Digestive System Tumors Research Articles

Pseudostellaria heterophylla (Miq.) Pax, a traditional folk medicine, ameliorates colorectal cancer by remodeling the tumor immune microenvironment.

Pseudostellaria heterophylla (Miq.) Pax (PH) is a traditional folk medicine, which is widely used clinically for digestive system tumors such as esophageal, gastric, colorectal, and liver cancers. The anti-tumor effect and mechanism of PH in colorectal cancer (CRC) deserves further study. The objective of this study is to examine the effects and the underlying mechanisms of aqueous extract of Pseudostellaria heterophylla (Miq.) Pax (AEPH) in the CRC. The components of AEPH were fully resolved using ultra-high-performance liquid chromatography coupled with quadrupole-orbitrap high-resolution mass spectrometry (UHPLC-Q/Orbitrap HRMS). The effect of AEPH was evaluated in vivo using the MC38 mouse colon cancer model, and its impact on the tumor microenvironment was analyzed by flow cytometry. Bioinformatics analysis, combined with transcriptome sequencing, was utilized to further investigate the signaling pathways of AEPH in CRC cells. A mass spectrometry analysis identified 371 compounds in AEPH, each with a comprehensive score exceeding 60. In vivo experiments demonstrated that AEPH suppressed the growth of MC38 tumors without exhibiting obvious toxicity. Mechanistic studies revealed that AEPH inhibited the JNK signaling pathway, reduced Chemokine C-C Motif Chemokine Ligand 5 (CCL5) secreted by CRC cells, hindered the recruitment of M2-like tumor-associated macrophages (TAMs), promoted the infiltration of IFN-γ+ CD8+ T cells, and improved the immunosuppressive microenvironment of CRC. AEPH contributes to the remodeling of the tumor immune microenvironment primarily through the inhibition of CCL5-mediated recruitment of M2-like TAMs. The findings of this study offer a novel perspective on the potential development of AEPH as a therapeutic agent for CRC.

Role of the m6A demethylase ALKBH5 in gastrointestinal tract cancer (Review).

N6‑methyladenosine (m6A) is one of the most universal, abundant and conserved types of internal post‑transcriptional modifications in eukaryotic RNA, and is involved in nuclear RNA export, RNA splicing, mRNA stability, gene expression, microRNA biogenesis and long non‑coding RNA metabolism. AlkB homologue 5 (ALKBH5) acts as a m6A demethylase to regulate a wide variety of biological processes closely associated with tumour progression, tumour metastasis, tumour immunity and tumour drug resistance. ALKBH5 serves a crucial role in human digestive system tumours, mainly through post‑transcriptional regulation of m6A modification. The present review discusses progress in the study of the m6A demethylase ALKBH5 in gastrointestinal tract cancer, summarizes the potential molecular mechanisms of ALKBH5 dysregulation in gastrointestinal tract cancer, and discusses the significance of ALKBH5‑targeted therapy, which may provide novel ideas for future clinical prognosis prediction, biomarker identification and precise treatment.

Exploration of the research hotspot and application rule of Tengligen in anti-digestive system tumor based on bibliometric analysis and data mining

Objective: Based on the systematic bibliometric and data mining of the literature on the anti-digestive system tumor of Tengligen, the state of research, research hotspots and medication rules in this field were explored. Methods: From January 2004 to October 2024, literature pertaining to Tengligen’s anti-digestive system tumor was obtained from the CNKI, Wanfang, and VIP databases. CiteSpace 6.3.R1 and VOSviewer 1.6.20 software were used to intuitively display the number of publications, authors, institutions, keywords and other information, and then analyzed. The medical record information of famous Chinese medicine treating digestive system tumors with prescriptions containing Tengligen was extracted, a database was established, and the association rule analysis and cluster analysis of Chinese medicine compatible with Tengligen were carried out by IBM SPSS Modeler18.0, SPSS Statistics 26.0 and other software. Results: There were 115 publications in all, and there was a growing tendency in the quantity of papers published in this area. There were 295 authors total, with 28 serving as key authors. The primary publishing institutions are Zhejiang Chinese Medicine University, the First Clinical School of Zhejiang Chinese Medicine University, and Nanjing University of Chinese Medicine. Seven core tags were obtained by keyword cluster analysis, and research focuses on the mechanism of action, extract of Tengligen, clinical efficacy, etc. A total of 41 prescriptions containing Tengligen were included, involving 125 Chinese medicines, among which Tengligen was the most associated with Fuling, Huangqi and Yiyiren, respectively. Cluster analysis showed that Tengligen, Ezhu, Yiyiren and Huangqi were the core prescriptions. Conclusion: The scientific knowledge graph directly shows the research progress and hot trends of Tengligen against digestive system tumors, analyzes the rule of its clinical application, and provides a cutting-edge perspective for new research.

