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08 May 2026, Volume 53 Issue 5 Previous Issue   

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Chinese expert consensus on the clinical management of cancer-related neuropathic pain Chinese Society of Clinical Oncology-Supportive Care and Rehabilitation Committee 2026, 53 (5):  257-267.  doi: 10.3760/cma.j.cn371439-20260118-00043 Abstract ( 9 )   HTML ( 7 )   PDF (1153KB) ( 2 )   Save Cancer-related neuropathic pain （CRNP） is a common type of pain among cancer patients， significantly impacting their quality of life. To standardize the clinical management of CRNP， the Chinese Society of Clinical Oncology-Supportive Care and Rehabilitation Committee organized experts from related fields to develop this consensus based on the GRADE evidence grading system. The consensus clarifies the definition and etiological classification of CRNP （cancer-induced， anticancer treatment-induced， and oncology multimorbidity-related）， systematically elaborates on the screening， diagnosis， and assessment processes of CRNP， recommends the use of scales such as DN4 and LANSS for screening， and confirms the diagnosis based on the NeuPSIG grading system. In terms of treatment， the consensus recommends selecting first-line drugs such as calcium channel modulators， tricyclic antidepressants， and serotonin-norepinephrine reuptake inhibitors based on the etiology， and emphasizes multimodal interventions such as combination therapy， local therapy， minimally invasive intervention， and physical therapy. Additionally， priority should be given to comprehensive patient education， evidence-informed psychological support， integration of traditional medicine and structured long-term follow-up management. This consensus provides evidence-based basis and practical guidance for the individualized and multidisciplinary comprehensive management of CRNP. Figures and Tables | References | Related Articles | Metrics

