The response of Tumor-Associated-Microphage to Irradiation

碩士 === 長庚大學 === 臨床醫學研究所 === 95 === Increasing evidence showed that tumor grown in vivo is an integrated structure. Reactions to the radiation damage by environmental components other than tumor cells per se, such as vascular damage and inflammatory responses, might play an important role in tumor k...

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Bibliographic Details
Main Authors: Tsai, Chien-Sheng, 蔡介生
Other Authors: Hong, Ji-Hong
Format: Others
Language:en_US
Published: 2007
Online Access:http://ndltd.ncl.edu.tw/handle/02935588786858899630
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Summary:碩士 === 長庚大學 === 臨床醫學研究所 === 95 === Increasing evidence showed that tumor grown in vivo is an integrated structure. Reactions to the radiation damage by environmental components other than tumor cells per se, such as vascular damage and inflammatory responses, might play an important role in tumor killing and growth. It has been known for many years that tumor-associated macrophages (TAMs) are a major cellular component of human and murine cancers. The purpose of this study is to investigate the effects of radiation on tumors and TAMs, and to elucidate the potential of TAMs to influence tumor growth. A murine prostate cell line, TRAMP-C1, was grown in C57Bl/6J mice and irradiated with either 25 Gy in a single dose, or 60 Gy in 15 fractions. The irradiated tumors were removed at the indicated times and assessed for a variety of markers related to TAM content, activation status and function, as compared to the un-irradiated tumors at the same size. Either after single or fractionated irradiation, increased levels of Arg-I, COX-2, and, to a lesser extent, iNOS protein were found to associate with TAMs 1–2 weeks after tumor irradiation. Function of TAMs was compared by mixing them with TRAMP-C1 cells and injecting them into mice. When mixing with TAMs from irradiated tumors, TRAMP-C1 cells grew significantly faster than those mixed with TAMs from unirradiated tumors or TRAMP-C1 alone. In conclusions, TAMs in the postirradiated tumor microenvironment express higher levels of Arg-1, COX-2, and iNOS, and promote early tumor growth in vivo.