Wilson disease complicated by Crohn disease: A case report and literature review.

RATIONAL: Wilson disease (WD), also known as hepatolenticular degeneration, is an autosomal-recessive hereditary disease with abnormal copper metabolism. Crohn disease (CD) is a chronic inflammatory gastrointestinal disease, which belongs to inflammatory bowel disease, all segments of the gastrointestinal tract can be affected, especially the terminal ileum and colon, accompanied by extraintestinal manifestations and related immune disorders. WD complicated by ulcerative colitis has been reported before, but WD complicated by CD has not been reported so far. PATIENT CONCERNS AND DIAGNOSIS: We presented the first report of a young patient with WD complicated by CD, who was admitted to the hospital because of repeated low fever, elevated C-reactive protein for 3 years, and anal fistula for 6 months. INTERVENTIONS AND OUTCOMES: In this complicated disease, Ustekinumab is safe and effective. LESSONS: We conclude that copper metabolism and oxidative stress play important roles in WD and CD.

Identification and validation of an epithelial-mesenchymal transition-related lncRNA pairs prognostic model for gastric cancer.

Background: Gastric cancer (GC) is a common malignancy. A mounting body of evidence has demonstrated the correlation between GC prognosis and epithelial-mesenchymal transition (EMT)-related biomarkers. This research constructed an available model using EMT-related long noncoding RNA (lncRNA) pairs to predict the survival for GC patients. Methods: The transcriptome data along with clinical information on GC samples were derived from The Cancer Genome Atlas (TCGA). Differentially expressed EMT-related lncRNAs were acquired and paired. Univariate and least absolute shrinkage and selection operator (LASSO) Cox regression analyses were applied to filter lncRNA pairs, and the risk model was built to investigate its effect on the prognosis of GC patients. Then, the areas under the receiver operating characteristic curves (AUCs) were calculated and the cutoff point for distinguishing low- or high-risk GC patients was identified. And the predictive ability of this model was tested in the GSE62254. Furthermore, the model was evaluated from the perspectives of survival time, clinicopathological parameters, infiltration of immunocytes, and functional enrichment analysis. Results: The risk model was built by using the identified twenty EMT-related lncRNA pairs, and it was not necessary to know the specific expression level of each lncRNA. Survival analysis pointed out that GC patients with high risk had poorer outcomes. Additionally, this model could be an independent prognostic variable for GC patients. The accuracy of the model was also verified in the testing set. Conclusions: The new predictive model constructed here is composed of EMT-related lncRNA pairs, with reliable prognostic values, and can be utilized to predict the survival of GC.

Recent developments in PD-1/PD-L1 blockade research for gastroesophageal malignancies.

Gastroesophageal cancers (GECs) comprise malignancies in the stomach, esophagus, and gastroesophageal junction. Despite ongoing improvements in chemoradiotherapy, the clinical outcomes of GEC have not significantly improved over the years, and treatment remains challenging. Immune checkpoint inhibitors (ICIs) have been the subject of clinical trials worldwide for several years. Encouraging results have been reported in different countries, but further research is required to apply ICIs in the clinical care of patients with GEC. This review summarizes completed and ongoing clinical trials with programmed death 1 (PD-1)/programmed death-ligand 1 (PD-L1) pathway blockers in GEC and current biomarkers used for predicting PD-1/PD-L1 blockade efficacy. This review captures the main findings of PD-1/PD-L1 antibodies combined with chemotherapy as an effective first-line treatment and a monotherapy in second-line or more treatment and in maintenance therapy. This review aims to provide insight that will help guide future research and clinical trials, thereby improving the outcomes of patients with GEC.

Fecal Microbiota Transplantation Effectively Cures a Patient With Severe Bleeding Immune Checkpoint Inhibitor-Associated Colitis and a Short Review.

Immune checkpoint inhibitors (ICIs) have opened up a new way for tumor therapy but simultaneously led to the occurrence of immune-related adverse events. We report a case of successful treatment of PD-1 inhibitor-associated colitis with fecal microbiota transplantation (FMT). The patient was a palatal malignant melanoma who developed diarrhea and hematochezia accompanied by fever, gastrointestinal bleeding, and infection after the third treatment with PD-1 (Toripalimab). The patient received general treatment unsuccessful, corticosteroid therapy after initial success but rapid loss of response, and finally successful treatment after fecal microbiota transplantation.

