A prognostic risk model based on lactate metabolism and transport-related lncRNAs for gastric adenocarcinoma.

BACKGROUND: Increased lactate levels and metastasis in tumours are strongly associated with dismal outcomes. But prognostic value of lactate metabolism and transport-related lncRNAs in gastric adenocarcinoma (GA) patients remains unaddressed. METHODS: Gene expression data of GA were provided by The Cancer Genome Atlas. Lactate metabolism and transport-related gene data were accessed from GSEA. LncRNAs related to lactate metabolism and transport were identified by correlation analysis. A prognostic model was built by regression analysis. Validity of prognostic model was confirmed through survival analysis and receiver operating characteristic (ROC) curve. Immunity of each risk group was evaluated by immune correlation analysis .LncRNA-mRNA network was built by correlation analysis using Cytoscape software. RESULTS: A 12-gene prognostic model based on lactate metabolism and transport-related lncRNAs was built in GA. Median riskscore was utilized to classify GA samples into high- and low-risk groups. Survival analysis and ROC curves demonstrated validity of prognostic model. Most immune checkpoint molecules and TIDE scores were lower in the low-risk group. LINC01303 and LINC01545 may be the key prognostic factors in patients with GA. CONCLUSION: This study successfully built a prognostic model of lactate metabolism and transport-related lncRNAs in GA. The findings guide prognostic management of GA patients.

WYC-209 inhibited GC malignant progression by down-regulating WNT4 through RARα.

Gastric cancer (GC) has been a major health burden all over the world but there are fewer promising chemotherapeutic drugs due to its multidrug resistance. It has been reported that WYC-209 suppresses the growth and metastasis of tumor-repopulating cells but the effect on GC was not explored. MTT, colony formation, and transwell assays were performed to examine the effects of WYC-209 on the proliferation, colony growth, and mobility of GC cells. Western blotting and qRT-PCR were used to detect the expression of proteins and mRNA. RNA-seq and enrichment analyses were conducted for the differentially expressed genes and enriched biological processes and pathways. The rescue experiments were carried out for further validation. Besides, we constructed xenograft model to confirm the effect of WYC-209 in vivo. The dual-luciferase reporter and Chromatin immunoprecipitation were implemented to confirm the underlying mechanism. WYC-209 exerted excellent anti-cancer effects both in vitro and in vivo. Based on RNA-seq and enrichment analyses, we found that Wnt family member 4 (WNT4) was significantly down-regulated. More importantly, WNT4 overexpression breached the inhibitory effect of WYC-209 on GC progression. Mechanically, WYC-209 significantly promoted the binding between retinoic acid receptor α (RARα) and WNT4 promoter. WYC-209 exerts anti-tumor effects in GC by down-regulating the expression of WNT4 via RARα.

ICOS/ICOSLG and PD-1 Co-Expression is Associated with the Progression of Colorectal Precancerous- Carcinoma Immune Microenvironment.

Purpose: This study aimed to investigate the expression of inducible T-cell co-stimulator (ICOS) and its ligand (ICOSLG), along with their association with clinicopathological features and influence on the immune profile in colorectal cancer (CRC). Patients and Methods: The Cancer Genome Atlas Colorectal Adenocarcinoma cohorts were used. We also analyzed 131 clinical samples of colon lesions, including precancerous lesions (hyperplastic polyps, low-grade dysplasia, and high-grade dysplasia) and CRC tissues. We conducted immunohistochemical (IHC) assays and multiple IHC (mIHC) of CD4+, Foxp3+ tumor-infiltrating lymphocytes (TILs), and PD-1/PD-L1 immune checkpoints in precancerous lesions and CRC samples from our patient subsets to determine changes and correlations in ICOS and ICOSLG expression during progression through the adenoma-carcinoma pathway. Results: High expression of ICOS and ICOSLG was a significant factor in CRC in multiple analyses and was positively correlated with CD4+/Foxp3+ TIL density and PD-1/PD-L1 expression, which increased with the sequential progression of lesions from precancerous tissues to carcinoma. Multivariable logistic regression analysis suggested that the location and expression level of ICOS/ICOSLG may be involved in precancerous-carcinoma progression. The co-expression status of PD-1 and ICOS/ ICOSLG could stratify patients with colorectal lesions into three groups of low, moderate, and high risk of progression. According to this classification and mIHC assays, we found a strong correlation between increased PD-1+ICOS+ or PD-1+ICOSLG+ co-expression and CRC, which might be deemed an independent factor in carcinogenesis. Conclusion: Increased ICOS/ICOSLG expression may be associated with the progressive formation of Foxp3+ TILs in the immune microenvironment and may further promote the development of the abnormal cytology of colorectal lesions from precancerous neoplasia to CRC. Our findings support the interpretation that enhanced co-expression of PD-1+ICOS+ or PD-1+ICOSLG+ contributes to the immune-active microenvironment of the colorectal adenoma-carcinoma sequence.

