Table of Content

25 February 2026, Volume 18 Issue 1 Previous Issue   

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Expert consensus on Bevacizumab treatment for recurrent respiratory papillomatosis (2026 Edition) Lung Cancer Integrated Prevention and Screening Committee of Chinese Anti?Cancer Association, Rare Tumor Committee of Shandong Rare Disease Prevention and Treatment Association, Rare Disease Branch of Shandong Medical Association 2026, 18 (1):  1-11.  doi: 10.3969/j.issn.1674--5671.2026.01.01 Abstract ( 16 )   PDF (714KB) ( 9 )   Save Abnormal angiogenesis is an important pathological characteristic of recurrent respiratory papillomatosis (RRP). Bevacizumab, by blocking the vascular endothelial growth factor (VEGF)/vascular endothelial growth factor receptor (VEGFR) signaling pathway, promotes the normalization of aberrant angiogenesis and vascular permeability in RRP lesions. This action results in a reduction of lesion burden, prolonging the interval between surgical interventions, and improving airway⁃related symptoms. Multiple studies have confirmed the therapeutic efficacy of Bevacizumab in the treatment of RRP, with acceptable short⁃term adverse events. This consensus was developed by the writing group based on published clinical evidence on Bevacizumab in RRP and clinical practice. Through multiple rounds of expert deliberation, a unified set of recommendation was formulated to guide the rational and standardized application of Bevacizumab in relevant clinical departments in China, thereby improving the standardization of RRP diagnosis and treatment. Related Articles | Metrics

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Analysis of leukemia incidence in Gansu Province from 2010 to 2021 and the future trend prediction Gong Qinli, Ye Yancheng, Liang Xuexue, Qin Tianyan, Ding Gaoheng, Zhu Jiahe, Wang Jia, Zhao Xiaoli, Wang Bole, Liu Yuqin, Zhang Yanshan 2026, 18 (1):  12-18.  doi: 10.3969/j.issn.1674-5671.2026.01.02 Abstract ( 7 )   PDF (908KB) ( 5 )   Save Objective In 2022, an estimated 81,900 new cases of leukemia were reported  in China, ranking 12th among domestic malignant tumors. The epidemiological characteristics of leukemia are influenced by regional environment and the distribution of medical resources. This study analyzes the trends in leukemia incidence within the cancer registration areas of Gansu Province from 2010 to 2021 and projects the incidence rates from 2022 to 2030. Methods Based on leukemia incidence data from 15 cancer registries in Gansu Province between 2010 and 2021, incidence rates were calculated by age, sex, and urban⁃rural distribution. The age⁃standardized incidence rate by Chinese standard population (ASIRC) was calculated using the 2000 Chinese standard population structure. The Joinpoint regression model was used to analyze incidence trends, calculating the annual percentage change (APC), average annual percentage change (AAPC), and their 95% confidence interval (CI). The Bayesian age⁃period⁃cohort (BAPC) model was applied to predict leukemia incidence in Gansu Province from 2022 to 2030. Results From 2010 to 2021, the overall ASIRC in Gansu Province showed a non‑significant downward trend (AAPC = −4.58%, 95%CI: −9.04% to 0.09%, P=0.055), with a significant decline observed from 2019 to 2021 (APC = −26.11%, P=0.014). The ASIRC level was higher in male than in female, but neither showed a statistically significant downward trend (all P>0.05). No significant change was found in urban areas (AAPC=0.24%, 95%CI: −5.62% to 6.46%, P=0.939), while rural areas exhibited a significant downward trend (AAPC=−7.76%, 95%CI: −14.04% to −1.03%, P=0.025). From 2010 to 2021 in Gansu Province, the ASIRC change of leukemia in the 0-29 and 40-49 age groups decreased at average annual rates of 5.09% and 1.89%, respectively. The results of birth cohort analysis showed that the ASIRC of leukemia in the early birth cohort was at a high level particularly among individuals aged over 70 years. Successive birth cohorts showed declining ASIRC for aged 0-49 years, while those aged ≥50 years demonstrated fluctuating upward trend. The BAPC model predicted that the ASIRC of leukemia for the overall population, male, urban areas, and rural areas would decline from 2.60/105, 3.00/105, 2.73/105, and 2.51/105 in 2021 to 0.93/105, 1.28/105, 0.93/105, and 2.17/105 in 2030, respectively. In contrast, the ASIRC for female would increase from 2.18/105 in 2021 to 2.94/105 in 2030. Conclusions From 2010 to 2021, the ASIRC of leukemia in Gansu Province declined overall, with a particularly noticeable decrease in rural areas. The ASIRC in the 0-49 age group showed a declining trend, while it fluctuates upward after the age 50. The ASIRC of leukemia further declines by 2030, suggesting that prevention and control measures have achieved results. However, continued efforts are needed to strengthen interventions for high⁃risk groups and maintain long⁃term surveillance. Related Articles | Metrics