Identification of specific role of SNX family in gastric cancer prognosis evaluation.

We here perform a systematic bioinformatic analysis to uncover the role of sorting nexin (SNX) family in clinical outcome of gastric cancer (GC). Comprehensive bioinformatic analysis were realized with online tools such as TCGA, GEO, String, Timer, cBioportal and Kaplan-Meier Plotter. Statistical analysis was conducted with R language or Perl, and artificial neural network (ANN) model was established using Python. Our analysis demonstrated that SNX4/5/6/7/8/10/13/14/15/16/20/22/25/27/30 were higher expressed in GC, whereas SNX1/17/21/24/33 were in the opposite expression profiles. GSE66229 was employed as verification of the differential expression analysis based on TCGA. Clustering results gave the relative transcriptional levels of 30 SNXs in tumor, and it was totally consistent to the inner relevance of SNXs at mRNA level. Protein-Protein Interaction map showed closely and complex connection among 33 SNXs. Tumor immune infiltration analysis asserted that SNX1/3/9/18/19/21/29/33, SNX1/17/18/20/21/29/31/33, SNX1/2/3/6/10/18/29/33, and SNX1/2/6/10/17/18/20/29 were strongly correlated with four kinds of survival related tumor-infiltrating immune cells, including cancer associated fibroblast, endothelial cells, macrophages and Tregs. Kaplan-Meier survival analysis based on GEO presented more satisfactory results than that based on TCGA-STAD did, and all the 29 SNXs were statistically significant, SNX23/26/28 excluded. SNXs alteration contributed to microsatellite instability (MSI) or higher level of MSI-H (hyper-mutated MSI or high level of MSI), and other malignancy encompassing mutation of TP53 and ARID1A, as well as methylation of MLH1.The multivariate cox model, visualized as a nomogram, performed excellently in patients risk classification, for those with higher risk-score suffered from shorter overall survival (OS). Compared to previous researches, our ANN models showed a predictive power at a middle-upper level, with AUC of 0.87/0.72, 0.84/0.72, 0.90/0.71 (GSE84437), 0.98/0.66, 0.86/0.70, 0.98/0.71 (GSE66229), 0.94/0.66, 0.83/0.71, 0.88/0.72 (GSE26253) corresponding to one-, three- and five-year OS and recurrence free survival (RFS) estimation, especially ANN model built with GSE66229 including exclusively SNXs as input data. The SNX family shows great value in postoperative survival evaluation of GC, and ANN models constructed using SNXs transcriptional data manifesting excellent predictive power in both OS and RFS prediction works as convincing verification to that.

A novel prognostic model based on epithelial-mesenchymal transition-related genes predicts patient survival in gastric cancer.

BACKGROUND: Gastric cancer (GC) represents a major malignancy and is the third deathliest cancer globally. Several lines of evidence indicate that the epithelial-mesenchymal transition (EMT) has a critical function in the development of gastric cancer. Although plentiful molecular biomarkers have been identified, a precise risk model is still necessary to help doctors determine patient prognosis in GC. METHODS: Gene expression data and clinical information for GC were acquired from The Cancer Genome Atlas (TCGA) database and 200 EMT-related genes (ERGs) from the Molecular Signatures Database (MSigDB). Then, ERGs correlated with patient prognosis in GC were assessed by univariable and multivariable Cox regression analyses. Next, a risk score formula was established for evaluating patient outcome in GC and validated by survival and ROC curves. In addition, Kaplan-Meier curves were generated to assess the associations of the clinicopathological data with prognosis. And a cohort from the Gene Expression Omnibus (GEO) database was used for validation. RESULTS: Six EMT-related genes, including CDH6, COL5A2, ITGAV, MATN3, PLOD2, and POSTN, were identified. Based on the risk model, GC patients were assigned to the high- and low-risk groups. The results revealed that the model had good performance in predicting patient prognosis in GC. CONCLUSIONS: We constructed a prognosis risk model for GC. Then, we verified the performance of the model, which may help doctors predict patient prognosis.

Potential Impact of ALKBH5 and YTHDF1 on Tumor Immunity in Colon Adenocarcinoma.

