Breast cancer is the most common neoplasm and the second leading cause of cancer death in American women. Radiotherapy (RT) is an effective adjuvant treatment after breast-conserving surgery for early-stage breast cancer. However, the majority of breast cancer patients undergoing RT develop acute skin reactions. We pilot tested the effects of RT on immune system and inflammatory cytokines in 12 breast cancer patients (6 with high and 6 with low skin toxicity). Using the Human Cytokine ELISA Plate Array I (Signosis Inc., Sunnyvale, CA), we evaluated 31 plasma cytokines in RT-related skin toxicity. The National Cancer Institute Common Terminology Criteria for Adverse Effects (version 3.0) was used to evaluate skin toxicity grade. Our data showed that RT induced epidermal growth factor (EGF); at baseline EFG was not detectable while post RT-treatment significant levels of EFG was observed (mean+SD: 395±620.4, p=0.0496). Interleukin (IL)-2 was significantly elevated by RT (6.5x106±1.01x106 vs. 4.85x106±1.44x106, p=0.0004). Adiponectin was significantly higher at post RT (3.09x106±1.31x106) than pre RT (1.77x106±1.52x106, p=0.0002). RT-related changes of IL-4 was significantly associated with skin toxicity at week 3 (p=0.018); IL-4 was decreased in patients without toxicity (-668.3±1691.5) and increased in patients with grade 2 toxicity (1830.0±1365.4). IL-12 showed similar trend but with marginal significance (p=0.076). RT-related changes of EGF was significantly associated with skin toxicity at week 6 (p=0.045); EGF was not changed in patients with no or low toxicity (grade 0/1) and increased in patients with grade 2/3 toxicity (592.5±686.4). In summary, our pilot data suggest that RT induces EGF, IL-2, and adiponectin. RT-related changes of IL-4 and EGF were associated with skin toxicity. Our ongoing study with a targeted sample size of 1,000 may shed light on the molecular mechanisms of cytokines in RT-related skin toxicity of breast cancer patients.

Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4352. doi:1538-7445.AM2012-4352