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Mortality trend and age-period-cohort model analysis of bladder cancer in Wuhan,2010—2019 Deng Qing, Liu Pulin, Zhang Xiaoxia, Zhao Yuanyuan, Xiong Jinmeng, Zhang Wei, Dai Juan 2026, 18 (1):  19-27.  doi: 10.3969/j.issn.1674-5671.2026.01.03 Abstract ( 13 )   PDF (580KB) ( 1 )   Save Objective To investigate the prognostic value of absolute lymphocyte count (ALC) in patients with natural killer/T⁃cell lymphoma (NKTCL) treated with programmed death⁃1 (PD⁃1) inhibitor, and to develop a prognostic model for predicting progression⁃free survival (PFS). Methods A cohort of 41 patients with NKTCL who underwent PD⁃1 inhibitor combination therapy at Beijing Tongren Hospital, Capital Medical University from June 2019 to June 2023 were enrolled. The optimal cut⁃off value for ALC was determined using the maximum selected rank statistics. The Cox proportional hazards regression model was used to analyze the correlation between ALC and prognosis, and a prognostic scoring model was constructed based on the identified prognostic factors. Results The optimal cut⁃off value of ALC was 1.35×10⁹/L. Significant differences in PFS and overall survival (OS) were observed between the low ALC group and high ALC group (P<0.001). The median PFS and median OS in the high ALC group were 216 days and 343 days, respectively, whereas both median PFS and OS were not reached in the low ALC group. Multivariable analysis demonstrated that ALC ≥1.35×109/L was an independent prognostic factor for PFS (HR=3.185, 95%CI: 1.146-8.851). The scoring model constructed based on age, disease status, Ann Arbor staging system and ALC could effectively distinguish low⁃risk from high⁃risk patients, with an area under the curve (AUC) of 0.924 for predicting PFS, which was significantly higher than that of the conventional nomogram⁃revised risk index (NRI) score (0.545, P<0.001). The clinical benefit rate (CBR) of the low⁃risk group reached 83.3%, significantly exceeding the 43.5% observed in the high⁃risk group (P=0.012). Conclusions Pretreatment ALC is an independent prognostic factor for PFS in NKTCL patients receiving PD⁃1 inhibitor combination therapy. The novel prognostic model integrating age, disease status, Ann Arbor stage and ALC improves risk stratification and may inform individualized treatment strategies. Related Articles | Metrics

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Prognostic value of absolute lymphocyte count in patients with NK/T-cell lymphoma receiving PD-1 monoclonal antibody therapy Liu Xindi, Yang Lei, Yao Na, Cong Jia, Ye Jin, Li Xin, Yang Jing, Wei Liqiang, Wang Liang 2026, 18 (1):  28-35.  doi: 10.3969/j.issn.1674-5671.2026.01.04 Abstract ( 7 )   PDF (658KB) ( 0 )   Save Objective To investigate the prognostic value of absolute lymphocyte count (ALC) in patients with natural killer/T⁃cell lymphoma (NKTCL) treated with programmed death⁃1 (PD⁃1) inhibitor, and to develop a prognostic model for predicting progression⁃free survival (PFS). Methods A cohort of 41 patients with NKTCL who underwent PD⁃1 inhibitor combination therapy at Beijing Tongren Hospital, Capital Medical University from June 2019 to June 2023 were enrolled. The optimal cut⁃off value for ALC was determined using the maximum selected rank statistics. The Cox proportional hazards regression model was used to analyze the correlation between ALC and prognosis, and a prognostic scoring model was constructed based on the identified prognostic factors. Results The optimal cut⁃off value of ALC was 1.35×10⁹/L. Significant differences in PFS and overall survival (OS) were observed between the low ALC group and high ALC group (P<0.001). The median PFS and median OS in the high ALC group were 216 days and 343 days, respectively, whereas both median PFS and OS were not reached in the low ALC group. Multivariable analysis demonstrated that ALC ≥1.35×109/L was an independent prognostic factor for PFS (HR=3.185, 95%CI: 1.146-8.851). The scoring model constructed based on age, disease status, Ann Arbor staging system and ALC could effectively distinguish low⁃risk from high⁃risk patients, with an area under the curve (AUC) of 0.924 for predicting PFS, which was significantly higher than that of the conventional nomogram⁃revised risk index (NRI) score (0.545, P<0.001). The clinical benefit rate (CBR) of the low⁃risk group reached 83.3%, significantly exceeding the 43.5% observed in the high⁃risk group (P=0.012). Conclusions Pretreatment ALC is an independent prognostic factor for PFS in NKTCL patients receiving PD⁃1 inhibitor combination therapy. The novel prognostic model integrating age, disease status, Ann Arbor stage and ALC improves risk stratification and may inform individualized treatment strategies. Related Articles | Metrics

