Portal vein tumor thrombus (PVTT) is a biologically aggressive and clinically heterogeneous form of hepatocellular carcinoma (HCC). Global guidelines generally classify macrovascular invasion as advanced disease and prioritize systemic therapy, whereas selected East Asian practice pathways incorporate hepatic arterial infusion chemotherapy (HAIC), radiotherapy, or resection. This review critically evaluates HAIC combined with an antiangiogenic agent and immune checkpoint inhibitor as a conversion strategy for HCC with PVTT. Randomized trials substantiate the efficacy of HAIC-based treatment in contrast to controls from the days of sorafenib but do not establish the incremental benefit of the contemporary triplet. Across prospective single-arm studies, RECIST 1.1 objective response rates ranged from approximately 36 to 77%, with higher estimates in some studies using mRECIST. Retrospective PVTT-focused comparisons also suggest longer progression-free and overall survival than with dual systemic therapy or HAIC alone, but these figures remain vulnerable to confounding by indication, heterogeneous regimens, inconsistent response criteria, and immortal-time bias related to surgery. Conversion should be defined as a prospectively documented transition from unresectable disease to an R0-resectable state with adequate liver reserve, not as radiological response alone. We propose an explicitly unvalidated multidisciplinary framework for candidate selection, reassessment, and perioperative management. Current evidence supports protocol-based use in clinical trials or experienced centers rather than routine global adoption. Randomized PVTT-stratified trials comparing the triplet to contemporary immunotherapy, with intention-to-treat reporting of resection and pathological response, are required.

Abstract Despite significant progress in immunotherapy for hepatocellular carcinoma (HCC), effective therapeutic targets remain limited, highlighting the urgent need for novel immunotherapeutic strategies. Intercellular communication is fundamental for maintaining homeostasis and responding to external stimuli, and while various modes such as ligand-receptor interactions and extracellular vesicle transfer are known, the potential role of tunneling nanotubes (TNTs) in macrophage-HCC cell communication has been unclear. In this study, using peritoneal macrophages from C57BL/6J mice co-cultured with Hepa1-6 HCC cells in vitro, we observed via field emission scanning electron microscopy and confocal microscopy that macrophages and HCC cells form TNTs—slender, straight, and suspended structures with vesicle-like protrusions indicative of cargo transport, composed of F-actin, α-tubulin, and Sec5. By physically inhibiting TNT formation using 0.4 μm transwell inserts and applying single-cell RNA sequencing, we found that in the TNT system, the HCC cell phenotype did not change significantly, but the proportion of MHC II+ macrophages greatly increased, and OT-II T cell activation assays further demonstrated enhanced antigen presentation ability in macrophages. Using specific markers for proteins, mitochondria, DNA, and RNA (CellTracker Blue, MitoTracker, Hoechst 34580, Click-iT RNA) and corresponding inhibitors (metformin, DNase, RNase), we obtained direct evidence that HCC cell-derived RNAs are transferred via TNTs to macrophages, leading to increased antigen presentation capability. Moreover, blocking macrophage RNA sensors with hydroxychloroquine suppressed the TNT-induced increase in MHC II+ macrophages, and in an orthotopic HCC mouse model, intratumoral injection of hydroxychloroquine-pretreated macrophages resulted in significantly larger tumor diameters by day 7 compared to the untreated group. In summary, our study reveals that macrophages and HCC cells establish a novel form of intercellular communication—TNTs—through which HCC cells transfer RNAs to macrophages, mediating an increase in MHC II+ macrophage proportion and enhanced antigen presentation capacity, thereby suppressing tumor progression. We propose that promoting efficient transfer of HCC-derived RNAs to macrophages by TNTs and enhancing macrophage recognition of these RNAs may provide novel insights and potential therapeutic targets for innovative anti-HCC treatments. Citation Format: Yutao He, Lin Wang, Zhitian Shi. Intercellular transfer of hepatocellular carcinoma-derived RNAs via tunneling nanotubes educates macrophages and enhances antigen presentation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 7397.

