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Prognostic Value of the Evolution of HER2-Low Expression after Neoadjuvant Chemotherapy
Youzhao Ma,Mingda Zhu,Jingyang Zhang,Minhao Lv,Xiuchun Chen,Zhenzhen Liu 대한암학회 2023 Cancer Research and Treatment Vol.55 No.4
Purpose Patients with human epidermal growth factor receptor 2 (HER2)–low advanced breast cancer can benefit from trastuzumab deruxtecan. Given the unclear prognostic characteristics of HER2-low breast cancer, we investigated the prognostic characteristics of HER2-low expression from primary tumor to residual disease after neoadjuvant chemotherapy (NACT). Materials and Methods The data of HER2-negative patients receiving NACT at our center were collected. Pathological complete response (pCR) rate were compared between HER2-0 and HER2-low patients. The evolution of HER2 expression from primary tumor to residual disease and its impact on disease-free survival (DFS) were examined. Results Of the 690 patients, 494 patients had HER2-low status, of which 72.3% were hormone receptor (HR)–positive (p < 0.001). The pCR rates of HER2-low and HER2-0 patients (14.2% vs. 23.0%) showed no difference in multivariate analysis regardless of HR status. No association was observed between DFS and HER2 status. Of the 564 non-pCR patients, 57 (10.1%) changed to HER2-positive, and 64 of the 150 patients (42.7%) with HER2-0 tumors changed to HER2-low. HER2-low (p=0.004) and HR-positive (p=0.010) tumors before NACT were prone to HER2 gain. HER2 gain patients had a better DFS compared with HER2-negative maintained patients (87.9% vs. 79.5%, p=0.048), and the DFS of targeted therapy group was better than that of no targeted therapy group (92.4% vs. 66.7%, p=0.016). Conclusion Although HER2-low did not affect the pCR rate and DFS, significant evolution of HER2-low expression after NACT creates opportunities for targeted therapy including trastuzumab.
Yang Guang,Li Jiajing,Xu Qian,Xie Huilan,Wang Lijun,Zhang Minhao 대한독성 유전단백체 학회 2022 Molecular & cellular toxicology Vol.18 No.4
Background Bone cancer pain (BCP) severely compromises the life quality of patients with advanced cancer or bone metastases . Objective This study investigates the analgesic effect of sodium aescinate (SA) on BCP, and the underlying mechanisms within the spinal cord (SC) and dorsal root ganglion (DRG). Walker 256 cells were intratibially inoculated into rats to establish a BCP model. 10, 20, and 40 g/L of SA was intrathecally injected, respectively, and then, hyperalgesia and allodynia were evaluated by measuring the paw withdrawal threshold (PWT) and paw withdrawal latency (PWL). The effect of SA on neuroinflammation was observed by detecting the production of the pro-inflammatory cytokines based on RT-qPCR and ELISA. The NF-κB and p38 MAPK/c-Fos signaling was detected by WB analysis. Furthermore, RT-qPCR and WB analyses of Iba-1and CD206 were performed to assess microglial activation. Result The development of hyperalgesia and allodynia, and an increase of pro-inflammatory cytokines production, as well as microglial activation, were observed in the BCP rats. SA (40 g/L) not only relieved the pain-related behaviors induced by BCP but also suppressed the release of pro-inflammatory cytokines and the activation of microglia in the SC and DRG. SA could also inhibit p38 MAPK/c-Fos signaling in both the SC and DRG, which might contribute to the suppression of microglial activation. Conclusion Our findings suggest that SA plays a promising analgesic role in the BCP rats by suppressing infl ammation and microglial activation, and these effects may be associated with the suppression of p38 MAPK/c-Fos signaling.