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Impact of postoperative adjuvant-transcatheter arterial chemoembolization on postoperative prognosis in cytokeratin 19-positive hepatocellular carcinoma patients: a propensity score matching cohort study Huang Hongyang, Tao Zheng, Zeng Can, Mo Kaixiang, Cen Weijie, Zeng Dandan, Luo Wenfeng, Su Jingting, Su Yuejiao, Lin Yan, Liang Rong, Wu Guobin, Ye Jiazhou, Mai Rongyun 2026, 18 (1):  36-42.  doi: 10.3969/j.issn.1674-5671.2026.01.05 Abstract ( 6 )   PDF (644KB) ( 2 )   Save Objective To investigate the prognostic value of postoperative adjuvant⁃transcatheter arterial chemoembolization (PA⁃TACE) in patients with cytokeratin 19 (CK19)⁃positive hepatocellular carcinoma (HCC). Methods This single⁃center retrospective cohort analysis enrolled patients with pathologically confirmed CK19⁃positive HCC who underwent radical hepatectomy at Guangxi Medical University Cancer Hospital from January 2013 to December 2018. Participants were stratified into the PA⁃TACE group (n=125) and Non⁃TACE group (n=255) based on postoperative receipt of PA⁃TACE. A 1∶1 propensity score matching (PSM) procedure was performed between the two groups, and differences in relapse⁃free survival (RFS) and overall survival (OS) were compared between the two groups pre⁃ and post⁃PSM. Results In a cohort of 380 patients, pre⁃PSM analysis showed that the PA⁃TACE group was younger, exhibited a higher rate of hepatitis B virus infection, and a higher proportion of multiple tumors compared with the Non⁃TACE group (all P<0.05). Across entire cohort, the median RFS in the PA⁃TACE group was significantly longer than that in the Non⁃TACE group (18.0 months vs 8.0 months; HR=0.69, 95%CI: 0.52-0.91， P<0.001), and the median OS was also significantly improved (not reached vs 39.0 months; HR=0.67, 95%CI: 0.49-0.92， P=0.013). Following  PSM, 124 matched patient pairs were obtained, and the PA⁃TACE group still had superior median RFS (17.0 months vs 7.0 months; HR=0.69,95%CI: 0.50-0.95， P<0.001) and median OS (not reached vs 41.0 months; HR=0.69, 95%CI: 0.48-0.99， P=0.044) compared with the Non⁃TACE group. Conclusions In this retrospective cohort study of patients CK19⁃positive HCC, postoperative PA⁃TACE was associated with prolonged RFS and OS. These findings suggest that PA⁃TACE may serve as a beneficial adjuvant therapeutic strategy for this population. Related Articles | Metrics

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Effect of BMI levels on arterial phase respiratory motion artifacts in patients with liver disease: based on gadoxetic acid disodium enhanced MRI Huang Fuling, Lu Feichen, Qiu Fuhe, Pan Haihui, Yang Zhengnan, Zhu Xuna, Li Qiang, Luo Ningbin 2026, 18 (1):  43-50.  doi: 10.3969/j.issn.1674-5671.2026.01.06 Abstract ( 10 )   PDF (564KB) ( 2 )   Save Objective Gadoxetic acid disodium (Gd‑EOB‑DTPA) enhanced magnetic resonance imaging (MRI) plays a crucial role in the detection and characterization of hepatic lesions, However, arterial phase images are frequently degraded by transient severe motion (TSM) artifacts, which may be associated with body mass index (BMI). This study aims to investigate the relationship and dose⁃response association between BMI and TSM in Gd⁃EOB⁃DTPA enhanced MRI, and to provide the evidence for the accurate identification and prevention of arterial⁃phase TSM. Methods This prospective study enrolled patients with liver lesions who underwent Gd⁃EOB⁃DTPA enhanced MRI at Guangxi Medical University Cancer Hospital from March 2024 to November 2025. Multivariable Logistic regression was used to evaluate the association between BMI and arterial⁃phase TSM. Four stepwise adjusted models were established. Model 1 was unadjusted, Model 2 adjusted for demographic factors, Model 3 additionally included lifestyle factors, and Model 4 was comprehensively adjusted for clinical covariates. Subgroup analysis was performed to observe the correlation between BMI and arterial TSM across different populations. Restricted cubic splines (RCS) were applied to explore potential non⁃linear relationships. Results A total of 792 patients were included in the study and categorized into three groups: the underweight/normal⁃weight group (n=484), the overweight group (n=158), and the obese group (n=150). Arterial⁃phase TSM occurred in 270 patients (34.1%). After adjustment for relevant confounders, compared with the underweight/normal⁃weight group, the obese group had a significantly higher risk of arterial⁃phase TSM (OR=2.88, 95%CI: 1.82-4.55; P<0.001). A 1⁃standard⁃deviation increase in BMI (4.51 kg/m²) was associated with a 49% higher risk of arterial⁃phase TSM (OR=1.49, 95%CI: 1.26-1.77; P<0.001). RCS analysis showed a linear positive association between BMI and arterial⁃phase TSM within a BMI range of 15-40 kg/m² (P for overall association<0.001; P for nonlinearity=0.927). Subgroup analyses indicated a significant interaction between prior Gd⁃EOB⁃DTPA enhanced MRI history and the BMI⁃TSM association (P for interaction=0.016). Conclusions Obesity is an independent risk factor for arterial⁃phase TSM on Gd⁃EOB⁃DTPA enhanced MRI, and the risk of arterial⁃phase TSM increasing with BMI. Clinical practice should pay particular attention to patients with elevated BMI, especially those undergoing first⁃time examinations, by implementing implement targeted preparation and acquisition strategies to improve arterial⁃phase image quality. Related Articles | Metrics