Infection with Helicobacter pylori (Hp) is associated with various gastric disorders, and its virulence factor cytotoxin-associated protein A (CagA) drives cytopathological changes, cellular transformation, and tumor progression. N6-methyladenosine (m6A) mRNA modification plays a key role in carcinogenesis, including gastric cancer (GC). However, whether Hp promotes GC malignancy by regulating m6A modification remains poorly understood. The expression levels of CagA and related genes were detected by RT-qPCR and Western blotting. Functional validation of CagA-mediated malignant phenotypes in GC cells was performed using CCK-8, colony formation, wound healing, and Transwell assays. Global m6A modification levels were evaluated by RNA dot blot analysis. The expression and distribution of METTL3 and other target genes in cells and tissues were assessed by immunofluorescence and immunohistochemistry. Co-immunoprecipitation (Co-IP) and ubiquitination assays were used to examine the interaction between METTL3 and USP7, as well as the ubiquitin-dependent degradation of METTL3. CagA promoted GC cell proliferation, metastasis, and glycolysis both in vitro and in vivo. Omics data analysis, RT-qPCR, and Western blotting results demonstrated that CagA increased METTL3 expression and global m6A levels in GC cells. Mechanistically, CagA enhanced the interaction between USP7 and METTL3, thereby inhibiting METTL3 ubiquitination and proteasomal degradation. CagA upregulates m6A modification of DUSP6 to boost glycolysis and accelerate GC progression.

Ulcerative colitis (UC) is a chronic inflammatory bowel disease closely associated with dysbiosis of the gut microbiome, encompassing not only bacterial communities but also fungal populations. Despite the growing recognition of the gut microbiome’s role in UC pathogenesis, the contribution of intestinal fungi has only recently garnered significant attention. In this review, we comprehensively examine the characteristics of intestinal fungi in both healthy individuals and UC patients, elucidating their role in disease pathogenesis and their interactions with bacterial communities. Additionally, we explore the impact of intestinal fungi on disease severity and therapeutic responses in UC. Furthermore, we evaluate the therapeutic potential of antifungal agents, probiotics, and fecal microbiota transplantation (FMT) in UC management, emphasizing the critical role of fungi in these treatment modalities. Future research should prioritize elucidating the multifunctional roles of fungi in UC pathogenesis and their implications for treatment strategies. Moreover, the identification of fungal biomarkers associated with FMT efficacy could pave the way for precision medicine approaches in FMT, offering novel insights into personalized therapeutic interventions for UC.

INTRODUCTION:Combined hepatocellular cholangiocarcinoma (cHCC-CCA) is a rare hepatic malignancy featuring both hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA) components, often leading to poor prognosis owing to its clinical complexity. CASE PRESENTATION:A middle-aged man presented with sudden abdominal pain and unexplained weight loss, leading to an initial diagnosis of CCA. The patient underwent laparoscopic left hepatectomy and lymph node dissection, and postoperative pathology confirmed cHCC-CCA with lymph node metastasis. Despite initial recovery, the disease recurred at 2 months and progressed to lung metastasis and multi-organ involvement by 7 months. Immuno-combination targeted therapy was ineffective, and the patient succumbed to the disease eight months after surgery. DISCUSSION:This case highlights the diagnostic and therapeutic challenges of cHCC-CCA, including its histological complexity, high recurrence rate, and limited treatment efficacy. Despite surgical resection, early recurrence and rapid progression to pulmonary metastasis were observed, emphasizing the need for improved treatment strategies for this condition. The failure of immune checkpoint inhibitors and targeted therapy suggests the need for alternative or combined therapeutic approaches. CONCLUSION:Future research should focus on integrating molecular profiling into treatment selection, optimizing adjuvant therapies, and exploring novel targeted or immunotherapy combinations to improve the long-term outcomes. This report contributes to the growing evidence on cHCC-CCA and underscores the urgency of developing precise diagnostic tools and personalized treatment strategies.