Reactive Nodular Fibrous Pseudotumor Mimicking Metastatic Tumor After Gastric Cancer Operation: A Case Report and Literature Review.

We describe a case of reactive nodular fibrous pseudotumor (RNFP) misdiagnosed as lymph node metastasis after gastric cancer surgery. Additionally, we summarize the clinical and imaging characteristics of RNFP, combined with the literature, to improve the understanding of preoperative diagnosis. Radiological features of RNFP are a homogenous, isodense, solid mass with gradually mild enhancement on multiphasic abdominal computed tomography (CT), and slight 18F-FDG uptake by positron emission tomography/computed tomography (PET/CT). To the best of our knowledge, this is the first report in the English literature of a case of reactive nodular fibrous pseudotumor associated with gastric cancer and its appearance on PET/CT images.

Surgical Treatment of Port-Site Metastases After Laparoscopic Radical Resection of Gastrointestinal Tumors.

Aim: This study was performed to investigate the feasibility of surgical treatment of port-site metastasis after laparoscopic radical resection of gastrointestinal tumors. Patients and Methods: We retrospectively analyzed the clinical data and follow-up data of 8 patients with port-site metastases after gastrointestinal cancer resection in our hospital from January 2014 to January 2018. Results: Six of port-site metastases occurred within 6 months after gastrointestinal tumor resection, one of port-site metastases occurred in 10 months after the operation, and one of port-site metastases occurred in 30 months after the operation. Any metastasis to the abdominal cavity or distant metastasis was ruled out before the surgical treatment of the port-site metastases, and all patients recovered well after the extended operation. No incisional infection or incisional hernia occurred. By December 2019, 4 patients had died (they had survived for 12, 13, 18, and 24 months, respectively) and 5 patients had survived. The follow-up duration ranged from 19 to 28 months. Conclusions: Surgical resection of port-site metastases is not difficult because of their superficial location. Surgical treatment can improve the prognosis of patients without abdominal metastasis or distant metastasis/recurrence.

FOXM1 functions collaboratively with PLAU to promote gastric cancer progression.

Background: Gastric cancer (GC) is one of the main mortality cause worldwide. Previously, we found Forkhead box protein (FOXM1) or Urokinase-type plasminogen activator (PLAU) are independent prognostic markers of GC. This study aims to explore the combining prognostic efficacy and the potential insights underlying additive effect of FOXM1 to PLAU in GC progression through in-silico analyses. Method: The expression of FOXM1 and PLAU were profiled in 33 cancer types using public data. A merged GC expression dataset containing 598 samples was used for evaluating prognostic significance of FOXM1/PLAU. Gene Set Enrichment Analysis (GSEA) was performed to elucidate the mechanisms underlying FOXM1/PLAU promoted GC progression. The Cancer Genome Atlas (TCGA) was used for analyzing the association between FOXM1/PLAU and tumor immune infiltration. Genomic and proteomic differences between FOXM1+PLAU+ and FOXM1-PLAU- groups were also computed using TCGA GC data. Drugs targeting FOXM1/PLAU associated gene expression pattern was analyzed using LINCs database. Results: FOXM1 and PLAU are overexpressed in 17/33 cancer types including GC. Kaplan-Meier analyses indicate that the FOXM1+PLAU+ subgroup have the worst prognosis, while FOXM1-PLAU- subgroup have the best survival. Bioinformatics analysis indicated that FOXM1+PLAU+ associated genes are enriched in TGF-beta, DNA repair and drug resistance signaling pathways; FOXM1 and PLAU expression are negatively correlated with tumor immune infiltration. Genomic and proteomic differences between FOXM1+PLAU+ and FOXM1-PLAU- groups were presented. Data mining from LINCs suggested several chemicals or drugs that could target the gene expression pattern of FOXM1+PLAU+ patients. Conclusion: FOXM1+PLAU+ can serve as effective prognostic biomarkers and potential therapeutic targets for GC. Due to the additive effect of these two genes, screening for drugs or chemicals that targeting the expression patterns PLAU+FOXM1+ subgroup may exert important clinical impact on GC management.