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Predictive value of preoperative contrast-enhanced CT and MRI arterial phase radiomics for microvascular invasion in hepatocellular carcinoma Lin Juyi, Wen Guoliang, Fang Hang, Lai Di, Mao Qinxiang, Wang Tian, Zhang Wei 2026, 18 (1):  51-58.  doi: 10.3969/j.issn.1674-5671.2026.01.07 Abstract ( 13 )   PDF (1299KB) ( 5 )   Save Objective To investigate the value of radiomics features derived from contrast⁃enhanced CT and MRI arterial phase images in predicting the microvascular invasion (MVI) status in hepatocellular carcinoma (HCC). Methods HCC patients who underwent surgery at Liuzhou People's Hospital and The First Affiliated Hospital of Guilin Medical University from January 2022 to January 2024, and had completed contrast⁃enhanced CT and MRI examinations within 1 month before surgery were retrospectively enrolled and divided into a training cohort and a test cohort. Patients were classified as MVI (-) and MVI (+) groups according to postoperative pathological results. Clinical predictors of MVI were screened by multivariable Logistic regression to construct a clinical model. Arterial⁃phase CT and MRI images were imported into the Yizhun Medical⁃Darwin research platform, and two radiologists manually delineated three⁃dimensional regions of interest (ROIs) along the margins. Radiomics features were automatically extracted and preprocessed with min⁃max normalization, features with good intraclass consistency (>0.80) were retained. The LASSO regression classifier in the platform was used for feature screening and dimensionality reduction. The optimal module identified five valuable radiomics features to construct CT, MRI, and CT+MRI models. The radiomics score (Radscore) of the CT+MRI model was calculated using the Logistic regression component in the platform. The clinical parameters related to MVI were combined with Radscore to construct a combined prediction model. Model performance was evaluated using the receiver operating characteristic curve (ROC), the goodness of fit was evaluated using the calibration curve, and the net benefit of predicting MVI was compared among the models using decision curve analysis (DCA). Results A total of 118 HCC patients was included, with 82 in the training cohort and 36 in the test cohort. Multivariate Logistic regression analysis showed that tumor size, AST, and Radscore were independent predictors of MVI (all P<0.05). In both the training cohort and the test cohort, the combined model demonstrated highest performance in predicting MVI (AUC: 0.892, 0.803), outperforming the other four models. The Delong curve showed that only the comprehensive model had better predictive performance than the clinical model in both the training and the test cohorts (P=0.001, 0.038). The calibration curve indicated the comprehensive model achieved a good fit, while DCA revealed that the comprehensive model had a higher clinical net benefit in predicting MVI  than other models (0.20⁃0.60 in the training cohort and 0.20-0.58 in the test cohort). Conclusions The construction of Radscore based on radiomics features from enhanced CT and MRI arterial phase images, when it combined with tumor size and AST, the comprehensive model yielded a high predictive value for the MVI status in HCC, supporting its utility in preoperative clinical decision⁃making. Related Articles | Metrics

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Clinical analysis of complete urinary tract exenteration for urothelial carcinoma in dialysis-dependent patients with end-stage renal disease Cui Jiayuan, Li Yuehan, Ren Kexin, Miao Qi, Wang Yuxuan, Zhang Ning, Hong Baoan 2026, 18 (1):  59-66.  doi: 10.3969/j.issn.1674-5671.2026.01.08 Abstract ( 9 )   PDF (593KB) ( 0 )   Save Objective This study aims to synthesize the principal  diagnostic and therapeutic considerations and short⁃term follow⁃up outcomes of complete urinary tract exenteration (CUTE) in end⁃stage renal disease (ESRD) patients undergoing long⁃term dialysis complicated by urothelial carcinoma (UC), and to provide references for surgical decision⁃making and perioperative management in this high⁃risk cohort. Methods The clinical data of two patients with ESRD receiving long⁃term maintenance hemodialysis and concomitant UC treated at Beijing Anzhen Hospital, Capital Medical University were analyzed retrospectively, including preoperative assessment, imaging findings, surgical procedures, postoperative pathology, and follow⁃up. Both patients underwent a CUTE⁃based strategy mainly composed of radical cystectomy combined with unilateral or bilateral nephroureterectomy. Follow⁃up was performed through clinical assessment along with chest and abdominopelvic imaging. Results The surgery was successfully completed for both patients, with operative durations of 65 and 83 minutes, respectively. Postoperative recovery was uneventful for both individuals, with hospital stay of 5 and 4 days, respectively. Postoperative pathology indicated high⁃grade urothelial carcinoma with multifocal involvement of the urinary tract in both cases. In case 1, there was invasive high⁃grade papillary urothelial carcinoma affecting the right kidney, ureter, and bladder, with vascular invasion. In case 2, the tumor involvement of the bladder muscularis propria (less than half the thickness), the muscular layer of the upper and middle segments of the right ureter (less than half the thickness), and the lamina propria of the right renal pelvis, without evidence of lymphovascular tumor thrombus or perineural invasion. Follow⁃up durations were 10 and 11 months, respectively; at the last follow⁃up, chest and abdominopelvic imaging showed no definite evidence of recurrence or metastasis. Conclusions With rigorous preoperative evaluation and standardized perioperative management, CUTE appears feasible for patients with ESRD on long⁃term dialysis complicated by UC and may enable radical resection of multifocal and occult urothelial involvement. No radiographic recurrence or metastasis was observed during short⁃term follow⁃up. Larger cohorts and longer follow⁃up are warranted to further clarify its safety and oncologic benefit. Related Articles | Metrics

