Levels In Gastric Cancer Research Articles

Immunogenomics Analysis Reveals that TP53 Mutations Inhibit Tumor Immunity in Gastric Cancer

Although immunotherapy continues to demonstrate efficacy in a variety of refractory cancers, currently, no any immunotherapeutic strategy is clinically used for gastric cancer (GC) except its microsatellite instable subtype. Thus, it is important to identify molecular biomarkers for predicting the responders to GC immunotherapy. TP53 mutations frequently occur in GC and are associated with unfavorable clinical outcomes in GC. We performed a comprehensive characterization of the associations between TP53 mutations and immune activities in GC based on two large-scale GC cancer genomics data. We compared expression and enrichment levels of 787 immune-related genes and 23 immune gene-sets among TP53-mutated GCs, TP53‐wildtype GCs, and normal tissue, and explored the correlations between p53-mediated pathways and immune activities in GC. Strikingly, almost all analyzed immune gene-sets were significantly downregulated in enrichment levels in TP53-mutated GCs compared to TP53‐wildtype GCs. These less active immune pathways and cell types in TP53-mutated GCs included 15 immune cell types and function, tumor-infiltrating lymphocytes, regulatory T cells, immune checkpoint, cytokine and cytokine receptor, human leukocyte antigen, pro‐inflammatory, and parainflammation. Moreover, we identified a number of p53-mediated pathways and proteins that were significantly associated with immune activities in GC. Furthermore, we demonstrated that the TP53 mutation itself could result in the depressed immune activities in GC and other cancer types. We revealed that chromosomal instability was an important mechanism for the depressed tumor immunity in TP53-mutated cancers. Finally, we showed that immune cell infiltration and immune activities were likely positively associated with survival prognosis in GC. Our findings suggest that p53 may play an important role in activating tumor immunity in GC and other cancer types and that the TP53 mutation status could be useful in stratifying cancer patients responsive to a certain immunotherapy.

Downregulation of peroxiredoxin II suppresses the proliferation and metastasis of gastric cancer cells.

Peroxiredoxin (Prx) II is an imperative member of the superfamily of peroxidases. It serves an essential role in scavenging organic hydroperoxide and H2O2. It is involved in the development of various malignant tumors. In order to investigate the significance of Prx II expressions level in gastric cancer (GC), downregulation of Prx II was performed to investigate its role in the proliferation and migration of gastric adenocarcinoma cells. In GC cells and 45 GC specimens, the mRNA and protein expression levels of Prx II were determined using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis, respectively. The Prx II expression profile in another 116 GC specimens was also detected with immunohistochemistry (IHC). The changes in the proliferation and migration of MKN45 and MGC-803 cells folllowing transfection with small interfering RNA (siRNA) were detected by cell counting kit (CCK)-8, western blot analysis, and Transwell migration and invasion assays. The results revealed that the expression of Prx II in GC tissues and GC cells were significantly upregulated compared with the normal control. There was a significant association between the expression level of Prx II and various factors, including tumor size, histological differentiation, the depth of invasion, the stage of tumor-node-metastasis (TNM) and lymph node metastasis in GC (P<0.05). Survival in patients with higher Prx II expression was significantly decreased compared with those with lower Prx II expression (P<0.01). Prx II, depth of invasion, lymph node metastasis and distant metastasis were identified as independent prognosis factors of GC (P<0.05). Knockdown of Prx II significantly suppressed the proliferation and the migration of GC cells. These experiments revealed that Prx II promotes the development of GC, affecting the survival of patients with GC.

Clinical significance of ADAM29 promoting the invasion and growth of gastric cancer cells in vitro.

ADAM metallopeptidase domain 29 (ADAM29) belongs to the ADAM family, is a type I integral membrane protein and secrets a glycoprotein that mediates cell-cell and cell-matrix interaction. Aberrant expression of ADAM29 is involved in a number of physiological processes diversification. The purpose of the present study was to investigate the expression and biological effect of ADAM29 in human gastric cancer (GC) specimens and cell lines in vitro. The expression of ADAM29 was examined in 83 GC samples and 25 adjacent normal gastric tissues using quantitative reverse transcriptase-quantitative polymerase chain reaction and immunohistochemistry. The association between ADAM29 expression and cellular function of GC cells was assessed in vitro. The ADAM29 mRNA levels were significantly elevated in GC tissues compared with paracancerous tissues. Increased levels of ADAM29 were associated with high-grade staging and high Tumor-Node-Metastasis stages. Kaplan-Meier survival curves demonstrated that patients with GC and low ADAM29 transcript levels exhibited longer overall survival (OS) (P<0.01) and progression-free survival (PFS) time (P<0.01) compared with patients with high ADAM29 expression levels. ADAM29 significantly promoted the proliferation, migration and invasion of GC cells in vitro when overexpressed in MGC803 cells and knocked down in AGS cells. ADAM29 was increased in GC and the elevated expression of ADAM29 was associated with a poor survival rate of patients. ADAM29 may become a prognostic factor and therapeutic candidate for human GC.

