 11.2 days, p < 0.05). In the intracranial model, a 10 mg polymer with 20% (w/w) BCNU polymers dramatically improved survival in animals with established 9L gliosarcoma. EVAc and pCPP SA polymers conferred respective survival advantages of 7.3-fold and 5.4-fold over controls. Systemic BCNU, in contrast, increased survival only 2.4-fold compared to controls. [Pg.335]

Surv-T34A (Survivin T34A) DNA fragmentation, aberrant nuclei formation, tumor cell apoptosis, tumor growth delay, 40-50% reduction in tumor mass Tat 12... [Pg.304]

BH3 domain of Bim Apoptosis of cancer cells, tumor growth delay Tat 14... [Pg.304]

Wn et al. demonstrates that a lipid-polymer hybrid drug delivery systan loaded with doxorubicin is effective for tnmor treatment in a well-established animal model. Tumor growth delay and tnmor necrosis were observed in tnmors treated with the lipid-polymer hybrid formulation of doxorubicin. It was fonnd that these lipid-polymer hybrids carrying anticancer agents were useful for loco-regional treatment of breast cancer with an improved therapeutic index. [Pg.1161]


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See also in sourсe #XX -- [ Pg.239 ]




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Tumor growth

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