Glutamine, Serine and Glycine at Increasing Concentrations Regulate Cisplatin Sensitivity in Gastric Cancer by Posttranslational Modifications of KDM4A.

Gastric cancer is a common digestive system tumor with a high resistance rate that reduces the sensitivity to chemotherapy. Nutrition therapy is an important adjuvant approach to favor the prognosis of gastric cancer. Dietary amino acids contribute greatly to gastric cancer progression by mediating tumor gene expressions, epigenetics, signal transduction, and metabolic remodeling. In the present study, 20 types of amino acids were screened and glutamine, glycine and serine were identified as the critical regulators of cisplatin (DDP) sensitivity in gastric cancer cells. Moreover, KDM4A acetylation drove the reduced chemotherapy sensitivity in gastric cancer cells by maintaining protein stability and activating DNA repair ability when the concentrations of glutamine (Gln), serine (Ser), and glycine (Gly) decreased. Conversely, Gln/Ser/Gly at increasing concentrations stimulated ubiquitination degradation of KDM4A, which in turn elevated the sensitivity of gastric cancer cells to chemotherapy. Our findings unveiled the role of amino acid nutrition in regulating chemotherapy sensitivity of gastric cancer and the underlying mechanism, thus providing a scientific basis for expanding the clinical significance of nutrition therapy for gastric cancer patients.

Mast cells: key players in digestive system tumors and their interactions with immune cells.

Mast cells (MCs) are critical components of both innate and adaptive immune processes. They play a significant role in protecting human health and in the pathophysiology of various illnesses, including allergies, cardiovascular diseases and autoimmune diseases. Recent studies in tumor-related research have demonstrated that mast cells exert a substantial influence on tumor cell behavior and the tumor microenvironment, exhibiting both pro- and anti-tumor effects. Specifically, mast cells not only secrete mediators related to pro-tumor function such as trypsin-like enzymes, chymotrypsin, vascular endothelial cell growth factor and histamine, but also mediators related to anti-tumor progression such as cystatin C and IL-17F. This dual role of mast cells renders them an under-recognized but very promising target for tumor immunotherapy. Digestive system tumors, characterized by high morbidity and associated mortality rates globally, are increasingly recognized as a significant healthcare burden. This paper examines the influence of mast cell-derived mediators on the development of tumors in the digestive system. It also explores the prognostic significance of mast cells in patients with various gastrointestinal cancers at different stages of the disease. Additionally, the article investigates the interactions between mast cells and immune cells, as well as the potential relationships among intratumoral bacteria, immune cells, and mast cell within digestive system microenvironment. The aim is to propose new strategies for the immunotherapy of digestive system tumors by targeting mast cells.

18F-FAPI-42 PET/CT and 18F-FDG PET/CT in Patients with Malignant Digestive System Neoplasms: A Head-to-Head Comparative Study.