Original Article

Effect and mechanism of IFITM1 gene silencing in mitigating cisplatin resistance in small cell lung cancer cells Qian Haihong, Wang Xuemei, Liu Siyan, Wang Hua, Zhang Hengjiao, Yang Donghai, Sun Qiong, Zhao Danye 2026, 53 (5):  268-275.  doi: 10.3760/cma.j.cn371439-20250712-00044 Abstract ( 8 )   HTML ( 4 )   PDF (1245KB) ( 2 )   Save Objective To investigate the effect of targeted silencing of interferon-induced transmembrane protein 1 （IFITM1） on cisplatin resistance in small cell lung cancer （SCLC） cells and to explore the underlying mechanisms. Methods Tumor tissue samples of 24 patients with SCLC who received chemotherapy with cisplatin regimen at the Tumor Center of People's Hospital of Yuxi City in Yunnan Province from January 2019 to December 2020 were collected and divided into the resistant group （n=12） and the non-resistant group （n=12）. The mRNA and protein expression levels of IFITM1 were detected by real-time quantitative PCR and enzyme-linked immunosorbent assay， respectively. After targeted silencing of IFITM1 in the cisplatin-resistant SCLC cell lines NCI-H82/cisplatin and SHP-77/cisplatin cells， changes in the IC50 of cisplatin were evaluated. IFITM1-silenced cisplatin-resistant cells were treated with low-dose cisplatin and divided into cisplatin-resistant cell group， IFITM1-silencing negative control group， IFITM1-silencing group， gradient cisplatin treatment group， IFITM1-silencing+gradient cisplatin treatment group， cisplatin （10 μmol/L） treatment group， IFITM1-silencing negative control+cisplatin（10 μmol/L） treatment group， IFITM1-silencing+cisplatin （10 μmol/L） treatment group. Cell proliferation was assessed using the CCK-8 assay， cell invasion was evaluated using the Transwell assay， cell apoptosis was detected by TUNEL staining， and protein expression levels were analyzed by Western blotting. Results The expression levels of IFITM1 mRNA and protein in the tissues of SCLC patients in the resistant group were both higher than those in the non-resistant group （both P<0.05）. IC50 analysis results showed that the IC50 values of cisplatin in NCI-H82/cisplatin cells were （43.12±8.00）， （41.48±10.57）， and （14.82±4.78）μmol/L in the cisplatin-resistant cell group， IFITM1-silencing negative control group， and IFITM1-silencing group， respectively， with a statistically significant difference （F=11.44， P=0.009）， and the IC50 values in the IFITM1-silencing group were lower than those in the cisplatin-resistant cell group and IFITM1-silencing negative control group （both P<0.05）. CCK-8 assay results showed that， the proliferation activities of NCI-H82/cisplatin cells in the cisplatin-resistant cell group， cisplatin treatment group， IFITM1-silencing negative control+cisplatin treatment group， and IFITM1-silencing+cisplatin treatment group were 1.35±0.18， 1.15±0.17， 1.06±0.18， and 0.52±0.08， respectively， with a statistically significant difference （F=15.17， P=0.001）， and proliferation activity in the IFITM1-silencing+cisplatin treatment group was significantly lower than that in the cisplatin-resistant group， cisplatin treatment group and IFITM1-silencing negative control+cisplatin treatment group （all P<0.05）. Transwell assay results indicated that， the numbers of invading NCI-H82/cisplatin cells in the cisplatin-resistant cell group， cisplatin treatment group， IFITM1-silencing negative control+cisplatin treatment group， and IFITM1-silencing+cisplatin treatment group were 1 380.00±166.43， 1 259.33±198.01， 1 143.00±169.14， and 563.00±127.39， respectively， with a statistically significant difference （F=15.11， P=0.001）， and the numbers of invasion were significantly lower in the IFITM1-silencing+cisplatin treatment group than those in the cisplatin-resistant cell group， cisplatin treatment group and IFITM1-silencing negative control+cisplatin treatment group （all P<0.05）. TUNEL staining results showed that， apoptosis rates of NCI-H82/cisplatin cells in the above four groups were （12.00±2.91）%， （15.83±3.50）%， （16.37±3.59）%， and （42.46±4.95）%， respectively， with a statistically significant difference （F=40.45， P<0.001）， and the apoptosis rate of the IFITM1-silencing+cisplatin treatment group was significantly higher than that of the cisplatin-resistant cell group， cisplatin treatment group and IFITM1-silencing negative control+cisplatin treatment group （all P<0.05）. The above experimental results for SHP-77/cisplatin cells were consistent with those of NCI-H82/cisplatin cells. The results of Western blotting showed that there were statistically significant differences in the protein expression levels of IFITM1， p-β-catenin， ABCB1， and ABCG2 among the NCI-H82/cisplatin resistant cell group， the IFITM1-silencing negative control group， and the IFITM1-silencing group （all P<0.05）. Compared with the cisplatin-resistant cell group and the IFITM1-silencing negative control group， the IFITM1-silencing group exhibited significantly higher p-β-catenin expression and significantly lower IFITM1， ABCB1， and ABCG2 expression levels （all P<0.05）. Conclusions IFITM1 plays a promotive role in cisplatin resistance of SCLC cells. Targeted silencing of IFITM1 effectively reduces cisplatin resistance by inhibiting the Wnt signaling pathway. Figures and Tables | References | Related Articles | Metrics