BACKGROUND: ALKBH5 and YTHDF1 are regarded as the eraser and reader, respectively, in N6-methyladenosine (m6A) modification. Recently, immune contexture has been drawing increasing attention in terms of the progression and treatment of cancers. This study aimed to determine the relationship between ALKBH5/YTHDF1 and immunological characteristics of colon adenocarcinoma (COAD). METHODS: Expression of ALKBH5 and YTHDF1 was investigated across TCGA and GEO validated in our study. Patients with COAD were divided into two clusters using consensus clustering based on the expression of ALKBH5 and YTHDF1. We then compared their clinical characteristics and performed gene set enrichment analysis (GSEA) to identify the functional differences. Immune infiltration analyses were conducted using ESTIMATE, CIBERSORT, and ssGSEA. In addition, we evaluated the expression of the targets of immune checkpoint inhibitors (ICIs) and calculated the tumor mutation burden (TMB) of the tumor samples. Weighted gene co-expression network analysis (WGCNA) was used to identify the genes related to both ALKBH5/YTHDF1 expression and immunity. GSE39582 was utilized for external validation of immunological features between the two clusters. RESULTS: Cluster 2 had high expression of ALKBH5 and lesser so of YTHDF1, whereas Cluster 1 had just the reverse. Cluster 1 had a higher N stage and pathological stage than Cluster 2. The latter had stronger immune infiltration, higher expression of targets of ICIs, more TMB, and a larger proportion of deficiency in mismatch repair-microsatellite instability-high (dMMR-MSI-H) status than Cluster 1. Moreover, WGCNA revealed 14 genes, including PD1 and LAG3, related to both the expression of ALKBH5/YTHDF1 and immune scores. CONCLUSIONS: ALKBH5 and YTHDF1 influence immune contexture and can potentially transform cold tumors into hot tumors in patients with COAD.

Visual impairment in immunoglobulin G4-related disease: A case report.

The present study reports on the case of a 50-year-old male with sinusitis, diplopia, secretory otitis media and skin eczema for >14 years. The patient presented with visual impairment in both eyes and subxiphoid pain on admission to the First Affiliated Hospital of China Medical University (Shenyang, China). Orbital CT revealed a slightly thickened left inferior rectus muscle. Due to a periocular mass, enlarged lymph nodes, elevated serum immunoglobulin G4 (IgG4) levels and enriched IgG4-positive plasma cells in the lymph nodes, the diagnosis of IgG4-related disease (IgG4-RD), possibly involving at least 10 organs, was established. Following treatment with methylprednisolone, the serum IgG4 levels decreased to normal and binocular vision returned to normal. Unlike previously reported cases, the present case exhibited no swollen masses around the optic nerve. The purpose of the present case report was to improve the understanding of IgG4-RD.

LncRNA-PCAT1 controls the growth, metastasis and drug resistance of human colon cancer cells.

PURPOSE: The long non-coding (lnc) RNAs have been shown to exhibit profound regulatory roles in maintaining the growth and proliferation of human cancer cells. Taking this fact into consideration, the current research work was scheduled to explore the regulatory control of lncRNA-PCAT1 in maintaining the growth and progression of human colon cancer cell. METHODS: The expression of lncRNA-PCAT1 was assessed through qRT-PCR method. DAPI and acridine orange (AO)/ethidium bromide (EB) staining protocols along with the colony formation protocols were performed to evaluate the viability of cancer cells. The migratory and invasion properties of cancer cells were examined by the wound-healing and transwell assays, respectively. Western blotting was used to assess the expression of proteins of interest. MTT assay was used for the assessment of cell proliferation. RESULTS: lncRNA-PCAT1 was highly up-regulated in the colon cancer tissues and cancer cell lines. The repression of lncRNA-PCAT1 in colon cancer cells reduced their viability through induction of Bax/Bcl-2 mediated apoptosis. The inhibition of lncRNA-PCAT1 expression further declined the migration and invasion of colon cancer cells along with the decline of cell proliferation and enhanced the chemosensitivity of colon cancer cells. CONCLUSION: lncRNA-PCAT1 expression may be utilized as a vital prognostic tool in colon cancer and highlighted its regulatory effects in maintaining the colon cancer growth and proliferation.

Prognostic significance of PD-L1 expression on cell-surface vimentin-positive circulating tumor cells in gastric cancer patients.