Radionuclide-labeled fibroblast activation protein inhibitor (FAPI) is an emerging tumor tracer. We sought to assess the uptake and diagnostic performance of 18F-FAPI-42 PET/CT compared with simultaneous 2-deoxy-2[18F]fluoro-D-glucose (18F-FDG) PET/CT in primary and metastatic lesions in patients with malignant digestive system neoplasms and to determine the potential clinical benefit. Forty-two patients (men = 30, women = 12, mean age = 56.71 ± 13.26years) who underwent 18F-FDG PET/CT and 18F-FAPI-42 PET/CT simultaneously for diagnosis, staging, and restaging were enrolled. Quantitative data, including standardized uptake value (SUV), tumor-to-liver ratio (TLR), and tumor-to-blood pool ratio (TBR), were analyzed. Two independent readers performed a visual assessment of lesion number and location on PET/CT images. Interobserver agreement between two examinations was calculated using Cohen's kappa (κ). Primary tumor locations included the liver (n = 20), stomach (n = 9), pancreas (n = 5), and intestine (n = 10). More intense 18F-FAPI-42 uptake and higher tumor-to-background contrast were detected in most primary and metastatic lesions compared with 18F-FDG, contributing to improved diagnostic accuracy ranging from 95.24% to 100%. Moreover, additional lesions showing 18F-FAPI-42 uptake in primary, locoregional and distant metastatic lesions were visualized, especially in multiple liver and peritoneal metastases. Patient-based interobserver agreement varied from moderate to strong, with suboptimal outcomes observed in primary tumors (κ = 0.441, P = 0.01) and preferable results derived from metastatic liver and bone lesions (κ = 1 and 0.896, both P < 0.01). 18F-FAPI-42 PET/CT resulted in modified treatment strategies for 40.48% (17/42) of patients, while 18F-FDG PET/CT led to altered therapeutic regimens in only 4.8% (2/42) of patients. In selected patients with malignant digestive system neoplasms, our study shows that 18F-FAPI-42 PET/CT is a promising alternative for assessing primary tumors and metastases and aiding staging, restaging, and decision-making, with higher uptake and better lesion visualization compared with 18F-FDG. Additionally, it may shed light into the treatment selection and response assessment for FAP-targeted therapy or immunotherapy.

The high efficacy of claudin18.2-targeted CAR-T cell therapy in advanced pancreatic cancer with a strategy to ensure the safety of patients.

Pancreatic cancer (PC) is one of the most lethal digestive system tumors. Claudin18.2 is highly expressed in PC tissue and could serve as a suitable target for CAR-T therapy. In the present study, we reported the utilization of tEGFR-expressing claudin18.2-targeted CAR-T cells to treat 3 patients with advanced PC. Intriguingly, all 3 patients achieved disease remission after CAR-T cell infusion, with 1 complete remission (CR) and 2 partial remissions (PR). However, gastric mucosal injury was observed, which was recognized as on-target off-tumor toxicity (OTOT) and may be due to the expression of claudin18.2 on normal gastric tissues. To control the severe OTOT in patient 3, cyclophosphamide and cetuximab were administered to deplete CAR-T cells, and they successfully controlled OTOT. Single cell transcriptome and TCR sequencing revealed the objective alterations of CAR-T cell clones after cetuximab treatment. Collectively, the present study showed the robust anti-tumor activity of claudin18.2-targeted CAR-T cells against PC, and reported the feasibility of antibody-dependent safety switch strategy to control the OTOT caused by CAR-T cells in patients. Our study may pave the way for the development of a novel strategy to treat patients with advanced PC in the future.

Research Progress in the Medicine-Food Dual Use of Angelica sinensis in Digestive System Tumors

Angelica sinensis (AS) is a widely used medicinal and culinary herb frequently considered critical in traditional prescriptions. Modern pharmacological studies have validated its beneficial effects, including nourishing, blood activation, anti-inflammatory and analgesic properties, liver and kidney protection, and tumor inhibition. Due to the lack of existing reviews on AS in treating digestive system tumors (DS-T), this study investigated the pharmacological effects of AS and its primary active components in combating DS-T from three main perspectives. First, we have summarized its mechanisms for treating various DS-T by analyzing in vitro and in vivo experimental studies. Second, we analyzed frequently used radiotherapy drugs and determined the potential of AS and its active ingredients to reduce toxicity and enhance efficacy. Additionally, AS can be integrated into both regular and medicated diets, thereby effectively preventing tumor development and facilitating post-surgery and radiotherapy recovery. In conclusion, AS exhibits potential as an anti-DS-T drug, providing a theoretical foundation for daily dietary and clinical medicinal use and offering insights for future scientific research and innovation.