MicroRNA­203a­3p is a candidate tumor suppressor that targets thrombospondin 2 in colorectal carcinoma.

The aim of the present study was to investigate the role of miR­203a­3p in colorectal cancer (CRC) and identify the target gene of microRNA (miR)­203a­3p. A total of 59 sets of cancer tissues and corresponding adjacent non­tumor tissues were collected from CRC patients (aged 31­78 years) between October 2016 and May 2017. Total RNA extraction and reverse transcription­quantitative polymerase chain reaction analysis, transfection assay, and Transwell and apoptosis assays, western blot analysis, a luciferase reporter assay and immunohistochemistry were performed. miR­203a­3p was found to be significantly downregulated in CRC tissues compared with adjacent normal tissues. The overexpression of miR­203a­3p was shown to inhibit the invasion and migration of human CRC SW480 and HT29 cells, and increase their apoptosis rates. Furthermore, miR­203a­3p downregulated the expression of thrombospondin 2 (THBS2) in SW480 and HT29 cells. It was also experimentally demonstrated that miR­203a­3p binds to the 3'­untranslated region of THBS2, downregulating THBS2 expression and thereby inhibiting CRC progression and metastasis. The expression of miR­203a­3p, which serves a tumor­suppressive role, in CRC tissues was significantly downregulated. As miR­203a­3p was determined to target THBS2 to inhibit CRC progression and metastasis; thus, miR­203a­3p may be considered as a potential novel approach to treating CRC.

Acute pancreatitis with abdominal bloating and distension, normal lipase and amylase: A case report.

RATIONALE: Acute pancreatitis is an inflammatory disorder of the pancreas, and its correct diagnosis is an area of interest for clinicians. In accordance with the revised Atlanta classification, acute pancreatitis can be diagnosed if at least 2 of the following 3 criteria are fulfilled: abdominal pain; serum lipase (or amylase) activity at least 3 times the upper limit of normal; or characteristic findings of acute pancreatitis on contrast-enhanced computed tomography (CT) or, less often, magnetic resonance imaging or transabdominal ultrasonography. Diagnostic imaging is essential in patients with no or slight enzyme elevation. If enzymes are normal in cases with abdominal distension, there is clinical doubt about the diagnosis of acute pancreatitis, so an early CT scan should be obtained and other life-threatening disorders excluded. PATIENT CONCERNS: A 50-year-old male presented with a 1-day history of abdominal bloating and distension. On physical examination, abdominal bulging and mild epigastric tenderness were detected. Laboratory evaluation showed normal amylase and lipase. There was no abnormality on abdominal ultrasound or CT of the abdomen and pelvis. On the fourth day of admission, CT of the abdomen and pelvis showed a hypodense lesion in the pancreas surrounded by a moderate amount of peripancreatic fluid. DIAGNOSES: In accordance with the revised Atlanta classification, acute pancreatitis was diagnosed, based on the presence of abdominal pain, and the results of the CT scan of the abdomen and pelvis. INTERVENTIONS: The patient was treated with fasting, gastrointestinal decompression bowel rest, intravenous rehydration, and somatostatin. OUTCOMES: After 2 days of treatment, his abdominal distension was significantly relieved, and the patient was discharged on the seventh day of admission. At the 3-month follow-up, the patient had no recurrence of pancreatitis. LESSONS: This case of abdominal distension could not be explained by common causes, such as ascites, bowel edema, hematoma, bowel distension, or ileus, which led us to suspect pancreatitis.

ERBB4 promotes the proliferation of gastric cancer cells via the PI3K/Akt signaling pathway.