Although circulating tumor cells (CTCs) have shown promise as potential biomarkers for diagnostic and prognostic assessment in gastric cancer (GC), determining the predictive and prognostic value of programmed death-ligand 1 (PD-L1)-positive CTCs in patients with GC is a challenge. Here, we identified that the expression of total vimentin (VIM) protein was positively correlated with PD-L1 and inhibited CD8+ T-cell activation in patients with GC according to bioinformatics analysis. Notably, coexpression of PD-L1 and cell-surface VIM (CSV) was detected by immunofluorescence and immunohistochemistry assay in locally advanced GC tumor specimens and metastatic lymph nodes. Likewise, CSV expression level was significantly decreased after transiently knocking down PD-L1 in GC cell lines. Based on our established CTC detection platform, CTCs were isolated from peripheral blood samples collected from 70 patients (38 resectable and 32 unresectable) with GC using magnetic positive selection and a CSV-specific monoclonal antibody, 84-1. CSV+ PD-L1+ CTCs were observed in 50 of 70 (71%) GC patient samples, ranging from 0 to 261 mL-1 . A higher number of CSV+ PD-L1+ CTCs were significantly associated with a short survival duration and poor therapeutic response. This study demonstrated that detection of PD-L1+ CTCs using a CSV-enrichment method has promising value as a clinically relevant prognostic marker for GC.

Growth arrest-specific protein 6 (Gas6) attenuates inflammatory injury and apoptosis in iodine-induced NOD.H-2h4 mice.

PURPOSE: Growth arrest-specific protein 6 (Gas6) is a vitamin K-dependent protein that plays an important role in the pathogenesis of autoimmune diseases. The purpose of this study was to explore the expression of Gas6 and its effects on autoimmune thyroiditis (AIT). METHOD: A total of 24 male NOD.H-2h4 mice were randomly assigned to three groups: (1) a control group supplied with regular water; (2) a sodium iodide (NaI) group supplied with 0.005% sodium iodide water; and (3) a group treated with recombinant mouse Gas6 (rmGas6) after iodine supplementation (NaI + Gas6 group). The severity of lymphocytic infiltration in the thyroid was measured through histopathology. Serum levels of tumor necrosis factor α (TNF-α), interleukin (IL) 6 and IL-1ß, as well as anti-thyroglobulin antibody (TgAb) titers were measured using an enzyme-linked immunosorbent assay. In addition, the expression of Gas6, Caspase 3, TAM receptors (Axl and MerTK), nuclear factor κB (NF-κB) and I-kappa-B α (IκB-α) were measured by Western blotting. Finally, the proportions of T cells were determined in the splenocytes of NOD.H-2h4 mice by flow cytometry. RESULTS: The mRNA and protein expression of Gas6 was significantly lower in the NaI group compared to the control group. Serum levels of TgAb, TNF-α, IL-6 and IL-1ß were also significantly higher in the NaI group but were dramatically reduced after rmGas6 injection. The prevalence of thyroiditis and the infiltration of lymphocytes were significantly lower in the NaI + Gas6 group compared to the NaI group. The protein expression of cleaved-Caspase 3, phosphorylation of MerTK, and NF-κB and IκB-α in the thyroid gland were significantly reduced after rmGas6 administration. The proportion of Th1, Th2 and Th17 cells in splenocytes were also significantly reduced after rmGas6 treatment, whereas there was a dramatic increase in the proportion of Treg cells. CONCLUSION: Gas6 exerts an anti-inflammatory effect in a mouse model of AIT and may therefore be a potential therapeutic target.

SIX1 is upregulated in gastric cancer and regulates proliferation and invasion by targeting the ERK pathway and promoting epithelial-mesenchymal transition.

Sine oculis homeobox homologue 1 (SIX1) is a Six class homeobox gene conserved throughout many species. It has been reported to act as an oncogene and is overexpressed in many cancers. However, the function and regulatory mechanism of SIX1 in gastric cancer (GC) remains unclear. In our study, we detected protein levels of SIX1 via immunohistochemistry (IHC) and its proliferation and invasion effects via CCK8 and transwell assays. Additionally, expression of cyclin D1, MMP2, p-ERK, and EMT-related proteins was measured by western blotting. We found that SIX1 had significantly higher expression in GC tissues and that it could promote GC cell proliferation and invasion. Also, overexpression of SIX1 increased the expression of cyclin D1, MMP2, p-ERK, and EMT-related proteins, which could all be inhibited by knocking down SIX1. In conclusion, SIX1 is upregulated in GC tissues. It can promote GC cell proliferation by targeting cyclin D1, invasion via ERK signalling, and EMT pathways by targeting MMP2 and E-cadherin. SIGNIFICANCE OF THE STUDY: Our study showed that SIX1 was upregulated in GC tissues, and promoted GC cell proliferation by targeting cyclin D1, invasion via ERK signalling, and EMT pathways by targeting MMP2 and E-cadherin. These results suggested the potential regulatory mechanism of SIX1 in proliferation and invasion of gastric cancer.