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CD36 promotes ovarian cancer metastasis and its association with STAT3 signaling pathway Xu Zhihong, Shuang Yuanjiang, Li Fudi, Xu Te, Tian Jiming, Huang Qichao, Wang Jing 2026, 18 (1):  67-76.  doi: 10.3969/j.issn.1674-5671.2026.01.09 Abstract ( 13 )   PDF (593KB) ( 7 )   Save bjective To identify the drivers of ovarian cancer metastasis by analyzing gene expression profiles of primary ovarian carcinomas and their corresponding omental metastases. Furthermore, it aims to explore the biological functions and potential regulatory mechanisms of these drivers. Methods Differential expression analyses were performed on paired datasets obtained from the Gene Expression Omnibus (GEO)，specifically GSE178913 and GSE222982，to identify common differentially expressed genes (DEGs), followed by pathway enrichment analysis. Candidate genes were subsequently assessed in cohorts from The Cancer Genome Atlas (TCGA)  for expression patterns and prognostic significance. The expression of the cluster of differentiation 36 (CD36) protein in paired primary and metastatic lesions was validated by immunohistochemistry. Functional studies were employed by CD36 silencing in A2780 cells and overexpressing in OVCAR⁃3 cells via plasmid transfection or lentiviral transduction. Cell migration and invasion were evaluated using wound healing and Transwell assays. Co⁃expression analysis, protein⁃protein interaction network construction, and transcription factor prediction collectively suggested an association between signal transducer and activator of transcription 3 (STAT3) signaling activity and CD36 expression. This association was further explored in vitro and in a mouse model of ovarian cancer peritoneal dissemination using the STAT3 inhibitor Stattic, with CD36 re⁃expression to assess whether metastasis⁃related phenotypes could be partially rescued. Results The common DEGs in primary ovarian tumors and matched omental metastases were significantly enriched in lipid metabolism⁃related pathways, particularly the PPAR signaling pathway. Within this pathway, the key fatty acid transporter CD36 was significantly upregulated in metastatic lesions and advanced⁃stage disease (P<0.05). Analyses of  TCGA data revealed that high CD36 expression independently predicted poor prognosis (HR=2.066, 95%CI: 1.414-3.035, P<0.001). Immunohistochemistry further confirmed higher CD36 protein levels in metastatic lesions relative to primary tumors. Functionally, CD36 knockdown markedly suppressed migration and invasion in A2780 cells (both P<0.01), whereas CD36 overexpression enhanced these phenotypes in OVCAR⁃3 cells (both P<0.05). STAT3 might be an upstream regulator of CD36. In A2780 cells, pharmacologic STAT3 inhibition with Stattic reduced CD36 expression and decreased migration/invasion (all P<0.01), and CD36 re⁃expression partially rescued these effects (all P<0.01). In vivo, STAT3 inhibition significantly reduced peritoneal metastatic nodule burden and ascites formation (both P<0.05). Conclusions CD36 potentially functions as a metastasis⁃promoting factor in ovarian cancer. Its expression  is upregulated in metastatic and advanced⁃stage disease，serving as an independent predictor of poor prognosis，and enhances the migration and invasion capabilities of ovarian cancer cells. Furthermore, STAT3 signaling activity is associated with CD36 expression and metastasis⁃related phenotypes. The STAT3/CD36⁃associated pathway may represent a potential therapeutic target, and CD36 may serve as a candidate biomarker for metastatic risk and adverse outcomes. Related Articles | Metrics