ERBB4 is one of the members of the epidermal growth factor receptor (EGFR) family. ERBB4 is a large transmembrane glycoprotein and has tyrosine kinase activity. Once combined with epidermal growth factor (EGF), ERBB4 can activate the related genes in the nucleus, thus promoting cell division and proliferation. In the present study, we investigated the effect of ERBB4 in the proliferation of gastric cancer cells. We found that high ERBB4 levels were closely related to the poor prognosis of gastric cancer patients. Furthermore, ERBB4 was highly expressed in gastric cancer cell lines when compared to the normal stomach cell line, GES. Clinical samples provided the same results. Two gastric cancer cell lines, SGC­7901 and MNK­45 were used to study the underlying mechanism of ERBB4 in the promotion of cell proliferation in gastric cancer cells both in vitro and in vivo. It was observed that after the expression of ERBB4 was suppressed, the proliferation of gastric cancer cells was markedly inhibited both in vitro and in vivo. Moreover, treatment with lentiviral vector siRNA­ERBB4 (Lv­siRNA­ERBB4) or the ERBB4 inhibitor AST­1306, markedly inhibited gastric cancer cell proliferation. Further experiments revealed that inhibition of the expression of ERBB4 could inhibit the activation of the PI3K/Akt signaling pathway. In addition, the use of the PI3K/Akt signaling pathway inhibitor LY294002 demonstrated the aforementioned results. Therefore, we believe that ERBB4 regulates cell proliferation mainly through the PI3K signaling pathway. Finally, nude mice xenografted with gastric cancer cells with low expression of ERBB4 exhibited smaller tumors and longer survival than those engrafted with control gastric cancer cells. These data indicated that ERBB4 promoted cell proliferation and is thus a potential therapeutic target for the treatment of gastric cancer.

Overexpression of MYC binding protein promotes invasion and migration in gastric cancer.

Gastric cancer (GC) is the second leading cause of cancer-associated mortality worldwide. Although the mortality rate of patients with GC has improved, it remains a significant health issue. The MYC proto-oncogene protein serves key roles in cellular proliferation, differentiation, transformation and apoptosis. Previous studies have identified the abnormal expression of MYC-binding protein (MYCBP) during tumorigenesis in multiple types of cancer. Furthermore, evidence demonstrates that the abnormal expression of MYCBP contributes to the invasion and migration of human cancer types, including colon cancer and glioma; however, its influence on GC remains unclear. In the present study, the expression of MYCBP in GC cells and tissues was analyzed by reverse transcription-quantitative polymerase chain reaction. Additionally, GC cell lines were transfected with small interfering RNAs against MYCBP or lymphoid enhancer-binding factor 1 (LEF-1) and assessed by in vitro transwell migration and invasion assays. The results indicated that the expression of MYCBP in GC cells and tissues was markedly increased compared with a normal gastric epithelial cell line and adjacent normal gastric mucosal tissues, respectively. Furthermore, MYCBP downregulation notably inhibited the metastatic capacity of GC cells, and LEF-1 knockdown was found to downregulate the expression of MYCBP. On the basis of the findings of the present study, MYCBP may be a direct target of the ß-catenin/LEF-1 pathway via binding LEF-1, and could potentially be used as a biomarker for the diagnosis and prognosis of GC.

Circular RNA hsa_circ_000984 promotes colon cancer growth and metastasis by sponging miR-106b.

Circular RNAs (circRNAs) as a novel type of noncoding RNAs (ncRNAs) are widely studied in the development of human various diseases, including cancer. Here, we found circular RNA hsa_circ_000984 encoded by the CDK6 gene was remarkably upregulated in the tissues of colorectal cancer (CRC) patients and in the CRC cell lines. Moreover, high expression level of hsa_circ_000984 was significantly associated with advanced colorectal cancer. Further analysis revealed that hsa_circ_000984 knockdown could inhibit cell proliferation, migration, invasion in vitro and tumor formation in vivo in CRC cell lines. Mechanically, we found that hsa_circ_000984 may act as a competing endogenous RNA (ceRNA) by competitively binding miR-106b and effectively upregulate the expression of CDK6, thereby inducing a series of malignant phenotypes of tumor cells. Taken together, these observations suggest that the hsa_circ_000984 could mediate the expression of gene CDK6 by acting as a ceRNA, which may contribute to a better understanding of between the regulatory miRNA network and CRC pathogenesis.

The clinicopathological significance of HES1 promoter hypomethylation in patients with colorectal cancer.

Hairy/enhancer of split 1 (HES1) is a basic helix-loop-helix transcriptional repressor. Aberrant demethylation has been considered a common mechanism of tumor promoter gene activation. In the current study, we aimed to investigate the methylation status of the HES1 promoter and correlations with clinicopathological parameters and prognosis in colorectal cancer (CRC). The expression of HES1 in 50 paired CRC specimens and adjacent normal tissues was determined by using quantitative real-time polymerase chain reaction and immunohistochemical analysis. Moreover, DNA methylation status was evaluated through methylation-specific polymerase chain reaction and bisulfite sequencing. The correlation of methylation status with HES1 expression level and clinicopathological parameters was statistically analyzed in CRC patients. Our data showed that the methylation level of HES1 was significantly decreased and negatively correlated with HES1 expression in CRC tissues. Moreover, HES1 hypomethylation was associated with a poor histological grade, Dukes' classification, lymph node metastasis, and clinical stages (P<0.05). Furthermore, survival analyses revealed that a decreased methylation status of HES1 was linked to poor prognosis of CRC patients. In conclusion, promoter hypomethylation upregulates HES1 expression and plays a critical role in the progression and prognosis of CRC patients.

