|Reference : Determination of TGF-β1 plasma levels. Authors' reply|
|Scientific journals : Article|
|Human health sciences : Oncology|
|Determination of TGF-β1 plasma levels. Authors' reply|
|Barthelemy, Nicole [Université de Liège - ULg > > Radiothérapie >]|
|De Jaeger, Katrien [ > > ]|
|SEPPENWOOLDE, Yvette [ > > ]|
|LEBESQUE, Joss [ > > ]|
|KAMINGA, Harm [ > > ]|
|International Journal of Radiation, Oncology, Biology, Physics|
|Yes (verified by ORBi)|
|Researchers ; Professionals ; Students ; General public ; Others|
|In patients with non–small-cell lung cancer, increasing radiotherapy (RT) dose improves eradication of intrathoracic disease, but increases the risk of side effects, especially radiation-induced lung injury. Many studies have been aimed at finding indices allowing the determination of the risk of treatment-related complications.
These indices include biologic factors and dosimetric parameters such as mean lung dose or the volume of lung receiving a threshold dose (e.g., 20 or 30 Gy). Among the biologic factors, interleukin-1α and interleukin-6 would be early circulatory cytokine markers for radiation pneumonitis (1 and 2). Transforming growth factor (TGF)-β1 is another potential marker. As recently shown in a human study determining local concentrations of TGF-β1 in the lung before, during, and after thoracic irradiation for lung cancer, TGF-β1 may contribute to the process leading to radiation response in human lung tissue (3). Anscher and his team found that elevated TGF-β1 plasma levels at the end of RT can identify patients at greater risk of pulmonary complication associated with thoracic irradiation for lung cancer (4). They proposed to use TGF-β1 plasma levels to assess the risk of treatment-related complications and consequently adjust the dose of radiotherapy. However, in a report published in the last issue of this journal, De Jaeger et al. failed to confirm that patients with increased TGF-β1 levels at the end of RT are at higher risk for developing symptomatic radiation pneumonitis (5).
Possible reasons for discrepancy include the use of different criteria to define treatment related complications and differences in the way plasma is collected and processed to determine TGF-β1 plasma levels. In humans, TGF-β1 is mainly found in the platelets α-granules and can be released in plasma in response to platelet activation (6). Therefore, platelet degranulation must be prevented during blood sampling and processing to measure true circulating TGF-β1 levels (7). In addition, because even the best methods of plasma collection and processing can result occasionally in some platelet degranulation, the extent of platelet activation must be assessed in studies reporting TGF-β1 plasma concentrations by determining plasma levels of platelet degranulation markers such as β-thromboglobulin or platelet factor 4 (7 and 8).
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