PurposeIntrahepatic cholangiocarcinoma (ICC) is a common primary hepatic tumors with a 5-year survival rate of less than 20%. Therefore, it is crucial to elucidate the molecular mechanisms of ICC. Recently, the advance of high-throughput chromosome conformation capture (Hi-C) technology help us look insight into the three-dimensional (3D) genome structure variation during tumorigenesis. However, its function in ICC pathogenesis remained unclear.MethodsHi-C and RNA-sequencing were applied to analyze 3D genome structures and gene expression in ICC and adjacent noncancerous hepatic tissue (ANHT). Furthermore, the dysregulated genes due to 3D genome changes were validated via quantitative real-time PCR and immunohistochemistry.ResultsPrimarily, the intrachromosomal interactions of chr1, chr2, chr3, and chr11 and the interchromosomal interactions of chr1-chr10, chr13-chr21, chr16-chr19, and chr19-chr22 were also significantly distinct between ANHT and ICC, which may potentially contribute to the activation of cell migration and invasion via the upregulation of WNT10A, EpCAM, S100A3/A6, and MAPK12. Interestingly, 56 compartment regions from 23 chromosomes underwent A to B or B to A transitions during ICC oncogenesis, which attenuated the complement pathway through the downregulation of C8A/C8B, F7, F10, and F13B. Notably, topologically associated domain (TAD) rearrangements were identified in the region containing HOPX (chr4: 57,514,154-57,522,688) and ACVR1 (chr2:158,592,958-158,732,374) in ICC, which may contribute to the hijacking of remote enhancers that were previously outside the TAD and increased expression of HOPX and ACVR1.ConclusionsThis study reveals relationship between 3D genome structural variations and gene dysregulation during ICC tumorigenesis, indicating the molecular mechanisms and potential biomarkers.

4104 Background: The combination of atezolizumab and bevacizumab is the standard treatment for advanced hepatocellular carcinoma approved in China and many other countries. However, the objective response rate of this combination treatment was around 30%. Consequently, identifying individuals with the potential to respond favorably prior to initiating therapy remains a pressing challenge. Methods: This multi-center retrospective study included advanced hepatocellular carcinoma patients who received atezolizumab plus bevacizumab as first-line therapy between December 2020 and February 2024. The training cohort consisted of eligible patients who have complete baseline, treatment and tumor evaluation records and MRI imaging data from Zhongshan Hospital, while eligible patients from other centers constituted the external validation cohort. A deep learning model based on nnU-Net was developed to automatically segment intrahepatic lesions. All segmentations were reviewed and revised by two radiologists. The radiomic features were extracted using PyRadiomics, then a radiomic feature-based model for predicting response to atezolizumab plus bevacizumab therapy was constructed using the Extreme Gradient Boosting Decision Tree (XGBoost) algorithm. Additionally, three radiologists evaluated 53 visually-assessed MRI features on MRI scans. Finally, the predictive performance of radiomic feature model, as well as the relationship between radiomic and MRI features, was assessed. Results: A total of 240 eligible patients were recruited from 14 centers in China, of which 161 and 79 were classified as training and validation cohorts, respectively. During a median follow-up period of 13.7 months (IQR: 8.3–20.6) in the training cohort and 10.5 months (IQR: 7.4–17.2) in the validation cohort, 19.0% (30/161) and 23.0% (18/79) of patients, respectively, achieved an objective response by RECIST v1.1 (p = 0.559). The radiomic feature model demonstrated a promising predictive performance, achieving an AUC of 0.913 (95% CI: 0.874–0.953) in the training cohort and 0.825 (95% CI: 0.700–0.949) in the validation cohort. Fat surpassing liver mass was the only MRI feature associated with an objective response (p = 0.020). When the MRI feature was combined with radiomic features, the predictive model further improved, yielding an AUC of 0.951 (95% CI: 0.924–0.979) in the training cohort and 0.835 (95% CI: 0.725–0.945) in the validation cohort. A significant correlation was observed between radiomic features and MRI features of intrahepatic lesions with a univariate analysis p < 0.2. Conclusions: Radiomic features derived from pretreatment MRI scans can effectively predict personalized objective responses to combination therapy with atezolizumab and bevacizumab in patients with unresectable or advanced HCC.

