TY  - JOUR
AU  - Jiang, Wenmei
AU  - Huang, Xiancong
AU  - Tian, Jiayuan
AU  - Wu, Yimin
AU  - Zhao, Jiazheng
AU  - Luo, Taobo
AU  - Zeng, Jian
AU  - Cai, Shunv
AU  - Wu, Leilei
PY  - 2026
DA  - 2026/01/29
TI  - Revisiting The Dual Role of Radiotherapy in EGFR-mutant NSCLC: Implications for Therapeutic Combination Strategies
JO  - Oncology Communications
T2  - Oncology Communications
JF  - Oncology Communications
VL  - 1
IS  - 1
SP  - 5
EP  - 7
DO  - 10.62762/OC.2025.306213
UR  - https://www.icck.org/article/abs/OC.2025.306213
KW  - non-small cell lung cancer
KW  - EGFR
KW  - radiotherapy
KW  - combination strategies
KW  - EGFR-TKI
AB  - The article by Piffkó A et al. elucidates the double-edged sword role of radiotherapy in cancer treatment. Radiotherapy stimulates tumor cells to secrete amphiregulin (AREG), which in turn activates EGFR$^+$ tumor-associated mononuclear phagocytes (MNPs). This activation feeds back into the EGFR signaling pathway, impairing the anti-tumor functions of MNPs. Moreover, AREG upregulates the expression of the immune checkpoint protein CD47 in tumor cells, thereby enabling them to evade immune-mediated phagocytosis. These insights hold important implications for clinical trial design and for optimizing therapeutic strategies.
SN  - 3142-8894
PB  - Institute of Central Computation and Knowledge
LA  - English
ER  - 

@article{Jiang2026Revisiting,
  author = {Wenmei Jiang and Xiancong Huang and Jiayuan Tian and Yimin Wu and Jiazheng Zhao and Taobo Luo and Jian Zeng and Shunv Cai and Leilei Wu},
  title = {Revisiting The Dual Role of Radiotherapy in EGFR-mutant NSCLC: Implications for Therapeutic Combination Strategies},
  journal = {Oncology Communications},
  year = {2026},
  volume = {1},
  number = {1},
  pages = {5-7},
  doi = {10.62762/OC.2025.306213},
  url = {https://www.icck.org/article/abs/OC.2025.306213},
  abstract = {The article by Piffkó A et al. elucidates the double-edged sword role of radiotherapy in cancer treatment. Radiotherapy stimulates tumor cells to secrete amphiregulin (AREG), which in turn activates EGFR\$^+\$ tumor-associated mononuclear phagocytes (MNPs). This activation feeds back into the EGFR signaling pathway, impairing the anti-tumor functions of MNPs. Moreover, AREG upregulates the expression of the immune checkpoint protein CD47 in tumor cells, thereby enabling them to evade immune-mediated phagocytosis. These insights hold important implications for clinical trial design and for optimizing therapeutic strategies.},
  keywords = {non-small cell lung cancer, EGFR, radiotherapy, combination strategies, EGFR-TKI},
  issn = {3142-8894},
  publisher = {Institute of Central Computation and Knowledge}
}