Role of infiltrating CD8 lymphocytes, microsatellite instability and h. pylori level in gastric cancer.

e16096Background: Modulation of immune system has demonstrated tumor response in Gastric Cancer. Tumor infiltrating lymphocytes and microsatellite instability are predictive biomarkers for response...

Overexpression of Kin of IRRE-Like Protein 1 (KIRREL) in Gastric Cancer and Its Clinical Prognostic Significance.

BackgroundThe aim of this study was to examine the expression level of IRRE-like protein 1 (KIRREL) in gastric cancer (GC) and to explore its prognostic significance.Material/MethodsBioinformatics methods were used to predict the differential expression levels of KIRREL mRNA in GC and normal gastric tissues by mining cancer-related databases (TCGA and Oncomine). Immunohistochemistry was done to verify the KIRREL protein expression levels in 71 cases of GC tissues combined with matched normal tissues. The relationship between clinicopathologic parameters and KIRREL differential expression levels in GC was investigated by the chi-square test. Kaplan-Meier univariate and Cox multivariate survival analyses were performed to explore the prognostic significance of KIRREL expression in GC patients.ResultsTCGA and GEO data analyses showed that KIRREL mRNA expression level was remarkably higher in GC than that in normal gastric tissues (both P<0.05). KIRREL mRNA levels were dramatically increased from stage I to stage IV (P=0.037). Immunohistochemical results showed that the high positive rate of KIRREL staining in GC was 61.97% (44/71). Moreover, GC patients with KIRREL mRNA or protein high levels had significantly shorter overall survival times than those with KIRREL mRNA or low protein levels (All P<0.05). Additionally, Cox multivariate survival analysis revealed that KIRREL differential expression levels (low vs. high) were the only independent parameter predicting the prognosis of GC patients (P=0.000).ConclusionsKIRREL was overexpressed in GC and the overexpression of KIRREL could serve as an independent predictor of poor prognosis in GC patients.

Overexpression of HACE1 in gastric cancer inhibits tumor aggressiveness by impeding cell proliferation and migration.

HACE1 E3 ligase was discovered to be down‐regulated in several cancers while its role in regulating tumors was merely understood. This study aimed to explore the specific effect of HACE1 played in gastric tumorigenesis and its potential mechanism. HACE1's expression was found significantly lower in gastric cancer tissues compared with the adjacent normal tissues (P < 0.001). Its protein level in gastric cancer negatively correlated to tumor pathological differentiation (P = 0.019). And in gastric cancer patients with TNM I‐IIIa, those with lower HACE1 protein level had poorer overall survival (P = 0.025). Studies, in vivo and in vitro, showed that overexpressing HACE1 inhibited tumor proliferation and migration, and enhanced cell apoptosis. Besides, ectopic expression of HACE1 down‐regulated the protein level of β‐catenin and inhibited the activity of the Wnt/β‐catenin signaling pathway. All the cellular functions were abolished when we overexpressed inactive HACE1‐deltaHECT. Above all, we demonstrated that HACE1 E3 ligase played a suppressive role in gastric tumorigenesis and inhibited the activity of the Wnt/β‐catenin signaling pathway. Circumventing the decline of HACE1 in early stage of carcinoma may impede the tumorigenesis and malignant process of gastric cancer.

High Expression of Retinoic Acid Induced 14 (RAI14) in Gastric Cancer and Its Prognostic Value.