AIMS:To assess the viability and safety of radiofrequency ablation (RFA) for intrahepatic tumors in hepatocellular carcinoma (HCC) treatment, as well as percutaneous ethanol injection (PEI) for portal vein tumor thrombus (PVTT). MATERIALS AND METHODS:From January 2010 to December 2020, a total of 25 HCC patients who underwent RFA for intrahepatic tumor combined with PEI for PVTT were enrolled. Treatment response (assessed using modified Response Evaluation Criteria in Solid Tumors [mRECIST] based on contrast-enhanced computed tomography [CECT] or contrast-enhanced ultrasound [CEUS]), overall survival (OS), progression-free survival (PFS), and safety profile were evaluated. Univariate and multivariate analyses were performed to identify the prognostic factors in predicting the OS and PFS. RESULTS:The overall response rate was 88%, including 12 (48%) patients achieving complete response (CR) and 10 (40%) patients achieving partial response (PR). Progressive disease (PD) was observed in 3 (12%) patients. The 1-, 3-, 6-, and 12- month PFS rates were 96%, 56%, 20%, and 4%, respectively. The OS rates at 6, 12, 24, 36, and 48 months were 96%, 52%, 28%, 8%, and 4%, respectively. The overall response was the only risk factor for the PFS in the univariate analysis (p=0.026), but not in the multivariate analysis (p=0.288). There was no independent prognostic factor of OS. No ablation-related mortality was observed. Major complication of liver abscess was observed in only 1 (4%) patient. CONCLUSIONS:RFA combined with PEI is a feasible treatment for HCC patients with PVTT, which might reduce the tumor burden and create conditions for further adjuvant therapy.

Pulmonary embolism (PE) is a significant cause of death in cancer patients. Although there are many reports on the clinical features and In-hospital prognosis for PE, but few studies on malignant tumors combined with pulmonary embolism. Early identification of high-risk populations, enhanced monitoring, and targeted therapeutic measures are crucial for improving patient prognosis. We conducted this study to identify reliable prognostic indicators through the analysis of real-world data. A total of 471 patients of malignant tumors complicated with PE were divided into two groups: (1) PE with poor prognosis group (n = 146). (2) PE without poor prognosis group (n = 325). Clinical characteristics, laboratory parameters and adverse prognostic events were recorded and analyzed. High diastolic blood pressure (Odds Ratio [OR] = 1.819, 95

The application of artificial intelligence (AI) technology in the medical field, particularly in surgical operations, has evolved from science fiction to a crucial tool. With continuous advancements in computational power and algorithmic technology, AI is reshaping the surgical medicine landscape. From preoperative diagnosis and planning to intraoperative real-time navigation and assistance and postoperative rehabilitation and follow-up management, AI technology has significantly enhanced the precision and safety of surgical procedures. This paper systematically reviews the development and current applications of AI in surgery, focusing on specific case studies of AI in surgical procedures, diagnostic assistance, intraoperative navigation, and postoperative management, highlighting its significant contributions to improving surgical precision and safety. Despite the obvious advantages of AI in improving surgical success, reducing postoperative complications, and accelerating patient recovery, its use in surgery still faces numerous challenges, including its cost-effectiveness, dependency, data privacy and security, clinical integration, and physician training. This review summarizes the current applications of AI in surgical medicine, highlights its benefits and limitations, and discusses the challenges and future directions of integrating AI into surgical practice.