Integrated analysis of genes associated with poor prognosis of patients with colorectal cancer liver metastasis.

Colorectal cancer (CRC) is one of the most common malignances in the gut. Liver is the most common metastasis site of CRC. This study focuses on the primary CRC and its liver metastasis, aiming to discover several liver metastasis related genes and provide therapeutic candidates. We compared gene expression patterns among the groups of normal colorectal mucosa, primary tumor and the liver metastasis using a CRC gene expression dataset. 84 genes were found to be upregulated in both primary tumor and liver metastases. Function enrichment analysis indicated that these genes are enriched in pathways such as chemotaxis, coagulation and lipid metabolism which are crucial in multi-step cancer metastasis. Gene network analysis identified several important hub genes that may be involved in carcinogenesis and liver metastasis. Then we used a validation dataset containing 562 CRC samples with detailed clinical information, to screen prognostic biomarkers for overall survival (OS) and relapse free survival (RFS). Finally, overexpression of THBS2 (thrombospondin 2), INHBB (inhibin, beta B) and BGN (biglycan) were proved to be correlated with poor OS and RFS. In conclusion, this study indicated that chemotaxis, coagulation and lipid metabolism might play critical roles in the processes of carcinogenesis and liver metastasis. THBS2, INHBB and BGN are prognostic markers and potential therapeutic targets for CRC.

[Efficacies of neoadjuvant chemotherapy plus nutritional support in advanced gastric cancer complicated with pylori obstruction].

OBJECTIVE: To explore the efficacies of neoadjuvant chemotherapy plus nutritional supports for gastric cancer complicated with pyloric obstruction. METHODS: Retrospective analyses were performed for a total of 116 patients of gastric cancer complicated with pyloric obstruction undergoing exploratory laparotomy from January 2004 to June 2013. RESULTS: Sixty-two patients (group A) received neoadjuvant chemotherapy (regimen of FOLFOX) plus preoperative nutritional support. And parenteral (PN, n = 30) and enteral (EN, n = 32) nutritional supports were provided. Another 54 patients (group B) underwent exploratory laparotomy alone. The serum level of albumin and score of quality of life in group A at the last preoperative day improved significantly. And EN was better than PN. The rate of excision/radical excision of group A (85.5%, 45.2%) was much higher than group B (64.8%, 18.5%) (both P < 0.05). CONCLUSION: Nutritional support, especially EN, can improve the nutritional status and quality of life in patients with gastric cancer complicated with pyloric obstruction. And nutritional support plus neoadjuvant chemotherapy increase the rate of tumor excision.

[Application of home enteral nutrition and its impact on the quality of life in patients with advanced gastric cancer].

OBJECTIVE: To investigate the application of home enteral nutrition (HEN) in patients with advanced gastric cancer and its impact on the quality of life. METHODS: Data of 60 consecutive patients with advanced gastric cancer, who could not underwent operation and had relapse metastasis, from June 2010 to June 2012 were retrospectively analyzed. According to familial nutritional pattern, these 60 patients were divided into HEN group (25 cases) receiving home enteral nutritional support and control group (35 cases). HEN patients were supported through jejunostomy tube or nasal gastric tube. Control patients were supported through total parental nutrition or purely eating respectively. All the patients received intravenous chemotherapy and evaluated by Karnofsky index and Spitzer system in the first, third, sixth and twelfth month. In the sixth month, patients were also examined by EORTC QLQ-C30. RESULTS: No significant differences were found between the two groups according to 8 elements containing age, sex, BMI, etc. A total of 53 patients died within one year, including 21 in HEN group and 32 in control group. The Karnofsky scales showed that HEN group scored meanly 57.4, 39.6 and 28.2 in the third, sixth and twelfth month respectively, which were significantly higher than those of control group (45.3, 29.2 and 20.1, P=0.041, P=0.012 and P=0.015 respectively). The Spitzer scales showed that HEN group scored meanly 5.12, 4.04 and 2.54 on average in the third, sixth and twelfth month respectively, which were significantly higher than those of control group (4.32, 3.01 and 1.97, P=0.048, 0.035 and P=0.024 respectively). The EROTC QLQ-C30 scales showed that HEN group scored higher than control group in functional scales (P<0.05), and lower in the symptom scales of short breathing, pain and tired (P=0.025, P=0.044, P=0.036 respectively), while higher in diarrhea (P=0.047). CONCLUSIONS: The quality of life of patients with advanced gastric cancer declines gradually with the nutritional status deteriorating. HEN can be applied to improve the nutritional status and quality of life.