Plasma levels of TAM receptors and ligands in severe preeclampsia.

BACKGROUND: Preeclampsia (PE) is a multifactorial dysfunction characterized by hypertension with characteristics of systematic endothelial activation. It is widely accepted that vascular disorder and deficient trophoblast invasion are involved in PE. Tyro3/Axl/MerTK (TAM) family receptors are tyrosine-kinase receptors and may exert a diverse range of functions such as cell proliferation, migration, and vascular angiogenesis. The role of TAM signaling in severe PE patients remains unclear. Therefore, the aim of this study was to investigate involvement of the TAM axis in the pathogenesis of PE. METHODS: A total of 36 severe PE patients and 40 age- and gender-matched healthy pregnant women (controls) were enrolled in this study. Plasma levels of soluble TAM receptors (Tyro3, Axl, MerTK) and ligands (Gas6 and ProS) were then measured using an enzyme-linked immunosorbent assay (ELISA). We evaluated the association between the expression of these proteins and the clinical features of PE. RESULTS: Plasma levels of sMerTK and sAxl were significantly higher in severe PE patients than in control women during pregnancy. The plasma concentrations of sMerTK and sAxl in severe PE patients correlated positively with systolic and diastolic blood pressure, and plasma sAxl levels demonstrated a significant correlation to proteinuria. In contrast, reduced levels of Gas6 were inversely associated with urine protein in PE patients. CONCLUSIONS: Elevated expression of the plasma levels of sMerTK and sAxl, as well as the reduction of Gas6 were observed in severe PE patients. Furthermore, these changes were correlated with disease activity. TAM signaling might play a role in the pathogenesis of PE.

Myeloid related proteins are up-regulated in autoimmune thyroid diseases and activate toll-like receptor 4 and pro-inflammatory cytokines in vitro.

PURPOSE: Myeloid-related protein (MRP) family plays an important role in the promotion of cell proliferation and the production of inflammatory cytokines. We investigated the expression of MRP6, MRP8 and MRP14 in thyroid tissues, serum, and peripheral blood monocular cells (PBMCs) in patients with autoimmune thyroid diseases (AITD). METHOD: The expression of MRP6, MRP8, and MRP14 was investigated using immunohistochemical staining and quantitative real-time polymerase chain reaction in the thyroid glands of 7 patients with Graves' disease (GD), 8 with Hashimoto's thyroiditis (HT), and 7 healthy controls (HC). The serum levels of MRP8/MRP14 complex and MRP6 were investigated in 30 patients with GD, 36 with HT, and 30 with HC. The mRNA expression of MRP proteins in PBMCs was also explored. PBMCs from each group were incubated with MPRs and their effect on Toll-like receptor 4(TLR4) expression and their effect on the levels of the pro-inflammatory cytokines in supernatant were analyzed upon incubating with TLR4 and signaling pathways inhibitors. RESULTS: Serum levels of MRP8/MRP14 and MRP6 were up-regulated in patients with AITD. In addition, mRNA expression of MRP proteins in PBMCs and the thyroid gland was markedly elevated in AITD patients. MRP6 and MPR8 promoted the secretion of TNF-α and IL-6 in cultured PBMCs, and this elevation was more pronounced in AITD patients; we also found that this up-regulation was regulated by TLR4/phosphoinositide 3-kinase/nuclear factor-κB signaling pathway. CONCLUSION: The expression of MRP proteins was elevated in AITD patients. Therefore, an MRP-TLR4 dependent signaling may play an important role in the pathogenesis of AITD.

High expression of HAX-1 protein is associated with tumor growth in papillary thyroid carcinoma.

Papillary thyroid carcinoma (PTC) is the most common type of endocrine malignancy. HS1-associated protein X-1 (HAX-1) is an anti-apoptotic factor involved in the development of many types of cancer. However, its functional role in human PTC remains unclear. Here we investigated HAX-1 overexpression in human PTC samples and correlated with tumor size and TNM stage. Decreased expression of HAX-1 significantly inhibited proliferation, migration, and invasion in papillary thyroid cancer cell lines TPC1 and K1. Furthermore, we found that down-regulation of HAX-1 induced cell apoptosis. Our results suggest that HAX-1 plays a significant role in regulating the biological behavior in PTC cells and may contribute to PTC target therapy.