T cells are involved in every stage of tumor development and significantly influence the tumor microenvironment (TME). Our objective was to assess T-cell marker gene expression profiles, develop a predictive risk model for human papilloma virus (HPV)-negative oral squamous cell carcinoma (OSCC) utilizing these genes, and examine the correlation between the risk score and the immunotherapy response. We acquired scRNA-seq data for HPV-negative OSCC from the GEO datasets. We performed cell‒cell communication, trajectory, and pathway enrichment analyses of T-cell-associated genes. In addition, we constructed and validated a T-cell-associated gene prognostic model for HPV-negative OSCC patients using TCGA and GEO data and assessed the immune infiltration status of HPV-negative OSCC patients .qRT-PCR was used to detect the expression level of prognosis-related genes in different risk groups. ScRNA-seq was conducted on 28,000 cells derived from 14 HPV-negative OSCC samples and 6 normal samples. We identified 4,635 T cells from these cells and identified 774 differentially expressed genes(DEGs) associated with T cells across five distinct T-cell subtypes. Through the integration of bulk-RNAseq data, we established a prognostic model based on DEGs related to T cells. By separating patients into high-risk and low-risk groups according to these prognostic related genes, we can accurately predict their survival rates and the immune infiltration status of the TME.qRT-PCR results showed that compared with the patients of low risk group, the expression of PMEPA1, SH2D2A, SMS and PRDX4 were significantly up-regulated in high risk group. This study provides a resource for understanding the heterogeneity of T cells in HPV-negative OSCC patients and associated prognostic risk models. It provides new insights for predicting survival and level of immune infiltration in patients with HPV-negative OSCC.

Dehydrocostus lactone (Dehy) is the main component of Saussurea lappa and has been shown to have anti-inflammatory and anti-cancer properties. This study aimed to explore the specific mechanism of action of Dehy in liver cancer. Dehy can effectively promote liver cancer cell apoptosis, and inhibit proliferation, invasion and migration, in a dose-dependent manner, using CCK-8 assay, flow cytometry, transwell invasion and wound healing assays. Identification of 2202 and 5549 differential expression genes with transcriptome sequencing analysis, respectively, at the gene expression level and transcript level, and discovered that they are related to ferroptosis. Then, discovered that only HMOX1 is the ferroptosis-related key gene using network pharmacology analysis. Dehy promoted liver cancer cell ferroptosis by up-regulating HMOX1. Moreover, HMOX1 negative regulation targets the gene CDK1. Dehy decreased the expression of CDK1 by up-regulating the expression of HMOX1, which promoted liver cancer cell ferroptosis. Subsequently, Dehy played an anti-tumor role and promoted the ferroptosis effect in vivo xenograft mouse models. Collectively, our findings demonstrate that Dehy can effectively promote liver cell ferroptosis in vitro and in vivo. Dehy exerts an anti-cancer function in liver cancer by regulating the HMOX1/CDK1 axis.

