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| Untersuchte Arbeit: Seite: 13, Zeilen: 1-7 (complete) |
Quelle: Matsumura et al 2008 Seite(n): 3099, 3106, Zeilen: 3099: right col 28-33; 3106:left col. 40-46 |
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| [Evidence is accumulating that ionizing radiation (IR) therapy, a treatment modality routinely used to kill cancer cells, can modulate the expression of several] receptors and cytokines by cancer cells and tumor stroma, resulting in modifications of the tumor microenvironment that can be exploited to enhance the effects of immunotherapy (Demaria and Formenti 2007). The molecular mechanism(s) responsible for up-regulation of chemokines following IR of cancer cells are presently undefined. A possible candidate is the PI3K/Akt signaling pathway, which is activated by IR in tumor and endothelial cells (Zingg et al. 2004). This pathway promotes survival of tumor cells and has been recently linked to the induction of CXCL16 in a mouse model of mammary tumorigenesis (Ju et al. 2007).
Demaria S, Formenti SC (2007) Sensors of ionizing radiation effects on the immunological microenvironment of cancer. Int J Radiat Biol 83:819-825 Ju X, Katiyar S, Wang C, Liu M, Jiao X, Li S, Zhou J, Turner J, Lisanti MP, Russell RG, Mueller SC, Ojeifo J, Chen WS, Hay N, Pestell RG (2007) Akt1 governs breast cancer progression in vivo. Proc Natl Acad Sci U S A 104:7438-7443 Zingg D, Riesterer O, Fabbro D, Glanzmann C, Bodis S, Pruschy M (2004) Differential activation of the phosphatidylinositol 3'-kinase/Akt survival pathway by ionizing radiation in tumor and primary endothelial cells. Cancer Res 64:5398-5406 |
[Page 3099]
Evidence is accumulating that ionizing radiation (IR) therapy, a treatment modality routinely employed to kill cancer cells, can modulate the expression of several receptors and cytokines by cancer cells and tumor stroma, resulting in modifications of the tumor microenvironment that can be exploited to enhance the effects of IT (reviewed in references 20 and 21). [Page 3106] The molecular mechanism(s) responsible for up-regulation of CXCL16 following IR of breast cancer cells are presently undefined. A possible candidate is the PI3K/Akt signaling pathway, which is activated by IR in tumor and endothelial cells (49). This pathway promotes survival of tumor cells, and has been recently linked to induction of CXCL16 in a mouse model of mammary tumorigenesis (50). 20. Demaria S, Bhardwaj N, McBride WH, Formenti SC. Combining radiotherapy and immunotherapy: a revived partnership. Int J Radiat Oncol Biol Phys 2005;63:655–666. [PubMed: 16199306] 21. Demaria S, Formenti SC. Sensors of ionizing radiation effects on the immunological microenvironment of cancer. Int J Radiat Biol 2007;83:1–7. [PubMed: 17357435] 49. Zingg D, Riesterer O, Fabbro D, Glanzmann C, Bodis S, Pruschy M. Differential activation of the phosphatidylinositol 3′-kinase/Akt survival pathway by ionizing radiation in tumor and primary endothelial cells. Cancer Res 2004;64:5398–5406. [PubMed: 15289348] 50. Ju X, Katiyar S, Wang C, Liu M, Jiao X, Li S, Zhou J, Turner J, Lisanti MP, Russell RG, Mueller SC, Ojeifo J, Chen WS, Hay N, Pestell RG. Akt1 governs breast cancer progression in vivo. Proc Natl Acad Sci U S A 2007;104:7438–7443. [PubMed: 17460049] |
The source is mentioned right before the passage starts on the previous page. Nothing has been marked as a citation though the wording (and the list of references) are identical. The reader should take note: The reference to "breast cancer" from the original source has been deleted since Iam does research with regard to liver cancer. |
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