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Expression of the long non-coding RNA KAZALD1-1 in hepatocellular carcinoma and its impact on the biological behavior of liver cancer cells Tan Lizheng, Mo Qiuyan, Zhou Zihan, Li Kezhi, Yu Hongping, Wen Qiuping 2026, 18 (1):  77-86.  doi: 10.3969/j.issn.1674-5671.2026.01.10 Abstract ( 9 )   PDF (7695KB) ( 2 )   Save Objective Hepatocellular carcinoma (HCC) is characterized by high malignancy, rapid progression, and poor survival rates. It is imperative to identify biomarkers for diagnosing HCC and predicting patient prognosis. Extensive research indicates that long non⁃coding RNAs (lncRNAs) play a crucial regulatory roles in the initiation and progression of HCC , thereby influencing patient outcomes. This study aims to investigate the expression of lncRNA Kazal type serine peptidase inhibitor domain 1 transcript variant 1 (KAZALD1⁃1) in HCC, evaluate its effects of cell proliferation, invasion, migration, cell cycle progression, and apoptosis in liver cancer cells, and explore its associated competitive endogenous RNA (ceRNA) network. Methods Five pairs of HCC tumor and matched adjacent non⁃tumor tissues were collected from patients undergoing liver resection at the Guangxi Medical University Cancer Hospital in October 2019. Whole⁃transcriptome sequencing data were analyzed to identify the significantly upregulated lncRNA KAZALD1⁃1 in HCC tissues. Tumor and matched adjacent non⁃tumor tissues were collected from 105 HCC patients who underwent liver resection at the hospital between October 2018 and November 2022. The expression levels of lncRNA KAZALD1⁃1 were detected by quantitative reverse transcription polymerase chain reaction (qRT⁃PCR). The differential expression of this lncRNA and its impact on overall survival (OS) in HCC patients were evaluated using data from The Cancer Genome Atlas (TCGA)  database. Stable knockdown and overexpression cell lines of lncRNA KAZALD1⁃1 were established in the liver cancer cell lines Huh7, HCCLM3, and SNU449. The effects of lncRNA KAZALD1⁃1 on liver cancer cell proliferation, migration, invasion, cell cycle progression, and apoptosis were evaluated using Cell Counting Kit⁃8 (CCK⁃8) assays, scratch assays, Transwell assays, and flow cytometry, respectively. Furthermore, the TCGA database was utilized to explore the ceRNA network associated with lncRNA KAZALD1⁃1. Results Bioinformatics analysis of sequencing data and the TCGA database demonstrated that lncRNA KAZALD1⁃1 was upregulated in HCC tissues, with its elevated expression was significantly associated  with the reduced OS in HCC patients (all P<0.05). qRT⁃PCR results confirmed that lncRNA KAZALD1⁃1 was significantly overexpressed in HCC tissues compared to adjacent non⁃cancerous tissues. Patients with high lncRNA KAZALD1⁃1 expression exhibited significantly poorer OS than those with lower expression levels. Further analysis using Cox proportional hazards regression identified high lncRNA KAZALD1⁃1 expression as an independent risk factor for poor prognosis in HCC patients. Subgroup analysis results indicated that high lncRNA KAZALD1‑1 expression was associated with reduced OS in HCC patients aged ≥54 years, those without cirrhosis, AFP≤400 ng/mL those presenting with solitary tumors, intact tumor capsules, absence of satellite nodules, and those classified as Edmondson stage Ⅰ-Ⅱ (all P<0.05). In vitro experiments demonstrated that knockdown of lncRNA KAZALD1⁃1 inhibited proliferation, migration, and invasion in Huh7 and HCCLM3 cells, while delaying cell cycle progression and promoting cell apoptosis (all P<0.05). Conversely, overexpression of lncRNA KAZALD1⁃1 enhanced proliferation, migration, and invasion in Huh7 and SNU449 cells, accelerated cell cycle progression and suppressed cell apoptosis (all P<0.05). The constructed ceRNA network indicated that hsa⁃miR⁃21028 and SC65 may serve as potential regulatory targets for lncRNA KAZALD1⁃1 in HCC progression. Conclusions LncRNA KAZALD1⁃1 is significantly overexpressed in HCC tissues and is associated with reduced OS rates in affected patients. It may promote HCC proliferation, invasion, and migration through the lncRNA KAZALD1⁃1/hsa⁃miR⁃21028/SC65 axis, accelerate cell cycle progression, and suppress cell apoptosis. Related Articles | Metrics

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Mechanism and clinical implications of FKBP10 drives bladder cancer progression through the extracellular matrix remodeling Qin Zezu, Liu Tao, Zheng Youwen, Song Wuyue, Cao Xuancheng, Tang Zhong, Wang Qiuyan, Feng Chao, Li Tianyu 2026, 18 (1):  87-97.  doi: 10.3969/j.issn.1674-5671.2026.01.11 Abstract ( 12 )   PDF (4251KB) ( 3 )   Save Objective Bladder cancer is a heterogeneous malignancy with highly metastasis and recurrence rates. Within the tumor microenvironment (TME), cancer⁃associated fibroblasts (CAFs) and extracellular matrix (ECM) remodeling critically influence tumor progression and therapeutic resistance. FK506⁃binding protein 10 (FKBP10) is a molecular chaperone involved in collagen folding and ECM homeostasis, has been implicated in various malignancies. However, its specific role and regulatory mechanisms within the bladder cancer TME remain insufficiently defined. This study aims to investigate the expression profile of FKBP10 in bladder cancer and to systematically elucidate its clinical significance and potential mechanisms in modulating the stromal niche to promote tumor malignancy. Methods Tumor tissue samples were collected from 92 bladder cancer patients who underwent radical cystectomy at The First Affiliated Hospital of Guangxi Medical University between January 2018 and February 2023. Patients were stratified into FKBP10 high⁃ and low⁃expression groups based on FKBP10 transcriptome levels to compare their prognosis and clinical characteristics. Based on Bulk RNA sequencing data, the intergroup heterogeneity were analyzed through differential gene analysis, Gene Set Enrichment Analysis (GSEA), and the xCell algorithm. Differentially upregulated genes in the FKBP10⁃high expression group were extracted and subjected to transcription factor prediction using ChEA3, which integrates ChIP⁃seq data from public repositories such as ENCODE and ReMap, along with RNA⁃seq co⁃expression datasets. Furthermore, the study applied the CellChat algorithm to decipher intercellular communication between FKBP10⁃positive cell subsets and other cell populations. Results In compared to the low⁃expression group (n=69), the high FKBP10 expression group (n=23) exhibited significantly shorter overall survival, along with higher T stage (all P<0.05). In patients with high FKBP10 expression, pathways associated with malignant tumor progression such as extracellular matrix (ECM) remodeling, epithelial⁃mesenchymal transition (EMT), and angiogenesis were significantly activated. PRRX1 and PRRX2 were identified as potential transcription factors regulating these processes. Analysis of the immune microenvironment revealed that the high⁃expression group indicated enrichment of M2 macrophages and elevated expression of immune checkpoint molecules. Single⁃cell RNA sequencing (scRNA⁃seq) analysis revealed that FKBP10 was predominantly expressed in CAFs. Ligand⁃receptor interaction analysis suggested that FKBP10+ CAFs may interact with endothelial cells through the VEGFB/PGF⁃VEGFR1 signaling axis. Conclusions FKBP10 acts as a driver of bladder cancer progression. High FKBP10 expression in bladder cancer is characterized by ECM remodeling and heightened angiogenic activity, which correlates with a poor clinical prognosis. The tumor⁃promoting mechanism likely involves FKBP10+ CAFs facilitating angiogenesis through ECM remodeling and activation of the VEGFB/PGF⁃VEGFR1 signaling axis. Related Articles | Metrics

