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T. Schimek-Jasch
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P3.04 - Poster Session/ Biology, Pathology, and Molecular Testing (ID 235)
- Event: WCLC 2015
- Type: Poster
- Track: Biology, Pathology, and Molecular Testing
- Presentations: 1
- Moderators:
- Coordinates: 9/09/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)
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P3.04-102 - CC Chemokine Ligand 18 as a Biomarker for the Prediction of Radiation Induced Lung Disease (RILD) (ID 2401)
09:30 - 09:30 | Author(s): T. Schimek-Jasch
- Abstract
Background:
In patients with fibrosing lung disease the CC Chemokine Ligand 18 (CCL18) is abundantly produced by alveolar macrophages and its concentration is increased in various inflammatory and fibrotic lung diseases. In this study we aimed to analyze the role of CCL18 as a prognostic biomarker for the development of radiation induced lung disease (RILD) after thoracic irradiation.
Methods:
Between August 2011 and February 2012, 60 patients were enrolled prospectively in the study. Forty-six patients were treated for lung cancer, thirteen had an esophageal cancer and one a thymoma. Patients were treated either with conventionally fractionated (n=47) or hypo-fractionated (n=13) radiotherapy. The CCL18 levels in serum were quantified with ELISA (enzyme-linked immunosorbent assay) at predefined time points; before treatment, after 30 Gy, after 60 Gy (for conventional fractionation), at 6 weeks after completion of treatment and 3 months after therapy. These results were then correlated with routinely performed computed tomographies at 6 weeks and 3 months after the last treatment.
Results:
Twenty three patients developed radiologic signs of RILD but only three of them developed symptoms. The mean CCL18 levels, for the whole group of patients, were, before treatment, 110 ng/ml (standard deviation, SD: 53) and at the end of treatment 85 ng/ml (SD: 73). During the first (6 weeks after treatment) and second follow-up (3 months after treatment) the mean CCL18 levels were 93 ng/ml (SD: 57) and 104 ng/ml (SD: 49), respectively. The CCL18 concentrations in serum were not significantly elevated in the group of patients who developed a RILD. The mean CCL18 levels, at six weeks and three months after treatment, were in the RILD-group 94 ng/ml (SD: 62) and 104 ng/ml (SD: 61) and in the non-RILD-group 93 ng/ml (SD: 54) and 103 ng/ml (SD: 39). Furthermore there was no statistical significant correlation between CCL18 levels or decreasing serum CCL18 concentrations and RILD, fibrosis, tumor volume, T-stage, histology, adjuvant therapy, dosimetric parameters such as V20, response after treatment and overall survival.
Conclusion:
These findings do not suggest that the chemokine CCL18 is involved in the development of RILD in patients undergoing radiotherapy for chest tumors.