MFOLFOX-HAIC+lenvatinib+PD-1 inhibitors versus GC/GS/GEMOX chemotherapy as a first line therapy for advanced biliary tract cancer: A single-center retrospective cohort study

Biliary tract tumors (BTC) account for about 3% of all digestive system tumors, with rising incidence and limited treatment options, particularly for advanced stages, underscoring the need for innovative therapies. This retrospective cohort study evaluated the safety and efficacy of a novel regimen combining hepatic artery infusion chemotherapy with 5-fluorouracil, leucovorin, and oxaliplatin (mFOLFOX-HAIC) alongside lenvatinib and programmed cell death protein-1 (PD-1) inhibitors (mFOLFOX-HAIC+lenvatinib+PD-1i) compared to standard regimens of gemcitabine plus cisplatin, gemcitabine plus S1, or gemcitabine plus oxaliplatin (GC/GS/GEMOX) in advanced BTC patients treated from March 2019 to November 2023. A total of 89 patients were analyzed, with 55 receiving hepatic arterial infusion chemotherapy and 34 receiving the GC/GS/GEMOX regimens. Among these, 23 patients were in the mFOLFOX-HAIC+lenvatinib+PD-1i group, while 24 were in the GC/GS/GEMOX group. The median progression-free survival (mPFS) for the mFOLFOX-HAIC+lenvatinib+PD-1i group was 15 months compared to 6 months for the GC/GS/GEMOX group. Similarly, the median overall survival (mOS) was 20 months for the mFOLFOXHAIC+lenvatinib+PD-1i group versus 13 months for the GC/GS/GEMOX group. The objective response rate (ORR) and disease control rate (DCR) for the mFOLFOX-HAIC+lenvatinib+PD-1i group were 48.5% and 87.0%, respectively, both significantly higher than those observed in the GC/GS/GEMOX group at three months of treatment. The incidence of adverse events (AEs) was similar between the mFOLFOX-HAIC+lenvatinib+PD-1i group and the GC/GS/GEMOX group, at 86.5% and 84.2%, respectively, with no statistically significant difference in complication rates. Overall, mFOLFOX-HAIC+lenvatinib+PD-1i appears to be a safe and well-tolerated treatment for advanced BTC, demonstrating superior mPFS and mOS compared to standard regimens.

MicroRNA-486-3p Targets Chymotrypsin C to Regulate Pancreatic Cancer Progression and Immunosuppressive Factor Expression

Pancreatic ductal adenocarcinoma (PDAC) is a common digestive system tumor with high mortality rates and a poor prognosis. Reports suggest that microRNA (miR)-486-3p in PDAC can be used as a diagnostic biomarker. This research aimed to elucidate the mechanisms by which miR-486-3p regulates PDAC progression. miR-486-3p and chymotrypsin C (CTRC) expression in PDAC were measured using quantitative real-time polymerase chain reaction. Changes in the biological properties of PDAC cells were assessed by Transwell assay, scratch-wound assay, cell counting kit (CCK)-8 assay, and plate cloning assay. The protein expression of immunosuppressive factors (vascular endothelial growth factor, interleukin-6, and transforming growth factor-β) in PDAC cells was detected by western blot. Additionally, a subcutaneous graft tumor model was constructed to explore the influence of silencing miR-486-3p on PDAC in vivo. PDAC showed a pronounced increase in miR-486-3p expression. Upregulation of miR-486-3p stimulated PDAC cell proliferation, migration, invasion, and immunosuppressive factor protein expression, whereas silencing miR-486-3p hindered PDAC malignant development. miR-486-3p targets and negatively regulates CTRC expression. Silencing CTRC partially rescued the restraining impact of silencing miR-486-3p on PDAC malignant progression. In vivo experiments also indicated that silencing miR-486-3p inhibited PDAC malignant progression and immunosuppressive factor expression in vivo. In summary, miR-486-3p promotes immunosuppressive factor protein expression by targeting and negatively regulating CTRC expression, which in turn promotes PDAC malignant progression.