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CMTM6 regulates epithelial-mesenchymal transition and malignant progression of  liver cancer by repressing CXCL8 Hu Yansong, Xu Li, Chen Yuhua, Tang Ye, Cui Huanyu, Tan Shengkui, Zhu Xiaonian 2026, 18 (1):  98-105.  doi: 10.3969/j.issn.1674-5671.2026.01.12 Abstract ( 7 )   PDF (1456KB) ( 0 )   Save Objective To investigate the regulatory effect of C⁃X⁃C motif chemokine ligand 8 (CXCL8) on the malignant biological behaviors of liver cancer cells, and to elucidate the underlying molecular mechanisms mediated by CKLF⁃like MARVEL transmembrane domain⁃containing protein 6 (CMTM6). The findings are expected to provide potential therapeutic targets and a theoretical foundation for the development of targeted therapy in liver cancer. Methods The expression levels of CXCL8 in the liver cancer cell lines HepG2, MHCC97H, Hep3B, and Huh7 were detected by real⁃time quantitative polymerase chain reaction (qPCR), and Hep3B cells which exhibited moderate expression levels, were selected for subsequent investigation. To establish Hep3B cell models, lentiviral and plasmid transfection were used to generate CXCL8 knockdown (CXCL8KD), CXCL8 overexpression (CXCL8OE), CMTM6 knockdown (CMTM6KD), and CMTM6KD combined with CXCL8OE cell lines. qPCR was performed to measure mRNA expression levels of CXCL8, CMTM6, and markers of epithelial⁃mesenchymal transition (EMT) , including E⁃cadherin, β⁃catenin, N⁃cadherin, and Vimentin. CCK⁃8, wound healing, and Transwell assays were used to detected the cell proliferation, migration, and invasion, respectively. Results CXCL8 knockdown significantly inhibited the proliferation, migration, and invasion of Hep3B cells (all P<0.01), which was associated with an upregulation of E⁃cadherin and β⁃catenin expression (all P<0.05), and a downregulation of N⁃cadherin and Vimentin expression (all P<0.01), whereas CXCL8 overexpression showed opposite effects (all P<0.05). CMTM6 overexpression significantly downregulated CXCL8 mRNA expression (P<0.001), while CMTM6 knockdown significantly upregulated CXCL8 mRNA expression (P<0.001). CMTM6 knockdown significantly inhibited Hep3B cell proliferation, migration, and invasion (all P<0.001), upregulated E⁃cadherin and β⁃catenin (all P<0.05), and downregulated N⁃cadherin and Vimentin (all P<0.05). Notably, simultaneous CXCL8 overexpression partially reversed these effects (all P<0.05). Conclusions CXCL8 has been identified as a downstream target gene of CMTM6 in liver cancer. CXCL8 may promote the proliferation, migration, and invasion of liver cancer cells by inducing EMT, and this mechanism may be associated with the negative regulation of CXCL8 expression by CMTM6 at the transcriptional level.This suggests that targeting the regulatory network involving CMTM6 and CXCL8 may offer a novel therapeutic strategy for the treatment of liver cancer. Related Articles | Metrics

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Advances in optimizing frontline therapy for mantle cell lymphoma Su Shuai, Xiao Yi 2026, 18 (1):  106-114.  doi: 10.3969/j.issn.1674-5671.2026.01.13 Abstract ( 9 )   PDF (568KB) ( 6 )   Save Mantle cell lymphoma is a clinically and biologically heterogeneous disease that necessitates individualized frontline treatment to balance efficacy and tolerability. Currently, intensified cytarabine⁃containing immunochemotherapy followed by consolidation with autologous hematopoietic stem cell transplantation remains a standard approach for achieving durable remission in transplant⁃eligible patients. In patients who are ineligible for transplantation, bendamustine combined with rituximab has emerged as a commonly used frontline regimen. In recent years, novel agents including Bruton tyrosine kinase inhibitors, BCL⁃2 inhibitors, and immunomodulatory agents have increasingly been integrated with existing standard strategies and shown promising therapeutic potential. This article systematically reviews recent advances in optimizing frontline treatment strategies for newly diagnosed patients with MCL and discusses current challenges and future directions. Related Articles | Metrics