BackgroundTo explore the expression level of retinoic acid induced 14 (RAI14) in gastric cancer (GC) patients and its potentially clinical prognostic value.Material/MethodsInitially, The Cancer Genome Atlas (TCGA) and Oncomine databases were mined to examine the differential expression levels and clinical prognostic significance of RAI14 mRNA in GC patients. Subsequently, 68 cases of GC and paired adjacent normal tissues were collected retrospectively, and the expression level of RAI14 protein was detected by immunohistochemical staining. In addition, Kaplan-Meier univariate and Cox multivariate survival analyses were used to verify the correlation between RAI14 expression and clinicopathological parameters in GC patients and its clinical prognostic significance.ResultsTCGA and GEO (from Oncomine database) data mining results found that RAI14 mRNA level was remarkably higher in GC than normal gastric tissues (All P<0.05). Besides, immunohistochemical results detected that RAI14 protein level in GC was dramatically higher (P=0.004) compared to that in the matched normal tissues. Moreover, TCGA database and Kaplan-Meier Plotter mining results showed that compared to those with RAI14 low mRNA expression levels, GC patients with RAI14 high mRNA expression levels had remarkably lower time of both overall survival and disease-free survival (All P<0.05). Additionally, based on the immunohistochemical results, Kaplan-Meier univariate and Cox multivariate survival analyses indicated that high expression of RAI14 was the only independent predictor of unfavorable prognosis in patients with gastric cancer (P=0.000).ConclusionsRAI14 was highly expressed in GC, and the high expression of RAI14 could be an independent predictor of poor prognosis in GC patients.

Circulating SH2B1 is associated with an increased risk of gastric cancer.

Gastric cancer (GC) is one of the most common types of cancer in humans and the second leading cause of cancer-associated mortality worldwide. Identifying novel risk factors will facilitate the development of therapeutic strategies to prevent and treat GC. Increased expression of the Src homology 2 B adaptor protein 1 (SH2B1) may stimulate the malignant progression of lung cancer, esophageal cancer and neuroblastoma. However, its function in GC has not yet been investigated. To identify whether increased serum SH2B1 is a risk factor for GC, the present study performed a nested case-control study of patients within the Chinese cohort study. Levels of serum SH2B1 were measured in 563 patients diagnosed with GC during the follow-up period and in 1,126 matched healthy controls. The results demonstrated that high levels of serum SH2B1 were associated with an increased GC risk (odds ratio, 3.23; 95% confidence interval, 2.45-5.65). When analyses were stratified further by sex, age and smoking, an association between increased levels of SH2B1 and GC was identified in males but not in females. Furthermore, the association between SH2B1 levels and GC was more evident in younger than in older participants, and statistically significant in current smokers but not in nonsmokers. These results were not altered following the exclusion of outliers. Furthermore, it was demonstrated that overexpression of SH2B1 contributes to the malignant transformation of normal gastric epithelial cells. Thus, the present study demonstrated that elevated serum SH2B1 levels may increase the risk of GC.

Clinical prognostic value of A FOXM1 related long non-coding RNA expression in gastric cancer.

The aim of this study was to explore FOXM1-related LncRNA 1(FRLnc1) expression level in gastric cancer (GC) and demonstrate its association with the prognosis. A total of 173 GC patients from Affiliated Hospital of Jining Medical University were enrolled in the study. GC tissue samples were quantified for FRLnc1 expression level using quantitative PCR (qPCR) method. The relevance between FRLnc1 expression and clinicopathological features was determined by x2-test. The association between FRLnc1 expression and overall survival was estimated by the Kaplan-Meier method. Multivariate and univariate analysis were performed to explore whether FRLnc1 was an independent prognostic factor for GC patients. We found that FRLnc1 expression was higher in GC tissues than corresponding adjacent tissues (p < 0.01). Increased FRLnc1 expression was associated with depth of tumor (p = 0.004), differentiation degree (p = 0.032), distant metastasis (p = 0.007), TNM stage (p = 0.006) and lymph node metastasis (p = 0.012). More importantly, Kaplan-Meier survival analysis demonstrated that overall patient survival for those with low FRLnc1 expression was significantly longer than those patients with high FRLnc1 expression (p < 0.001). Multivariate analysis suggested that FRLnc1 expression was an independent prognostic marker for survival in patients with GC. The data presented in this work firstly suggested that FRLnc1 may be a prognostic predictor in GC.

Overexpression of NEK3 is associated with poor prognosis in patients with gastric cancer.

The NIMA-related kinase 3 (NEK3) plays an important role in cell migration, cell proliferation, and cell viability. Recently, NEK3 was reported to enhance the malignancy of breast cancer. However, its role in gastric cancer has not been completely characterized. In this study, we explored the prognostic significance of NEK3 in human gastric cancer. Reverse transcription-polymerase chain reaction and western blot were performed to detect the NEK3 mRNA and protein expression in 6 paired fresh human gastric cancer tissues and surrounding normal tissues. NEK3 levels in gastric cancer and its adjacent normal samples of 168 cases were detected by immunohistochemistry, and the relationships between the NEK3 level and various clinicopathological features were analyzed. NEK3 mRNA and protein were significantly overexpressed in gastric cancer tissues, compared with adjacent normal tissues. Immunohistochemistry staining assay showed the percentage of high NEK3 expression in gastric cancer samples was higher than that in adjacent normal samples. NEK3 overexpression was significantly correlated with pT stage, pathologic TNM stage, lymph node metastasis, and poor prognosis of gastric cancer. Cox multivariate regression analyses suggested that NEK3 was an independent prognostic factor for survival of patients with gastric cancer. The data demonstrate that NEK3 is overexpressed in gastric cancer, which promotes the malignancy of gastric cancer. NEK3 may be as a prognostic biomarker and a potential therapeutic target for gastric cancer.