Background: Trigeminal neuralgia (TN) is a severe facial pain disorder with complex etiology. Inflammation has been suggested as a contributing factor to TN pathogenesis. This study investigates the causal relationship between inflammatory biomarkers, including 41 circulating inflammatory cytokines, C-reactive protein (CRP), and procalcitonin (PCT), and TN using Mendelian randomization (MR) analysis. Methods: A two-sample MR approach was employed using genome-wide association study (GWAS) data from 8293 Finnish individuals for inflammatory cytokines and data from the FinnGen database for TN. Instrumental variables (IVs) were selected based on genome-wide significance and clumping thresholds to avoid linkage disequilibrium. Inverse variance weighting (IVW) was used as the primary method, complemented by MR Egger regression, weighted median, simple mode, and weighted mode methods. Additionally, Bayesian Weighted MR (BWMR) and Multivariable MR (MVMR) were utilized to validate the findings and explore potential confounders. Results: The present MR analysis identified significant causal associations for three inflammatory cytokines with TN. Stem cell growth factor beta (SCGF-β) (OR = 1.362, 95% CI = 1.049–1.770, p = 0.021) and Interleukin-4 (IL-4) (OR = 1.533, 95% CI = 1.014–2.316, p = 0.043) were positively associated with TN, while Interleukin-16 (IL-16) (OR = 0.720, 95% CI = 0.563–0.921, p = 0.009) had a protective effect. CRP levels were also linked to TN risk (OR = 0.751, 95% CI = 0.593–0.951, p = 0.017). No significant causal effect of PCT on TN was observed. Sensitivity analyses confirmed the robustness of these findings, showing no evidence of horizontal pleiotropy or heterogeneity. Conclusion: This study highlights specific inflammatory biomarkers that may play pivotal roles in TN pathogenesis. SCGF-β and IL-4 are potential therapeutic targets due to their facilitative effects on TN, while IL-16 could offer protective benefits. CRP's association with TN further supports the involvement of systemic inflammation in this condition. These findings provide novel insights into TN's inflammatory mechanisms, suggesting new avenues for targeted interventions.

Cellular senescence, an emerging hallmark of cancer, has garnered increasing attention in recent years. However, its role in hepatocellular carcinoma (HCC) is still not well understood. Furthermore, there is a lack of comprehensive biomarkers to predict prognosis and assess senescence and immune characteristics in HCC patients. To address these gaps, we conducted functional studies on bleomycin-induced senescent Hepa1-6 cells and developed the Cellular Senescence Score (CSS) based on four core cellular senescence-related genes. We found that the cellular senescence signaling pathway was enriched among the risk genes associated with unfavorable prognosis in HCC patients. The senescence associated secretory phenotype (SASP) derived from senescent Hepa1-6 cells induced an increase in CD3+ CD8+ CD279+ T cells. The senescent Huh7 cells expressed higher levels of pro-angiogenic genes compared to their immortal counterparts. The CSS was constructed on the basis of BMI1, EZH2, NPM1, and ME1. HCC Patients in the high-CSS group had significantly shorter overall survival compared to those in the low-CSS group. In contrast to the low-CSS group, the high-CSS group exhibited more senescence characteristics at both the overall tumor microenvironment and single-cell levels. Three distinct senescence patterns were identified in hepatoma cells: oxidative stress related senescence, metabolism related senescence, and immune related senescence. The high-CSS group showed elevated TP53 mutation rate, diminished immune cell infiltration, and enhanced expression levels of immune checkpoint molecules compared to the low-CSS group. Moreover, the high-CSS group displayed a greater proportion of patients responsive to immune checkpoint therapy compared to the low-CSS group. In summary, the impacts of cellular senescence on HCC are multifaceted, and the tumor-promoting effects may be caused by SASP remodeling the HCC microenvironment rather than by the senescent hepatoma cells themselves. The CSS is a promising biomarker capable of predicting prognosis and assessing senescence and immune characteristics in HCC.

CD27 as a marker of memory B cells is belong to the tumor necrosis factor receptor (TNFR) superfamily, CD27 is ligated by CD70, they can co-stimulate T-cell growth and differentiation through their interaction. Uncertainty surrounds CD27's function in esophageal cancer (EC). This study investigated the role of CD27 in the prognosis of EC using the TCGA, cbioportal, linkedomics and GEPIA databases as well as the proliferation assay was applied. CD27 differential expression may be a key factor in the development of EC. different level of CD27 expression in EC has profound impacts on TOR complex, and many kinds of kinase (KIT proto-oncogene receptor tyrosine kinase, transforming growth factor beta receptor 1, and G protein-coupled receptor kinase 3.), as well as the cell membrane, and survival analysis revealed that it had a significant impact on both the overall survival and disease-free survival of EC. CD27 overexpression will suppress the viability of the KYSE150 and TE3 cells. Our findings suggested that the degree of CD27 expression could serve as an esophageal cancer prognosis biomarker.