Progress in application and research of tsRNAs in digestive system tumors

Progress in application and research of tsRNAs in digestive system tumors

Application of Spatial Transcriptomics in Digestive System Tumors.

In the field of digestive system tumor research, spatial transcriptomics technologies are used to delve into the spatial structure and the spatial heterogeneity of tumors and to analyze the tumor microenvironment (TME) and the inter-cellular interactions within it by revealing gene expression in tumors. These technologies are also instrumental in the diagnosis, prognosis, and treatment of digestive system tumors. This review provides a concise introduction to spatial transcriptomics and summarizes recent advances, application prospects, and technical challenges of these technologies in digestive system tumor research. This review also discusses the importance of combining spatial transcriptomics with single-cell RNA sequencing (scRNA-seq), artificial intelligence, and machine learning in digestive system cancer research.

Prognostic role of long noncoding RNA CASC11 in cancer patients: A meta-analysis.

Long noncoding RNA (lncRNA) is a significant component of the noncoding genome and refers to RNA molecules that exceed 200 nucleotides in length. It plays a crucial role in both promoting and suppressing cancer by regulating the proliferation, invasion, and metastasis of tumor cells. We have found a correlation between cancer susceptibility candidate 11 (CASC11) experssion and tumorigenesis development prognosis in a number of studies on tumors. Hence, this meta-analysis was conducted to further investigate the effects of CASC11 expression on clinicopathological features and outcome. Furthermore, CASC11 can act both as a therapeutic target and a cancer biomarker. We conducted a thorough search of PubMed, Embase, Web of Science, and Cochrane Library to identify all eligible studies until September 20, 2023. These studies examined the potential relationship between the expression levels of CASC11 and survival or the range of pathological feature in cancer patients. The impact of CASC11 expression on overall survival (OS) was evaluated using pooled hazard ratios and 95% confidence intervals (CI). The relationship between CASC11 expression and clinicopathological features was assessed through pooled odds ratios and 95% CI. A total of 11 studies, involving 660 patients, were examined in this analysis. The results revealed that the overexpression of CASC11 was significantly associated with poor OS (hazard ratios = 2.07, 95%CI = 1.64-2.60) in cancer. Further subgroup analysis demonstrated that the overexpression of CASC11 was consistently linked to poorer OS in diverse types of cancer, including digestive system neoplasm, respiratory neoplasms, and gynecologic tumor. Overall, this analysis established a strong correlation between CASC11 expression and tumor prognosis, suggesting its potential as a predictive marker for tumor progression in diverse cancer types.

Systematic Characterization of Splicing Dysregulation in Pan Solid Tumor Transcriptome.

Splicing dysregulation arising from spliceosomal mutations contributes to disease progression and treatment resistance, mostly in hematologic malignancy. Whereas spliceosomal mutations are less common in solid tumors, splicing disorders are pervasive and proven to promote tumorigenesis. However, there is a lack of systematic understanding of the overall splicing dysregulation patterns and how widespread different patterns occur within or across solid tumor lineage. To address these questions, a computational method called SMNPLS (Sparse Multi-Network Regularized Partial Least Squares) is developed to uncover the pan-cancer splicing dysregulation landscape by extracting joint modular patterns from paired matrices of splicing factors (SFs) expressions and alternative splicing events (ASEs). Six unique patterns illustrated by ASE-SF co-modules are summarized, which involve 1,570 ASEs and altered expression of 170 SFs, covering 40% of TCGA solid tumors. Cross-cancer commonalities of splicing dysregulation are observed among digestive system neoplasms, renal-associated tumors, and urogenital tumors. By contrast, brain tumors demonstrate a distinct splicing pattern with the highest ASE-SF correlation. In addition, some new splicing regulatory relationships are identified that are potentially oncogenic. Overall, the study characterizes the full spectrum of splicing dysregulation patterns, indicating the similarity and specificity of splicing-derived pathogenesis across 31 human solid tumors.