Long noncoding RNA MALAT1 regulates autophagy associated chemoresistance via miR-23b-3p sequestration in gastric cancer

BackgroundChemoresistance has long been recognized as a major obstacle in cancer therapy. Clarifying the underlying mechanism of chemoresistance would result in novel strategies to improve patient’s response to chemotherapeutics.MethodslncRNA expression levels in gastric cancer (GC) cells was detected by quantitative real-time PCR (qPCR). MALAT1 shRNAs and overexpression vector were transfected into GC cells to down-regulate or up-regulate MALAT1 expression. In vitro and in vivo assays were performed to investigate the functional role of MALAT1 in autophagy associated chemoresistance.ResultsWe showed that chemoresistant GC cells had higher levels of MALAT1 and increased autophagy compared with parental cells. Silencing of MALAT1 inhibited chemo-induced autophagy, whereas MALAT1 promoted autophagy in gastric cancer cells. Knockdown of MALAT1 sensitized GC cells to chemotherapeutics. MALAT1 acts as a competing endogenous RNA for miR-23b-3p and attenuates the inhibitory effect of miR-23b-3p on ATG12, leading to chemo-induced autophagy and chemoresistance in GC cells.ConclusionsTaken together, our study revealed a novel mechanism of lncRNA-regulated autophagy-related chemoresistance in GC, casting new lights on the understanding of chemoresistance.

Ten-eleven translocation 1 dysfunction reduces 5-hydroxymethylcytosine expression levels in gastric cancer cells.

A sixth base, 5-hydroxymethylcytosine (5hmC), is formed by the oxidation of 5-methylcytosine (5mC) via the catalysis of the ten-eleven translocation (TET) protein family in cells. Expression levels of 5hmC are frequently depleted during carcinogenesis. However, the detailed mechanisms underlying the depletion of 5hmC expression in gastric cancer cells remains unclear, and further research is required. The present study examined the expression levels of 5mC and 5hmC and the expression levels of TET1 and TET2 in gastric cancer tissues using immunohistochemistry. The results revealed that 5hmC expression levels were markedly lower in gastric cancer tissues compared with corresponding adjacent normal tissues. Furthermore, a decrease in 5hmC expression levels was associated with a decrease in TET1 protein expression levels in gastric cancer tissues. The ectopic expression level of TET1 may increase the 5hmC expression level in gastric cancer cells. In addition, the results revealed that TET1 protein expression was markedly different in regards to subcellular localization, and mislocalization was significantly associated with the depletion of 5hmC expression levels in gastric cancer. Together, the results of the present study indicated that TET1 dysfunction reduces 5hmC expression levels, and this phenomenon may serve a crucial role in gastric cancer progression.

MDM2 binding protein as a predictor of metastasis and a novel prognostic biomarker in patients with gastric cancer.

MDM2 binding protein (MTBP) has been revealed to be involved in cancer progression and metastasis. However, the role and clinical implication of MTBP expression in gastric cancer (GC) remains poorly understood. The present study aimed to investigate the clinicopathological significance of MTBP and the prognostic determinant in GC. The expression level of MTBP was examined in cancerous and matched adjacent noncancerous gastric mucosa tissues by reverse transcription-quantitative polymerase chain reaction and western blotting. MTBP expression levels were evaluated by immunohistochemical analysis of tissue microarrays for 352 patients, and association between the expression levels and prognosis in patients with GC were investigated. Kaplan-Meier analysis and Cox's regression models were used to investigate the associations between MTBP expression and prognosis of GC patients. The results of the present study revealed decreased MTBP mRNA (P=0.005) and protein (P=0.001) expression levels in tumor tissue compared with in matched adjacent normal tissue mucosa. MTBP expression level in GC was associated with gender (P=0.026), lymph node metastasis (P<0.001), distant metastasis (P=0.026) and pathological tumor-node-metastasis stage (P<0.001). Kaplan-Meier survival analysis demonstrated that patients with high MTBP expression levels exhibited longer survival times compared with patients with low MTBP expression levels. The multivariate logistic regression analysis revealed that MTBP was independently associated with the presence of lymph node [OR, 0.282; 95% confidence interval (CI), 0.161–0.494; P<0.001] and distant metastasis (OR, 0.365; 95% CI, 0.138–0.965; P=0.042). Furthermore, the multivariate Cox analysis revealed that low MTBP expression level was significantly associated with longer overall survival time and was recognized as an independent prognostic factor of patient's survival. MTBP expression level was significantly associated with progression and metastasis in GC, suggesting that MTBP may be used as a predictive marker for patient prognosis of GC.

