17 research outputs found

    Function-preserving in colorectal cancer surgery assisted by laparoscopy and da Vinci robotic surgical system

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    [Abstract] Minimally invasive surgery has become the mainstream approach for treating colorectal cancer, with function-preserving being a focal point of recent surgical discussions. Compared with open surgery, laparoscopic surgery and da Vinci robotic surgery align more closely with the surgical principles of minimal invasion, “bloodlessness”, and function-preserving. This article delves into the aspects of function-preserving in laparoscopic and da Vinci robot-assisted colorectal cancer surgery, including visual surgical techniques, surgical manipulation-related injuries, preservation of autonomous nerves, sphincter-preserving surgery, holistic integrative medicine concept and natural orifice specimen extraction surgery, and precise preoperative evaluation and the application of novel technologies. The aim is to share insights with colleagues in the field

    Tumor-Stroma Ratio is a Critical Indicator of Peritoneal Metastasis in Gastric Cancer

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    Lin Zhong,1,* Hongyun Huang,2,* Dong Hou,1,* Shihai Zhou,3 Yu Lin,4 Yue Yu,4 Jinhao Yu,1 Fanghai Han,5 Lang Xie6 1Department of Gastrointestinal Surgery, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, Guangdong, 510120, People’s Republic of China; 2Department of General Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100010, People’s Republic of China; 3Department of Tumor Surgery, Zhongshan City People’s Hospital, Zhongshan, Guangdong, 528403, People’s Republic of China; 4Department of Pathology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, 510282, People’s Republic of China; 5Department of Gastrointestinal Surgery, Guangdong Second Provincial General Hospital, Guangzhou, Guangdong, 5181025, People’s Republic of China; 6Department of General surgery, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, 510282, People’s Republic of China*These authors contributed equally to this workCorrespondence: Lang Xie; Fanghai Han, Email [email protected]; [email protected]: This study aims to investigate the correlation between the tumor-stroma ratio (TSR) and peritoneal metastasis (PM) in gastric cancer (GC) and constructs a diagnostic model based on preoperative examination data.Methods: To determine the feasibility of obtaining TSR in GC patients through preoperative examinations, the consistency of TSR between endoscopic biopsy tissues and postoperative histopathological tissues was evaluated. Additionally, the correlation between TSR and PM in GC was analyzed using Gene Expression Omnibus (GEO) datasets. To validate TSR’s clinical potential in diagnosing PM, 640 GC patients from two medical centers were enrolled. A training cohort of 330 patients evaluated TSR and synchronous PM correlation, and a validation cohort of 310 patients was used. An additional cohort of 510 patients was established to investigate TSR and metachronous PM. A diagnostic model based on preoperative data was developed and a nomogram constructed.Results: The TSR shows good consistency between endoscopic biopsy tissues and postoperative histopathological tissues. A significant correlation between TSR and PM was observed. The TSR-based model, combined with CA125, CA724 and Borrmann type, exhibited strong diagnostic effectiveness and considerable predictive efficacy, with an Area Under the Curve (AUC) of 0.85 in the training cohort, 0.73 in the external validation cohort, and 0.72 in the metachronous PM cohort.Conclusion: The TSR emerges as a crucial marker for PM in GC, with the developed model, based on TSR and preoperative examination data, demonstrating substantial diagnostic and predictive capabilities.Keywords: tumor-stroma ratio, peritoneal metastasis, gastric cancer, preoperative examinations, nomogra

    Immune-Related LncRNAs to Construct a Prognosis Risk-Assessment Model for Gastric Cancer

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    Background: Gastric cancer is a prevalent cause of tumor death. Tumor immunotherapy aims to reshape the specific immunity to tumors in order to kill the tumor. LncRNAs play a pivotal role in regulating the tumor immune microenvironment. Herein, immune-related lncRNAs were used to establish a prognosis risk-assessment model for gastric cancer and provide personalized predictions while providing insights and targets for gastric cancer treatment to enhance patient prognosis. Methods: Gastric adenocarcinoma transcriptome and clinical data were acquired from the The Cancer Genome Atlas (TCGA) database to screen the immune-related lncRNAs. Then, LASSO COX regression was utilized to construct the prognosis risk-assessment model. Afterward, the reliability of the model was evaluated the relationship between immune infiltration, clinical characteristics, and the model was analyzed. Results: We identified 13 lncRNAs and constructed the prognosis assessment model. According to the median risk score of the training set, the patients were assigned to different risk groups. Overall survival time was shorter in the high-risk group. In the high-risk group, higher infiltration of mono-macrophages, dendritic cells, CD4+ T cells, and CD8+ T cells was observed. Moreover, the model was positively related to tumor metastasis. Conclusion: The prognosis risk-assessment model developed in this research can effectively predict the prognosis of gastric cancer patients. This tool is expected to be further applied to clinics in the future, thus providing a novel target for immunotherapy in gastric cancer patients

    FMO family may serve as novel marker and potential therapeutic target for the peritoneal metastasis in gastric cancer