Leveraging the synergy between anti-angiogenic therapy and immune checkpoint inhibitors to treat digestive system cancers.

The response rates to immunotherapy vary widely depending on the type of cancer and the specific treatment used and can be disappointingly low for many solid tumors. Fortunately, due to their complementary mechanisms of action, immunotherapy and anti-angiogenic therapy have synergistic effects in cancer treatment. By normalizing the tumor vasculature, anti-angiogenic therapy can improve blood flow and oxygenation to facilitate better immune cell infiltration into the tumor and enhance the effectiveness of immunotherapy. It also reduces immunosuppressive factors and enhances immune activation, to create a more favorable environment for immune cells to attack the tumor. Their combination leverages the strengths of both therapies to enhance anti-tumor effects and improve patient outcomes. This review discusses the vasculature-immunity crosstalk in the tumor microenvironment and summarizes the latest advances in combining anti-angiogenic therapy and immune checkpoint inhibitors to treat digestive system tumors.

Scutellaria baicalensis and its flavonoids in the treatment of digestive system tumors.

Scutellaria baicalensis has been used for the treatment of digestive system disorders for thousands of years in China and other regions. Modern research have revealed its therapeutic efforts in digestive system tumors. Thus, to review the updated progress of S. baicalensis and its main flavonoids in the treatment of digestive system tumors in the past 10 years, this article summarized the therapeutic effect and molecular mechanisms of S. baicalensis and its 5 flavonoids on tumors in oral cavity, esophagus, stomach, colon, liver, pancreas by inhibiting tumor cell proliferation, inducing autophagy, stimulating immune response, and increasing drug sensitivity. In conclusion, S. baicalensis and its flavonoids could be applied to treat digestive system tumors with different type of methods.

The effect of thyroid cancer on the survival of patients with digestive system tumors using SEER database

The number of cancer survivors worldwide is increasing every year, making secondary primary cancers (SPC) is a growing health threat. Studies have been conducted to investigate the risk of occurrence between digestive system tumors (DST) and thyroid cancer (TC). However, existing studies have tended to focus more on the risk of developing SPC and less on the impact of SPC on the survival of cancer survivors. In this study, using the Surveillance, Epidemiology, and End Results database, we aimed to explore the impact of TC on the survival of patients with DST by data between 2000 and 2018. The study employed the standardized incidence ratio to assess the relative risk of SPC, propensity score matching was conducted to mitigate confounding effects, Kaplan-Meier, Cox proportional risk model and competitive risk model were used to analyze the factors affecting the overall survival and cancer-specific survival. We furthermore explored the influence of pathological types and radiotherapy of TC on the survival of DST patients. 518,901 patients with DST only, 801 patients with TC occurring earlier than DST (TC-1st), and 744 patients with DST occurring earlier than TC (DST-1st) were included. The total incidence rate of small intestine cancer after TC was higher than that of the general population, and the incidence of TC after DST was higher than in the general population. DST patients with a history of TC had better overall survival and lower cancer-specific mortality and this difference was particularly significant in patients with DST-1st. In addition, radiotherapy for TC had no effect on cancer-specific mortality in patients with DST.

Interplay between lncRNAs and the PI3K/AKT signaling pathway in the progression of digestive system neoplasms (Review).

Long non‑coding RNA (lncRNA) is a class of non‑coding RNA molecules located in the cytoplasm or nucleus, which can regulate chromosome structure and function by interacting with DNA, RNA, proteins and other molecules; binding to mRNA bases in a complementary manner, affecting the splicing, stabilization, translation and degradation of mRNA; acting as competing endogenous RNA competitively binds to microRNAs to regulate gene expression and participate in the regulation of various vital activities of the body. The PI3K/AKT signalling pathway plays a key role in numerous biological and cellular processes, such as cell proliferation, invasion, migration and angiogenesis. It has been found that the lncRNA/PI3K/AKT axis regulates the expression of cancer‑related genes and thus tumour progression. The abnormal regulation of lncRNA expression in the lncRNA/PI3K/AKT axis is clearly associated with clinicopathological features and plays an important role in regulating biological functions. In the present review, the expression and biological functions of PI3K/AKT‑related lncRNAs both in vitro and in vivo over recent years, were comprehensively summarized and analyzed. Their correlation with clinicopathological features was also evaluated, with the objective of furnishing a solid theoretical foundation for clinical diagnosis and the monitoring of efficacy in digestive system neoplasms. The present review aimed to provide a comprehensive overview of the expression and biological functions of PI3K/AKT‑related lncRNAs in digestive system neoplasms and to assess their correlation with clinicopathological features. This endeavor seeks to establish a solid theoretical foundation for the clinical diagnosis and efficacy monitoring of digestive system tumors.