Role of the tumour necrosis factor-like weak inducer of apoptosis (TWEAK)/fibroblast growth factor-inducible 14 (Fn14) axis in autoimmune thyroid disease.

BACKGROUND: TNF-like weak inducer of apoptosis (TWEAK), its receptor fibroblast growth factor-inducible 14 (Fn14) and its scavenger receptor CD163 (sCD163) have known associations with many autoimmune diseases. However, the role of the TWEAK axis in autoimmune thyroid disease (AITD) remains unclear. Therefore, the aim of this study was to investigate the role of the TWEAK-Fn14 axis in the pathogenesis of AITD. METHODS: Serum levels of soluble TWEAK (sTWEAK) and sCD163 were measured in 38 patients with Graves' disease (GD), 40 patients with Hashimoto's thyroiditis (HT) and 40 healthy controls (HCs). Additionally, the mRNA expression of TWEAK and Fn14 in peripheral blood mononuclear cells (PBMCs) was explored, and the protein expression of TWEAK and Fn14 in thyroid glands surgically removed from 10 patients with GD, 10 patients with HT and 10 HCs was studied by immunohistochemical staining. RESULTS: The results showed that the serum levels of sTWEAK were significantly reduced in patients with HT and inversely correlated with antithyroid peroxidase antibody (TPOAb) levels. Additionally, high levels of sCD163 and a high sCD163/sTWEAK ratio were positively associated with the TPOAb levels in patients with HT and the thyrotropin receptor antibody (TRAb) levels in patients with GD. TWEAK mRNA expression and protein expression were upregulated in thyroid glands and PBMCs from patients with HT. CONCLUSION: Expression of the TWEAK-Fn14 axis was upregulated in patients with AITD and might play a role in the pathogenesis of AITD.

Expression of pyruvate dehydrogenase is an independent prognostic marker in gastric cancer.

AIM: To investigate the expression and prognostic role of pyruvate dehydrogenase (PDH) in gastric cancer (GC). METHODS: This study included 265 patients (194 male, 71 female, mean age 59 years (range, 29-81 years) with GC who underwent curative surgery at the First Affiliated Hospital of China Medical University from January 2006 to May 2007. All patients were followed up for more than 5 years. Patient-derived paraffin embedded GC specimens were collected for tissue microarrays (TMAs). We examined PDH expression by immunohistochemistry in TMAs containing tumor tissue and matched non-neoplastic mucosa. Immunoreactivity was evaluated independently by two researchers. Overall survival (OS) rates were determined using the Kaplan-Meier estimator. Correlations with other clinicopathologic factors were evaluated by two-tailed χ(2) tests or a two-tailed t-test. The Cox proportional-hazard model was used in univariate analysis and multivariate analysis to identify factors significantly correlated with prognosis. RESULTS: Immunohistochemistry showed that 35.47% of total cancer tissue specimens had cytoplasmic PDH staining. PDH expression was much higher in normal mucosa specimens (75.09%; P = 0.001). PDH expression was correlated with Lauren grade (70.77% in intestinal type vs 40.0% in diffuse type; P = 0.001), lymph node metastasis (65.43% with no metastasis vs 51.09% with metastasis; P = 0.033), lymphatic invasion (61.62% with no invasion vs 38.81% with invasion; P = 0.002), histologic subtypes (70.77% in intestinal type vs 40.0% in diffuse type; P = 0.001) and tumor-node-metastasis (TNM) stage (39% in poorly differentiated vs 65.91% in well differentiated and 67.11% in moderately differentiated; P = 0.001) in GC. PDH expression in cancer tissue was significantly associated with higher OS (P < 0.001). The multivariate analysis adjusted for age, Lauren classification, TNM stage, lymph node metastasis, histological type, tumor size, depth of invasion and lymphatic invasion showed that the PDH expression in GC was an independent prognostic factor for higher OS (HR = 0.608, 95%CI: 0.504-0.734, P < 0.001). CONCLUSION: Our study indicated that PDH expression is an independent prognostic factor in GC patients and that positive expression of PDH may be predictive of favorable outcomes.