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    ObjectiveTo explore the relationship between flavin-containing monooxygenases (FMOs) and peritoneal metastasis (PM) in gastric cancer (GC).Materials and methodsTIMER 2.0 was used to perform pan-cancer analysis and assess the correlation between the expression of FMOs and cancers. A dataset from The Cancer Genome Atlas (TCGA) was used to analyze the correlation between FMOs and clinicopathological features of GC. PM is well established as the most common mode of metastasis in GC. To further analyze the correlation between FMOs and PM of GC, a dataset was obtained from the National Center for Biotechnology Information Gene Expression Omnibus (GEO) database. The results were validated by immunohistochemistry. The relationship between FMOs and PM of GC was explored, and a novel PM risk signature was constructed by least absolute shrinkage and selection operator (LASSO) regression analysis. The regression model’s validity was tested by multisampling. A nomogram was established based on the model for predicting PM in GC patients. The mechanism of FMOs in GC patients presenting with PM was assessed by conducting Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses in TCGA and GEO datasets. Finally, the potential relationship between FMOs and immunotherapy was analyzed.ResultsThe pan-cancer analysis in TCGA and GEO datasets showed that FMO1 was upregulated, while FMO2 and FMO4 were downregulated in GC. Moreover, FMO1 and FMO2 correlated positively with the T and N stage of GC in the TCGA dataset. FMO1 and FMO2 expression was a risk factor for GC (hazard ratio: 1.112 and 1.185). The overexpression of FMO1 was significantly correlated with worse disease-free-survival (DFS) and overall survival (OS). However, no relationship was found between FMO2 expression in GC and DFS and OS. PM was highly prevalent among GC patients and typically associated with a worse prognosis. FMO1 was highly expressed in GC with PM. FMO1 and FMO2 were positively correlated with PM in GC. We identified a 12-gene panel for predicting the PM risk signature by LASSO (Area Under Curve (AUC) = 0.948, 95%CI: 0.896–1.000). A 10-gene panel for PM prediction was identified (AUC = 0.932, 95%CI: 0.874–0.990), comprising FMO1 and FMO2. To establish a model for clinical application, a 7-gene panel was established (AUC = 0.927, 95% CI: 0.877–0.977) and successfully validated by multisampling. (AUC = 0.892, 95% CI: 0.878–0.906). GO and KEGG analyses suggest that FMO1 and FMO2 regulate the extracellular matrix and cell adhesion. FMO1 and FMO2 were positively correlated with the immune score of GC, and their expression was associated with the infiltration of immune cells.ConclusionPM in GC is strongly correlated with FMOs. Overall, FMO1 and FMO2 have huge prospects for application as novel diagnostic and therapeutic targets

    A β‑Galactosidase-Activated Fluorogenic Reporter for the Detection of Gastric Cancer In Vivo and in Urine

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    Although gastric cancer (GC) is one of the most frequent malignant tumors in the digestive tract with high morbidity and mortality, it remains a diagnostic dilemma due to its reliance on invasive biopsy or insensitive assays. Herein, we report a fluorescent gastric cancer reporter (FGCR) with activatable near-infrared fluorescence (NIRF) signals and high renal-clearance efficiency for the detection of orthotopic GC in a murine model via real-time imaging and remote urinalysis. In the presence of gastric-tumor-associated β-galactosidase (β-Gal), FGCR can be fluorescently activated for in vivo NIRF imaging. Relying on its high renal-clearance efficiency (∼95% ID), it can be rapidly excreted through kidneys to urine for the ultrasensitive detection of tumors with a diameter down to ∼2.1 mm and for assessing the prognosis of oxaliplatin-based chemotherapy. This study not only provides a new approach for noninvasive auxiliary diagnosis and prognosis of GC but also provides guidelines for the development of fluorescence probes for cancer diagnosis

    New Anti-Cancer Strategy to Suppress Colorectal Cancer Growth Through Inhibition of ATG4B and Lysosome Function

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    Autophagy inhibition has been proposed to be a potential therapeutic strategy for cancer, however, few autophagy inhibitors have been developed. Recent studies have indicated that lysosome and autophagy related 4B cysteine peptidase (ATG4B) are two promising targets in autophagy for cancer therapy. Although some inhibitors of either lysosome or ATG4B were reported, there are limitations in the use of these single target compounds. Considering multi-functional drugs have advantages, such as high efficacy and low toxicity, we first screened and validated a batch of compounds designed and synthesized in our laboratory by combining the screening method of ATG4B inhibitors and the identification method of lysosome inhibitors. ATG4B activity was effectively inhibited in vitro. Moreover, 163N inhibited autophagic flux and caused the accumulation of autolysosomes. Further studies demonstrated that 163N could not affect the autophagosome-lysosome fusion but could cause lysosome dysfunction. In addition, 163N diminished tumor cell viability and impaired the development of colorectal cancer in vivo. The current study findings indicate that the dual effect inhibitor 163N offers an attractive new anti-cancer drug and compounds having a combination of lysosome inhibition and ATG4B inhibition are a promising therapeutic strategy for colorectal cancer therapy
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