Correlation between the changes in sPD-1 after neoadjuvant therapy in patients with esophageal squamous cell carcinoma and pathological response Gu Lei, Han Jihua, Tian Wenze, Zhou Wubi, Xin Yong 2026, 53 (5):  276-282.  doi: 10.3760/cma.j.cn371439-20251019-00045 Abstract ( 9 )   HTML ( 1 )   PDF (937KB) ( 2 )   Save Objective To investigate the correlation between dynamic changes in serum soluble programmed death-1 （sPD-1） during neoadjuvant camrelizumab combined with chemotherapy and pathological response in patients with esophageal squamous cell carcinoma （ESCC）， and to evaluate the feasibility of sPD-1 as a predictive indicator of therapeutic efficacy. Methods A total of 125 patients with locally advanced ESCC who received neoadjuvant treatment with camrelizumab combined with albumin paclitaxel and cisplatin at Affiliated Huai′an No.1 People's Hospital of Nanjing Medical University from January 2019 to December 2021 were selected as the research subjects. Serum sPD-1 levels were measured at baseline， after the first cycle， after the second cycle， and before surgery. Patients were divided into the decreasing group （n=45） and non-decreasing group （n=80） based on early sPD-1 reduction （≥30% vs. <30%）. Correlations between sPD-1 dynamic changes and pathological complete response （pCR）， major pathological response （MPR）， and event-free survival （EFS） were analyzed using generalized estimating equation （GEE） models. Logistic regression model was used to identify the influencing factors of patients' pathological response； Kaplan-Meier curves were plotted to assess EFS in patients from the decreasing and non-decreasing groups， and the log-rank test was conducted； the Cox proportional hazards regression model was used to evaluate the influencing factors of patients' EFS. Results All 125 patients completed neoadjuvant therapy and surgery， with an R0 resection rate of 100% and no perioperative deaths. The baseline sPD-1 levels in the decreasing and non-decreasing groups were 5.9 （4.5， 7.3） and 5.7 （4.3， 7.6） ng/ml， respectively， with no statistically significant difference （Z=0.52， P=0.472）. Following the first treatment cycle， sPD-1 levels decreased to 3.1 （2.4， 4.0） ng/ml in the decreasing group and 4.8 （3.7， 6.5） ng/ml in the non-decreasing group， with a statistically significant difference （Z=19.26， P<0.001）. After the second treatment cycle， levels were 2.8 （2.2， 3.7） and 4.5 （3.4， 6.0） ng/ml， respectively， with a statistically significant difference （Z=22.13， P<0.001）. Before surgery， sPD-1 levels were 2.6 （2.0， 3.5） and 4.2 （3.3， 5.7） ng/ml，with a statistically significant difference （Z=21.84， P<0.001）. GEE analysis revealed that both the main effects of time （χ2=112.40， P<0.001） and group （χ2=7.63， P=0.006） were significant， and a significant interaction effect between time and group was observed （χ2=9.18， P=0.027）. After the first treatment cycle， the pCR rate for patients in decreasing group was 42.2% （19/45）， significantly higher than the 19.5% （16/80） in the non-decreasing group （χ2=7.59， P=0.006）. The MPR rate in the decreasing group was 68.9% （31/45）， significantly higher than that in the non-decreasing group， which was 48.1% （38/80） （χ2=5.35， P=0.021）. The survival analysis showed that the median EFS in the decreasing group was 34 months， longer than that of 28 months in the non-decreasing group （χ2=8.33， P=0.004）. Multivariate analysis indicated that an early reduction in sPD-1 of ≥30% （OR=2.34， 95%CI： 1.18-4.63， P=0.015） and baseline sPD-1 levels （OR=0.89， 95%CI： 0.80-0.98， P=0.023） were independent influencing factors of pCR in patients with locally advanced ESCC. Furthermore， early sPD-1 reduction ≥30% （HR=0.44， 95%CI： 0.23-0.85， P=0.014） and baseline sPD-1 （HR=1.09， 95%CI： 1.02-1.18， P=0.021） were identified as independent influencing factors for EFS in patients with locally advanced ESCC. The total incidence of adverse events was 52.0% （65/125）， mainly consisting of bone marrow suppression and mild to moderate immune-related reactions； the incidence of grade ≥3 adverse events was 9.6% （12/125）， with no treatment-related deaths. Conclusions Both baseline sPD-1 levels and early dynamic decline during neoadjuvant camrelizumab plus chemotherapy are significantly associated with pathological response and EFS in patients with locally advanced ESCC. Serum sPD-1， as a simple and dynamically monitorable peripheral blood marker， is expected to become a predictive tool for the efficacy of neoadjuvant immunotherapy. Figures and Tables | References | Related Articles | Metrics

