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- W2895822422 abstract "Purpose This study examined tumor growth delay resulting from partial irradiation in preclinical mouse models. Methods and Materials We investigated 67NR murine orthotopic breast tumors in both immunocompetent and nude mice. Treatment was delivered to 50% or 100% of the tumor using a 2 × 2 cm collimator on a microirradiator. Radiation response was modulated by treatment with anti-CD8 and anti—intercellular adhesion molecule (anti-ICAM) antibodies. Similar experiments were performed using the less immunogenic Lewis lung carcinoma mouse model. Tumor growth delay and γ-H2AX phosphorylation were measured, and immune response was assessed by immunofluorescence and flow cytometry at 1 and 7 days after radiation therapy. Tumor expression of cellular adhesion molecules was also measured at different times after radiation therapy. Results Partial irradiation led to tumor responses similar to those of fully exposed tumors in immunocompetent mice, but not in nude mice. After a single dose of 10 Gy, infiltration of CD8+ T cells was observed along with increased expression of ICAM. The response to 10 Gy in hemi-irradiated tumors was abrogated by treatment with either anti-CD8 or anti-ICAM antibodies. Similar responses were obtained in the less immunogenic Lewis lung carcinoma mouse model delivering 15 Gy to half the tumor volume. Treatment with FTY720, a compound that inhibits T-cell egress from lymph nodes, did not affect tumor response at the time of CD8+ T cells infiltration in the nonirradiated area of the tumor. This result indicated that the most likely source of these cells is the irradiated portion of the hemi-irradiated tumors. In addition, a significant abscopal effect was observed after partial irradiation with a single dose of 10 Gy in the 67NR model. Conclusions In these models, radiation controls tumor growth both directly through cell killing and indirectly through immune activation. This outcome raises the possibility that this effect could be induced in the clinic. This study examined tumor growth delay resulting from partial irradiation in preclinical mouse models. We investigated 67NR murine orthotopic breast tumors in both immunocompetent and nude mice. Treatment was delivered to 50% or 100% of the tumor using a 2 × 2 cm collimator on a microirradiator. Radiation response was modulated by treatment with anti-CD8 and anti—intercellular adhesion molecule (anti-ICAM) antibodies. Similar experiments were performed using the less immunogenic Lewis lung carcinoma mouse model. Tumor growth delay and γ-H2AX phosphorylation were measured, and immune response was assessed by immunofluorescence and flow cytometry at 1 and 7 days after radiation therapy. Tumor expression of cellular adhesion molecules was also measured at different times after radiation therapy. Partial irradiation led to tumor responses similar to those of fully exposed tumors in immunocompetent mice, but not in nude mice. After a single dose of 10 Gy, infiltration of CD8+ T cells was observed along with increased expression of ICAM. The response to 10 Gy in hemi-irradiated tumors was abrogated by treatment with either anti-CD8 or anti-ICAM antibodies. Similar responses were obtained in the less immunogenic Lewis lung carcinoma mouse model delivering 15 Gy to half the tumor volume. Treatment with FTY720, a compound that inhibits T-cell egress from lymph nodes, did not affect tumor response at the time of CD8+ T cells infiltration in the nonirradiated area of the tumor. This result indicated that the most likely source of these cells is the irradiated portion of the hemi-irradiated tumors. In addition, a significant abscopal effect was observed after partial irradiation with a single dose of 10 Gy in the 67NR model. In these models, radiation controls tumor growth both directly through cell killing and indirectly through immune activation. This outcome raises the possibility that this effect could be induced in the clinic." @default.
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- W2895822422 date "2019-03-01" @default.
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- W2895822422 title "An Antitumor Immune Response Is Evoked by Partial-Volume Single-Dose Radiation in 2 Murine Models" @default.
- W2895822422 cites W1706972008 @default.
- W2895822422 cites W1825962579 @default.
- W2895822422 cites W1955548161 @default.
- W2895822422 cites W1959227906 @default.
- W2895822422 cites W1964476212 @default.
- W2895822422 cites W1969464492 @default.
- W2895822422 cites W1980137951 @default.
- W2895822422 cites W1984367232 @default.
- W2895822422 cites W1997122877 @default.
- W2895822422 cites W1999020268 @default.
- W2895822422 cites W2001438671 @default.
- W2895822422 cites W2001816519 @default.
- W2895822422 cites W2017453499 @default.
- W2895822422 cites W2024222590 @default.
- W2895822422 cites W2025421597 @default.
- W2895822422 cites W2032166347 @default.
- W2895822422 cites W2043043829 @default.
- W2895822422 cites W2044179999 @default.
- W2895822422 cites W2061342795 @default.
- W2895822422 cites W2064641323 @default.
- W2895822422 cites W2077871003 @default.
- W2895822422 cites W2079265161 @default.
- W2895822422 cites W2087673211 @default.
- W2895822422 cites W2093424661 @default.
- W2895822422 cites W2099675490 @default.
- W2895822422 cites W2100143139 @default.
- W2895822422 cites W2100928937 @default.
- W2895822422 cites W2112682556 @default.
- W2895822422 cites W2115538252 @default.
- W2895822422 cites W2117280704 @default.
- W2895822422 cites W2117352925 @default.
- W2895822422 cites W2117878645 @default.
- W2895822422 cites W2118863472 @default.
- W2895822422 cites W2127733313 @default.
- W2895822422 cites W2133739473 @default.
- W2895822422 cites W2140828776 @default.
- W2895822422 cites W2153929368 @default.
- W2895822422 cites W2163182836 @default.
- W2895822422 cites W2167876561 @default.
- W2895822422 cites W2428697703 @default.
- W2895822422 cites W2578888194 @default.
- W2895822422 cites W2605630275 @default.
- W2895822422 cites W2606378959 @default.
- W2895822422 cites W2749319028 @default.
- W2895822422 cites W2760326418 @default.
- W2895822422 cites W2787553571 @default.
- W2895822422 cites W2884207647 @default.
- W2895822422 doi "https://doi.org/10.1016/j.ijrobp.2018.10.009" @default.
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