Shared and specific competing endogenous RNAs network mining in four digestive system tumors

BackgroundDigestive system malignancies, including esophageal carcinoma (ESCA), stomach adenocarcinoma (STAD), liver hepatocellular carcinoma (LIHC), and colon adenocarcinoma (COAD), pose significant global health challenges. Identifying shared and distinct regulatory mechanisms across these cancers can lead to improved therapies. This study aims to construct and compare competing endogenous RNA (ceRNA) networks across ESCA, STAD, LIHC, and COAD to identify RNA biomarkers that could serve as precision therapeutic targets to enhance clinical outcomes and advance personalized cancer care. MethodsClinical and transcriptomic data from The Cancer Genome Atlas (TCGA) were analyzed to predict differentially expressed RNAs using the edgeR package. The ceRNA networks were constructed using the miRcode and ENCORI databases. Functional enrichment analysis and prognostic RNA screening were performed with ConsensusPathDB and univariate Cox regression analysis. Resultswe identified 6, 88, 55, and 41 RNA biomarkers in ESCA, STAD, LIHC, and COAD, respectively. Network analysis revealed shared and specific elements, with shared nodes enriched in cell cycle and mitotic processes. Several biomarkers, including HMGB3 and RGS16 (ESCA), COL4A1 and COL6A3 (STAD), CDCA5 and CDCA8 (LIHC), and LIMK1 and OSBPL3 (COAD), were consistent with prior studies, while novel biomarkers, such as C3P1 (ESCA), P2RY6 (STAD), and N4BP2L1 and PPP1R3B (LIHC), were discovered. Based on RNA correlation analysis, 1, 23, and 2 potential ceRNA regulatory axes were identified in STAD (PVT1/miR-490-3p/HMGA2), LIHC (DLX6-AS1/miR-139-5p/TOP2A, etc.), and COAD (STRCP1 & LINC00488/miR-142-3p/GAB1), respectively. ConclusionsThis study advances the understanding of ceRNA networks in digestive cancers, highlighting RNA biomarkers with potential as therapeutic targets for personalized treatment strategies.

Multi‐omics graph convolutional networks for digestive system tumour classification and early‐late stage diagnosis

AbstractThe prevalence of digestive system tumours (DST) poses a significant challenge in the global crusade against cancer. These neoplasms constitute 20% of all documented cancer diagnoses and contribute to 22.5% of cancer‐related fatalities. The accurate diagnosis of DST is paramount for vigilant patient monitoring and the judicious selection of optimal treatments. Addressing this challenge, the authors introduce a novel methodology, denominated as the Multi‐omics Graph Transformer Convolutional Network (MGTCN). This innovative approach aims to discern various DST tumour types and proficiently discern between early‐late stage tumours, ensuring a high degree of accuracy. The MGTCN model incorporates the Graph Transformer Layer framework to meticulously transform the multi‐omics adjacency matrix, thereby illuminating potential associations among diverse samples. A rigorous experimental evaluation was undertaken on the DST dataset from The Cancer Genome Atlas to scrutinise the efficacy of the MGTCN model. The outcomes unequivocally underscore the efficiency and precision of MGTCN in diagnosing diverse DST tumour types and successfully discriminating between early‐late stage DST cases. The source code for this groundbreaking study is readily accessible for download at https://github.com/bigone1/MGTCN.