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Tumor physiology

D. Zhao, L. Jiang, E.W. Hahn, R.P. Mason, Tumor physiological response to com-bretastatin A4 phosphate assessed by MRI, Int. J. Radiat. Oncol. Biol. Phys 62 (2005) 872-880. [Pg.268]

Evelhoch, J. L., Bissery, M.-C., Chabot, G. G., Simpson, N. E., McCoy, C. L., Heilbrun, L. K., and Corbett, T. H. (1988) Flavone acetic acid (NSC 347512)-induced modulation of murine tumor physiology monitored by in vivo nuclear magnetic resonance spectroscopy. Cancer Res. 48, 4749-4755. [Pg.152]

A prerequisite for reproducible and predictable modification of tumor physiology is a fundamental understanding of the parameters which govern blood flow and transport in tumors. Since there are a limited number... [Pg.192]

The heterogeneity of tumor cells and tumor physiology, metastasis of tumor, and cancer stem-like cells restricts research on polymeric carriers. These hurdles still remain as challenges for the development of multifunctional and custom-made polymeric carriers. Nonetheless, the combined findings from polymer chemistry and tumor biology provide researchers with the potential tools to overcome such barriers in the future. [Pg.232]

Yasuda, H. (2008). Solid tumor physiology and hypoxia-induced chemo/radio-resistance Novel strategy for cancer therapy Nitric oxide donor as a therapeutic enhancer. Nitric Oxide 19, 205-216. [Pg.132]

Jain RK. Delivery of novel therapeutic agents in tumors Physiological barriers and strategies. / Natl Cancer Inst 1989 81 570-576. [Pg.1665]

Tannock, I.F., 2001. Tumor physiology and drug resistance. Cancer Metastasis Rev. 20,... [Pg.495]

Phosphorothioates generally protect normal tissues more than tumors. Tumor protection reported in some animal studies can pardy be explained by physiological effects of the particular dmgs, which are specific to rodents (4). WR-2721 does not appear to protect human and most animal tumors, apparentiy because of the low availabiUty of the dmg to tumor cells (4). Many tumors appear to have a reduced capillary density (44), which may mean that these tumors have altered levels of alkaline phosphatase, the enzyme that converts WR-2721 to WR-1065. A reduced abiUty of thiols to protect the hypoxic cells characteristic of many tumors may also contribute to their selectivity for normal tissues. The observation that WR-1065 protects cultured normal human fibroblasts, but not fibrosarcoma tumor cells, suggests that additional factors may contribute to the selectivity of radioprotection by WR-2721 m vivo (18). [Pg.489]

It has been estimated that using available neutron intensities such as 10 neutrons/(cm -s) concentrations of B from 10—30 lg/g of tumor with a tumor cell to normal cell selectivity of at least five are necessary for BNCT to be practical. Hence the challenge of BNCT ties in the development of practical means for the selective deUvery of approximately 10 B atoms to each tumor cell for effective therapy using short neutron irradiation times. Derivatives of B-enriched /oj o-borane anions and carboranes appear to be especially suitable for BNCT because of their high concentration of B and favorable hydrolytic stabiUties under physiological conditions. [Pg.253]

Despite recent developments, effectiveness of chemotherapy is still rather limited for most types of cancer, including tumors of the colon, lung, kidney, pancreas, and liver. Why some cancers respond better than others may be explained by factors relating to the anatomy and physiology of the cancer-ridden organ or... [Pg.750]

In cancer treatment, passive targeting of macromolecular carriers to tumors is a commonly used approach. This passive targeting is based on the enhanced permeability and retention (EPR) effect, which leads to an accumulation of the high molecular weight carrier in the tumor tissue. The EPR effect arises from the different physiology of tumor vasculature, where the vessel walls are highly porous and lack the tight junctions that are present in healthy tissue. As a result, macromolecular carriers extravasate and accumulate preferentially in tumor tissue relative to normal tissues [63, 64]. [Pg.85]

Tsukamoto Y, Kato Y, Ura M, Horii I, Ishitsuka H, Kusuhara H, Sugiyama Y. A physiologically based pharmacokinetic analysis of capecitabine, a triple prodrug of 5-FU, in humans the mechanism for tumor-selective accumulation of 5-FU. Pharm Res 2001 Aug 18(8) 1190-202. [Pg.551]


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See also in sourсe #XX -- [ Pg.1330 ]




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