Impact of imatinib adjuvant therapy on the postoperative prognosis of patients with non-gastric primary high-risk GIST Yang Song, Zheng Xiangyun, Pan Yingxue, Wang Jiaming, Zhang Huanhu 2026, 53 (5):  283-289.  doi: 10.3760/cma.j.cn371439-20250826-00046 Abstract ( 6 )   HTML ( 1 )   PDF (1331KB) ( 2 )   Save Objective To analyze the impact of imatinib adjuvant therapy on the postoperative prognosis of patients with non-gastric primary high-risk gastrointestinal stromal tumor （GIST）. Methods A retrospective analysis was conducted on the clinical data， postoperative treatment and survival information of 40 patients with non-gastric primary high-risk GIST admitted to Weihai Municipal Hospital Affiliated to Shandong University from January 1， 2010 to May 30， 2022. All patients underwent radical surgical resection. Patients receiving imatinib （400 mg/d） as adjuvant therapy started taking the medication 4 to 8 weeks after the surgery. Univariate and multivariate analyses of factors influencing patient prognosis were performed using the Cox proportional hazards regression model. Kaplan-Meier survival curves were plotted， and patients were stratified based on whether they completed 3-year or 5-year postoperative imatinib adjuvant therapy. Inter-group comparisons were made using the log-rank test. Results By the end of the follow-up period， among the 40 patients， 37 received adjuvant therapy， of whom 16 experienced tumor progression and 7 of these died due to tumor progression； 3 patients did not receive adjuvant therapy， and 2 of them died due to tumor progression. The 3-， 5-， and 10-year disease-free survival （DFS） rates were 79.1%， 60.0%， and 25.3%， respectively， while the 3-， 5-， and 10-year overall survival （OS） rates were 94.1%， 90.6%， and 54.1%， respectively. Univariate analysis revealed that the Ki-67 （HR=4.01， 95%CI： 1.04-15.27， P=0.048） and imatinib adjuvant therapy （HR=4.59， 95%CI： 1.05-20.23， P=0.041） were factors influencing DFS. Tumor number （HR=5.83， 95%CI： 1.06-21.93， P=0.042） and imatinib adjuvant therapy （HR=5.05， 95%CI： 1.03-24.26， P=0.044） were factors influencing OS. Multivariate analysis identified Ki-67>5% （HR=4.21， 95%CI： 1.03-20.73， P=0.046） and without postoperative imatinib adjuvant therapy （HR=6.23， 95%CI： 1.23-31.59， P=0.027） as independent risk factors for DFS. Multiple tumor numbers （HR=8.77， 95%CI： 1.40-55.01， P=0.020） and not receiving postoperative imatinib adjuvant therapy （HR=7.70， 95%CI： 1.28-46.41， P=0.026） were independent risk factors for OS. The 5-year DFS and OS rates were 46.2% and 90.0% in the group receiving postoperative imatinib adjuvant therapy for less than 3 years， compared to 90.0% and 100.0% in the group receiving therapy for more than 3 years， with statistically significant differences （χ2=8.24， P=0.004； χ2=6.34， P=0.012）. The 5-year DFS and OS rates were 55.0% and 92.2% in the group receiving postoperative imatinib adjuvant therapy for less than 5 years， compared to 100% and 100% in the group receiving therapy for more than 5 years. There was a statistically significant difference in the 5-year DFS rate between the two groups （χ2=3.94， P=0.047）， but no statistically significant difference in the 5-year OS rate （χ2=2.10， P=0.147）. Conclusions Ki-67>5%， multiple tumor numbers and without postoperative imatinib adjuvant therapy are independent risk factors affecting the postoperative prognosis of non-gastric primary high-risk GIST patients. 5-year imatinib adjuvant therapy can prolong the postoperative DFS of non-gastric primary high-risk GIST patients and improve their prognosis. Figures and Tables | References | Related Articles | Metrics