Expression of TRAF6 and ubiquitin mRNA in skeletal muscle of gastric cancer patients.

OBJECTIVE: To investigate the prognostic significance of tumor necrosis factor receptor (TNFR),-associated factor 6 (TRAF6),-and ubiquitin in gastric cancer patients. METHODS: Biopsies of the rectus abdominis muscle were obtained intra operatively from 102 gastric cancer patients and 29 subjects undergoing surgery for benign abdominal diseases, and muscle TRAF6 and ubiquitin mRNA expression and proteasome proteolytic activities were assessed. RESULTS: TRAF6 was significantly upregulated in muscle of gastric cancer compared with the control muscles. TRAF6 was upregulated in 67.65% (69/102) muscle of gastric cancer. Over expression of TRAF6 in muscles of gastric cancer were associated with TNM stage, level of serum albumin and percent of weight loss. Ubiquitin was significantly upregulated in muscle of gastric cancer compared with the control muscles. Ubiquitin was upregulated in 58.82% (60/102) muscles of gastric cancer. Over expression of ubiquitin in muscles of gastric cancer were associated with TNM (Tumor-Node-Metastasis) stage and weight loss. There was significant relation between TRAF6 and ubiquitin expression. CONCLUSIONS: We found a positive correlation between TRAF6 and ubiquitin expression, suggesting that TRAF6 may up regulates ubiquitin activity in cancer cachexia. While more investigations are required to understand its mechanisms of TRAF6 and ubiquitin in skeletal muscle. Correct the catabolic-anabolic imbalance is essential for the effective treatment of cancer cachexia.

[Current status and prospect of surgical treatment for diabetes mellitus].

Diabetes surgery is a new concept in recent years, which means controlling blood sugar or curing diabetes through some surgical methods. From the commencement of bariatric surgery in the 1950s to the discovery of the special function of decreasing blood sugar after these surgeries in 1970s, and then the fast developing of diabetes surgery in the past 30 years, now there seems be a different answer to the question that if we can cure diabetes. In this article, we review the historical evolution, surgical procedure, potential mechanism and outlook of diabetes surgery.

[Effect of early enteral nutrition supplemented with glutamine on postoperative intestinal mucosal barrier function in patients with gastric carcinoma].

OBJECTIVE: To investigate the effect of early enteral nutrition (EEN) supplemented with glutamine on postoperative intestinal mucosal barrier function of patients with gastric carcinoma. METHODS: Eighty patients with gastric carcinoma who underwent intraoperative peritoneal hyperthermic chemotherapy(IPHC) were randomized into two groups: EEN+glutamine (EEN+Gln) group(n=40) and EEN group(n=40). Intestinal mucosal barrier function was evaluated by serum diamine oxidase (DAO), ratio of lactulose to mannitol(L/M), endotoxin lipopolysaccharides(LPS), and tumor necrosis factor-α(TNF-α) at 1 day before operation, 1 day, 7 days, 12 days after operation. Time to first flatus and tolerance to EEN were recorded as well. RESULTS: There were no significant differences in the two groups in demographics(all P>0.05). Two cases(5%) in the EEN+Gln group and 1 case (2.5%) in the EEN group could not tolerate well(P>0.05). On postoperative day 1, there were no differences in serum DAO, L/M ratio, LPS, TNF-α between the two groups (P>0.05). On postoperative day 7, all the parameters for mucosal barrier function were significantly lower in the EEN+Gln group. On postoperative day 12, the urinary L/M and DAO, LPS, and TNF-α were still significantly lower in the EEN+Gln group, however, urinary L/M was comparable between the two groups. There were no differences between the two groups in the time to first flatus (P>0.05). CONCLUSION: The immunologic tolerance of enteral nutrition supplemented with glutamine is favorable, which provides protective effect on intestinal mucosal barrier in patients with gastric carcinoma undergoing IPHC.