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Tissue TGF-beta expression following conventional radiotherapy and pulsed low-dose-rate radiation
Cell Cycle. 2017 Jun 18;16(12) :1171-1174
PMID: 28486014    PMCID: PMC5499842    URL: https://www.ncbi.nlm.nih.gov/pubmed/28486014
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Abstract
The release of inflammatory cytokines has been implicated in the toxicity of conventional radiotherapy (CRT). Transforming growth factor beta (TGF-beta) has been suggested to be a risk marker for pulmonary toxicity following radiotherapy. Pulsed low-dose rate radiotherapy (PLDR) is a technique that involves spreading out a conventional radiotherapy dose into short pulses of dose with breaks in between to reduce toxicities. We hypothesized that the more tolerable toxicity profile of PLDR compared with CRT may be related to differential expression of inflammatory cytokines such as TGF-beta in normal tissues. To address this, we analyzed tissues from mice that had been subjected to lethal doses of CRT and PLDR by histology and immunohistochemistry (IHC). Equivalent physical doses of CRT triggered more cellular atrophy in the bone marrow, intestine, and pancreas when compared with PLDR as indicated by hematoxylin and eosin staining. IHC data indicates that TGF-beta expression is increased in the bone marrow, intestine, and lungs of mice subjected to CRT as compared with tissues from mice subjected to PLDR. Our in vivo data suggest that differential expression of inflammatory cytokines such as TGF-beta may play a role in the more favorable normal tissue late response following treatment with PLDR.
Notes
Meyer, Joshua E Finnberg, Niklas K Chen, Lili Cvetkovic, Dusica Wang, Bin Zhou, Lanlan Dong, Yanqun Hallman, Mark A Ma, Chang-Ming C El-Deiry, Wafik S eng 2017/05/10 06:00 Cell Cycle. 2017 Jun 18;16(12):1171-1174. doi: 10.1080/15384101.2017.1317418. Epub 2017 May 9.