Background. The mRNA vaccine has become a promising platform for cancer therapy. Lots of studies have been focusing on discovering novel potent cancer-associated antigens to develop mRNA vaccines against cancers. Besides, immunotyping shows the immune status, and immune microenvironment of immunotyping is related with therapeutic reaction. However, potential antigens for mRNA vaccines and immunotyping of liver hepatocellular carcinoma (LIHC) remain far from being understood. Methods. In this study, we collected gene expression data and clinical information data from ICGC and TCGA databases. Using GEPIA2, we calculated differential expression genes and prognostic indices. We applied TIMER to calculate the correlation coefficient between immune infiltrating cells and each gene. Consensus cluster was used for immunotyping of LIHC. Results. We uncovered four most potential candidates including PES1, MCM3, PPM1G, and KPNA2, which were all related with antigen-presenting cell (APC) infiltration and poor survival in LIHC in two independent datasets. Furthermore, three immune-related subtypes (IS1-IS3) of LIHC were identified. All these results were validated in two independent datasets. Furthermore, we validated our results in vitro. Conclusions. The above candidates will be expected to be potential antigen genes for developing anti-LIHC mRNA vaccine, and furthermore, patients with IS2 and IS3 tumors are supposed to be appropriate for mRNA vaccine in LIHC.

To explore the RNA biomolecular marker associated with hepatocellular carcinoma (HCC) prognosis, we constructed a regulatory network of competitive endogenous RNAs (ceRNAs), which provides favorable conditions for the early diagnosis, prognostic monitoring, and personalized treatment of HCC. In this study, the differentially expressed genes (DEGs) of patients with HCC were obtained from the Gene Expression Omnibus. We identified 574 upregulated genes and 274 downregulated genes relevant to HCC occurrence (p < 0.05). Subsequently, we constructed the protein–protein interaction (PPI) network using these DEGs and identified the hub genes from the PPI. We then determined the expression and prognostic values of the hub genes from the GEPIA and Kaplan–Meier plotter databases. After the upstream microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) were respectively identified by miRTarBase and miRNet, we validated the expression of the key miRNAs in the serum using qPCR experiments. Moreover, we identified a two-lncRNA (LINC01184 and ADORA2A-AS1) signature from the upstream lncRNA that effectively predicted overall survival and had promotive effects for HCC. To verify the clinical significance of the signature, we validated the expression of the lncRNA in HCC tissues. Finally, we discovered and identified four mRNAs, four miRNAs, and five lncRNAs associated with the prognosis of HCC and constructed a new ceRNA regulatory network, which will be beneficial for the accurate diagnosis and treatment of HCC.

由于肝细胞癌的发生与发展机理复杂,目前还未充分揭示.作为人体基因组中规模最大的转录因子家族,锌指蛋白现已证实在包括肝癌在内的许多癌症中起到了关键性作用,现将对探讨锌指蛋白的构成、类型,以及在肝细胞癌中的作用机制方面进行综述.