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Research advances in risk prediction models for venous thromboembolism following colorectal cancer surgery Liu Dan, Zhou Bin, Shi Yunjie, Qian Yiyi 2026, 18 (1):  115-121.  doi: 10.3969/j.issn.1674?5671.2026.01.14 Abstract ( 4 )   PDF (531KB) ( 0 )   Save Venous thromboembolism (VTE) constitutes a severe postoperative complication of colorectal cancer (CRC), significantly increases patient mortality and healthcare burden. In China, the incidence of post⁃CRC VTE reaches 11.2% within one month, while adherence to guideline⁃compliant prophylaxis rates remains low at 10.3%. This highlights the critical need for precise risk assessment tools. While widely utilized generic models such as Caprini may lack CRC specificity, and the Khorana score shows moderate discrimination (C⁃statistic 0.7), emerging CRC⁃specific models (e.g., CRC⁃VTE score, AUC 0.72) and machine learning approaches (e.g., XGBoost, AUC up to 0.908) demonstrate better performance. Nonetheless, the majority of these models are derived from single⁃center retrospective data, which limits their generalizability. Consequently, there is a pressing necessity to develop and validate the dynamic population⁃tailored prediction models to optimize perioperative VTE prevention and reduce related morbidity and mortality. This review systematically examines the risk factors associated with VTE formation following CRC surgery, synthesizes research progress and clinical applications of predictive models, aims to provide evidence⁃based support for optimizing perioperative VTE prevention and treatment strategies in CRC. Related Articles | Metrics

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Mechanisms and clinical application potential of solute carrier transporters in colorectal cancer Han Ling, Tong Ling 2026, 18 (1):  122-128.  doi: 10.3969/j.issn.1674-5671.2026.01.15 Abstract ( 12 )   PDF (671KB) ( 2 )   Save The solute carrier (SLC) transporter family constitutes a vital transmembrane protein system for maintaining cellular metabolic homeostasis. It is extensively involved in the transmembrane transport of diverse substances, including amino acids, glucose, lipids, metal ions and vitamins. In recent years, numerous studies have demonstrated that multiple SLC family members are aberrantly expressed in colorectal cancer (CRC). These aberrantly expressed SLC transporters drive the malignant progression of tumors through multiple mechanisms, such as mediating tumor metabolic reprogramming, promoting tumor invasion and metastasis, regulating the tumor immune microenvironment, and participating in therapeutic resistance. This article systematically reviews the molecular mechanisms underlying the involvement of SLC transporters in the initiation and progression of CRC, with a focus on summarizing their roles in metabolic regulation, immune evasion and therapeutic response of CRC. It further explores their clinical application value as diagnostic and prognostic biomarkers as well as potential therapeutic targets, aiming to provide a theoretical basis for the precision diagnosis and treatment of colorectal cancer. Related Articles | Metrics

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Research progress on the mechanism of microglial polarization in radiation-induced cognitive impairment Zhang Qingqing, Li Ling 2026, 18 (1):  129-134.  doi: 10.3969/j.issn.1674-5671.2026.01.16 Abstract ( 11 )   PDF (632KB) ( 3 )   Save Radiotherapy serves as a primary therapeutic approach for head and neck tumors. However, it subsequently develops radiation⁃induced brain injury and radiation⁃induced cognitive impairment (RICI). RICI is characterized by progressive deficits in  memory, attention, and executive function, yet the underlying mechanisms remain inadequately understood. As the innate immune effector cells of the central nervous system (CNS), the dynamic polarization of microglia is a critical role in the pathological processes of RICI. Accumulating evidence suggests that dysregulation of microglial polarization significantly contributes to the etiology of RICI. Beyond direct neuronal damage, ionizing radiation disrupts immune homeostasis, thereby amplifying secondary injury. During the acute phase of radiotherapy, damaged cells release injury⁃related molecular patterns such as HMGB1, which activate the TLR4/NF⁃κB signaling pathway and the NLRP3 inflammasome. This activation prompts microglia to rapidly polarize into the M1 phenotype (pro⁃inflammatory/damage type), subsequently releasing inflammatory mediators such as IL⁃1β and TNF⁃α. As the disease progresses to the chronic stage, the transformation of microglia from M1 to M2 phenotype (anti⁃inflammatory/repair type) is blocked, leading to persistent chronic neuroinflammation, which in turn compromises hippocampal neurogenesis and synaptic plasticity, ultimately resulting in cognitive dysfunction. This review summarizes the spatiotemporal characteristics of microglial polarization in RICI and elucidates the associated molecular regulatory mechanisms, aims to provide a theoretical basis for the prevention and treatment of radiation⁃induced cognitive impairment.  Related Articles | Metrics