Value of Gd-EOB-DTPA enhanced MRI combined with DWI in evaluating vessels encroachment tumor clusters in hepatocellular carcinoma Zhang Zhuang, Wang Qian, Yang Yujia, Wei Haikuo, Liu Chang 2026, 53 (5):  290-295.  doi: 10.3760/cma.j.cn371439-20250704-00047 Abstract ( 6 )   HTML ( 1 )   PDF (981KB) ( 2 )   Save Objective To investigate the value of gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid （Gd-EOB-DTPA） enhanced MRI combined with diffusion weighted imaging （DWI） in evaluating vessels encroachment tumor clusters （VETCs） in patients with hepatocellular carcinoma （HCC）. Methods A retrospective study was conducted and 116 patients with HCC admitted to the Second Hospital of Qinhuangdao from January 2023 to December 2024 were selected for the study. All patients underwent Gd-EOB-DTPA-enhanced MRI and DWI examinations within 7 d before surgery. Based on postoperative pathological results， the patients were divided into VETC positive group （n=35） and VETC negative group （n=81）. Imaging features and apparent diffusion coefficient （ADC） values of the two groups were compared. Multivariate logistic regression was utilized to analyze the influencing factors of VETC in patients with HCC， and the receiver operator characteristic （ROC） curve was plotted to analyze the value of each parameters in evaluating VETC in patients with HCC. Results The incidence rates of rough tumor margins， peritumoral enhancement in arterial phase， and hepatobiliary specific peritumoral hypointensity in the VETC positive group [51.43% （18/35）， 42.86% （15/35）， 54.29% （19/35）] were higher than those in the VETC negative group [25.93% （21/81）， 16.05% （13/81）， 18.52% （15/81）]， with statistically significant differences （χ2=7.12， P=0.008； χ2=9.59， P=0.002； χ2=15.09， P<0.001）. The ADC value of the VETC positive group [（1.05±0.30）×10-3 mm2/s] was lower than that of the VETC negative group [（1.28±0.44）×10-3 mm2/s] （t=2.82， P=0.006）. Multivariate logistic regression analysis showed that peritumoral enhancement in arterial phase （OR=1.40， 95%CI： 1.12-1.74， P=0.003）， hepatobiliary specific peritumoral hepatobiliary （OR=1.43， 95%CI： 1.13-1.81， P=0.003）， and decreased ADC value （OR=1.49， 95%CI： 1.20-1.86， P<0.001） were independent risk factors for VETC in patients with HCC. ROC curve analysis showed that the values of the area under the curve （AUC） of peritumoral enhancement in arterial phase， hepatobiliary specific peritumoral hypointensity， decreased ADC value， and the combined detection of the three for predicting VETC in HCC patients were 0.695， 0.684， 0.725， and 0.855， respectively. The AUC of the combined detection of the three for predicting VETC in HCC patients was higher than that of the individual detection （Z=2.08， P=0.038； Z=2.86， P=0.004； Z=2.97， P=0.003）. Conclusions Gd-EOB-DTPA enhanced MRI combined with DWI is of high value in evaluating VETC in patients with HCC， and can help to guide individualized treatment plan and evaluate the prognosis. Figures and Tables | References | Related Articles | Metrics

Review

Research progress on the CD300 family and its mechanism of regulating the anti-tumor effects of immune cells Yu Xinjing, Yang Yang, Li Shuyao, Qiao Xiaojuan 2026, 53 (5):  296-300.  doi: 10.3760/cma.j.cn371439-20251106-00048 Abstract ( 11 )   HTML ( 1 )   PDF (831KB) ( 7 )   Save As an important member of the immunoglobulin （Ig） superfamily， the CD300 family possesses conserved Ig domains and diverse intracellular signaling motifs， and is widely present in various immune cells and tumor cells. Due to differences in the structural composition of different subtypes， members of this family are classified into inhibitory or activating receptors， exhibiting functional heterogeneity. They play a dual role in the tumor immune microenvironment： they can either promote immune activation or mediate immune suppression. By directly or indirectly regulating the functions of myeloid cells （macrophages， dendritic cells， polymorphonuclear-like myeloid-derived suppressor cells） and lymphocytes （natural killer cells， T cells） in the tumor immune microenvironment， the CD300 family serves as a key node in tumor immune escape. Based on the anti-tumor effect of CD300 family regulating immune cells， this article reviews the biological functions of CD300 family and its correlation with tumor occurrence and development， which can provide new research ideas for tumor immunotherapy and drug resistance. References | Related Articles | Metrics