BACKGROUND:Lung cancer is a leading cause of death worldwide, and its incidence shows an upward trend. A study of the long-term changes in the premature death rate in lung cancer in a developed region of China has great exploratory significance to further clarify the effectiveness of intervention measures.OBJECTIVE:This study examined long-term changes in premature lung cancer death rates in order to understand the changes in mortality and to design future prevention plans in Pudong New Area (PNA), Shanghai, China.METHODS:Cancer death data were collected from the Mortality Registration System of PNA. We analyzed the crude mortality rate (CMR), age-standardized mortality rate by Segi's world standard population (ASMRW), and years of life lost (YLL) of patients with lung cancer from 1973 to 2019. Temporal trends in the CMR, ASMRW, and YLL rate were calculated by joinpoint regression expressed as an average annual percentage change (AAPC) with the corresponding 95% CI.RESULTS:All registered permanent residents in PNA (80,543,137 person-years) from 1973 to 2019 were enrolled in this study. There were 42,229 deaths from lung cancer. The CMR and ASMRW were 52.43/105 and 27.79/105 person-years, respectively. The YLL due to premature death from lung cancer was 481779.14 years, and the YLL rate was 598.16/105 person-years. The CMR and YLL rate showed significantly increasing trends in men, women, and the total population (P<.001). The CMR of the total population increased by 2.86% (95% CI 2.66-3.07, P<.001) per year during the study period. The YLL rate increased with an AAPC of 2.21% (95% CI 1.92-2.51, P<.001) per year. The contribution rates of increased CMR values caused by demographic factors were more evident than those caused by nondemographic factors.CONCLUSIONS:Lung cancer deaths showed an increasing trend in PNA from 1973 to 2019. Demographic factors, such as the aging population, contributed more to an increased CMR. Our research can help us understand the changes in lung cancer mortality and can be used for similar cities in designing future prevention plans.

Background The need for intraoperative endoscopic nasobiliary drainage during laparoscopic cholecystectomy and laparoscopic common bile duct exploration with primary closure is controversial in the treatment of cholecystolithiasis combined with choledocholithiasis. The aim of this study was to evaluate the safety and efficacy of laparoscopic cholecystectomy + laparoscopic common bile duct exploration + intraoperative endoscopic nasobiliary drainage + primary closure (LC + LCBDE + IO-ENBD + PC). The safety of different intubation methods in IO-ENBD was also evaluated. Method From January 2018 to January 2022, 168 consecutive patients with cholecystolithiasis combined with choledocholithiasis underwent surgical treatment in our institution. Patients were divided into two groups: group A ( n = 96) underwent LC + LCBDE + IO-ENBD + PC and group B ( n = 72) underwent LC + LCBDE + PC. Patient characteristics, perioperative indicators, complications, stone residual, and recurrence rates were analyzed. Group A was divided into two subgroups. In group A 1 , the nasobiliary drainage tube was placed in an anterograde way, and in group A 2 , nasobiliary drainage tube was placed in an anterograde–retrograde way. Perioperative indicators and complications were analyzed between subgroups. Results No mortality in the two groups. The operation success rates in groups A and B were 97.9% (94/96) and 100% (72/72), respectively. In group A, two patients were converted to T-tube drainage. The stone clearance rates of group A and group B were 100% (96/96) and 98.6% (71/72), respectively. Common bile duct diameter was smaller in group A [10 vs. 12 mm, P < 0.001] in baseline data. In perioperative indicators, group A had a longer operation time [165 vs.135 min, P < 0.001], but group A had a shorter hospitalization time [10 vs.13 days, P = 0.002]. The overall complications were 7.3% (7/96) in group A and 12.5% (9/72) in group B. Postoperative bile leakage was less in group A [0% (0/96) vs. 5.6% (4/72), P = 0.032)]. There were no residual and recurrent stones in group A. And there were one residual stone and one recurrent stone in group B (all 1.4%). The median follow-up time was 12 months in group A and 6 months in group B. During the follow-up period, 2 (2.8%) patients in group B had a mild biliary stricture. At subgroup analysis, group A 1 had shorter operation time [150 vs. 182.5 min, P < 0.001], shorter hospitalization time [9 vs. 10 days, P = 0.002], and fewer patients with postoperative elevated pancreatic enzymes [32.6% (15/46) vs. 68% (34/50), P = 0.001]. Conclusion LC + LCBDE + IO-ENBD + PC is safer and more effective than LC + LCBDE + PC because it reduces hospitalization time and avoids postoperative bile leakage. In the IO-ENBD procedure, the antegrade placement of the nasobiliary drainage tube is more feasible and effective because it reduces the operation time and hospitalization time, and also reduces injury to the duodenal papilla.