Research progress on preoperative radiotherapy for breast cancer Li Lina, Liu Shuai, Zhang Nan 2026, 53 (5):  301-305.  doi: 10.3760/cma.j.cn371439-20251112-00049 Abstract ( 4 )   HTML ( 1 )   PDF (790KB) ( 3 )   Save Preoperative radiotherapy is an important development direction in the field of comprehensive treatment of breast cancer. Its clinical value lies not only in tumor downstaging and improving the pathological complete response rate， but also in optimizing the timing of breast reconstruction and reducing long-term complications. With the rapid advancement of precise radiotherapy and immunotherapy， increasing attention has been paid to the biological synergistic effects of preoperative radiotherapy in inducing immunogenic cell death and regulating the tumor microenvironment. This review provides an in-depth discussion of the clinical value， key technical models， and multidisciplinary joint strategies of preoperative radiotherapy for breast cancer， systematically summarizes the latest evidence， and delineates the key challenges， which may guide the clinical practice of preoperative radiotherapy in patients with breast cancer and improve patient prognosis. References | Related Articles | Metrics

Research progress of neurokinin-1 receptor antagonists in the treatment of lung cancer Li Yiping, Tang Zhuang, Ouyang Surui, Li Jin, He Jingdong 2026, 53 (5):  306-310.  doi: 10.3760/cma.j.cn371439-20251009-00050 Abstract ( 4 )   HTML ( 1 )   PDF (836KB) ( 3 )   Save The neuropeptide substance P （SP） and its receptor， neurokinin-1 receptor （NK-1R）， play a critical role in the occurrence and development of tumors. As a member of the G protein-coupled receptor superfamily， aberrant activation of NK-1R is closely related to the proliferation and metastasis of lung cancer. Studies have shown that SP/NK-1R promotes the proliferation of tumor cells by regulating signal pathways such as MAPK and PI3K/Akt， and anticipates in the remodeling of the tumor microenvironment to drive angiogenesis. In recent years， an increasing number of preclinical studies have found that NK-1R antagonists not only serve as antiemetic drugs widely used for the prevention of chemotherapy-induced nausea and vomiting， but also have direct anti-tumor effects. Some of the mechanisms include reversing epithelial-mesenchymal transition and inhibiting the vascular endothelial growth factor pathway. The systematic elaboration of NK-1R's mechanisms in lung cancer and research progress of its antagonists can lay a foundation for exploring new treatment paths for lung cancer and ultimately improving therapeutic efficacy and the quality of patients′ lives. References | Related Articles | Metrics

Research progress on myocarditis associated with immunotherapy in lung cancer Zhao Juan, Yu Jiaofeng, Wei Aojiao, Dai Yixue, Zhao Yan, Fu Ye, Zhao Mingli 2026, 53 (5):  311-316.  doi: 10.3760/cma.j.cn371439-20251106-00051 Abstract ( 5 )   HTML ( 1 )   PDF (808KB) ( 3 )   Save Immune checkpoint inhibitor treatment is an important treatment option for lung cancer. However， it can cause immune-related adverse events， including potentially severe cardiac toxicity， such as myocarditis， which can lead to treatment delays or discontinuation. Severe cardiac toxicity events can even result in patient death. Increasing attention to immune checkpoint inhibitor-associated myocarditis and implementing appropriate preventive and intervention measures for high-risk patients in clinical applications can minimize the risk and severity of myocarditis. References | Related Articles | Metrics