Differential expression of two genes Oct-4 and MUC5AC associates with poor outcome in patients with gastric cancer.

Gastric cancer (GC) is the most frequent leading cause of cancer-associated mortality worldwide that is linked to poor prognosis due to the lack of appropriate biomarkers. Our aim was to evaluate the MUC5AC and Oct-4 expression levels in GC and to assess their association with clinical factors. Immunohistochemical analysis (IHC) and qRT-PCR were performed in GC patients to examine the MUC5AC and Oct-4 expression levels. The mRNA level of MUC5AC was significantly decreased in tumour tissues compared with non-cancerous tissues (1.11±0.69 vs 3.7±0.71; P=.024). On the other hand, Oct-4 mRNA level was upregulated in tumour tissues as compared to normal tissues (2. 86±0.78 vs 0.87±0.54; P=.0015). Decreased expression of MUC5AC was detected in 27 patients (67.5%), while high to moderate expression levels were observed in 13 cases (32.5%), but in normal tissues the expression levels of MUC5AC were increased (P=.001). The decreased expression of MUC5AC was associated with aggressive tumour characteristics, such as TNM stage (P=.023), histologic type (P=.012) and lymph node metastasis (P=.001). High expression of Oct-4 was detected in 24 tumour tissues (60%), while 16 cases (40%) showed low expression level. Increased Oct-4 expression was correlated with clinicopathological characteristics such TNM stage (P=.002), histologic type (P=.008) and lymph node metastasis (P=.001). Our results showed that high Oct-4 expression and the reduction of MUC5AC expression may be involved in the progression and an unfavorable prognosis of GC.

High level of homeobox A9 and PBX homeobox 3 expression in gastric cancer correlates with poor prognosis.

The homeobox protein homeobox (HOXA9) is a transcriptional factor that regulates patterning during embryogenesis and controls cell differentiation. HOXA9 dysfunction has been implicated in certain cancers. However, the role of HOXA9 in gastric cancer is poorly understood. The present study investigated HOXA9 and its cofactor PBX homeobox 3 (PBX3) expression in patients with gastric cancer. Paired tissue samples from 24 patients and paraffin embedded tissues of gastric cancer patients (104 males and 24 females) were included. HOXA9 and PBX3 expression levels were determined by reverse transcription quantitative polymerase chain reaction in fresh tissues, and by immunohistochemical staining in paraffin embedded tissues. The association between HOXA9/PBX3 expression and clinicopathological features was established. The results demonstrated that HOXA9 and PBX3 mRNA levels were significantly upregulated (P=0.032 for HOXA9 and P=0.031 for PBX3) in gastric cancer tissue. Immunohistochemical staining revealed that HOXA9 expression was associated with differentiation, lymph node metastasis and tumor-node-metastasis (TNM) stage, and PBX3 expression was associated with lymph node metastasis and TNM stage. Correlation analysis revealed a high coincidental expression of HOXA9 and PBX3 levels in gastric cancer (r=0.391; P<0.001). Survival analysis showed that high expression of HOXA9 or PBX3 was associated with poor survival of gastric cancer, and multivariate analysis using Cox's regression model showed that PBX3 expression was an independent prognostic factor in gastric cancer. There was elevated expression of HOXA9 and PBX3 in gastric cancer patients, and high-level expression of those proteins was associated with poor prognosis of gastric cancer. The present study underlines the significance of HOXA9/PBX3 in the development of gastric cancer.

MECP2 expression in gastric cancer and its correlation with clinical pathological parameters.

This study is to investigate the expression of methyl CpG binding protein 2 (MECP2) in gastric cancer (GC) and its clinical significance.Expression of MECP2 was analyzed in 69 cases of GC tissues and 12 paracancerous tissues, either by qRT-PCR at the mRNA level or by Western blot and immunochemistry at the protein level. The correlation of MECP2 expression with clinicopathological parameters was analyzed in the 69 GC patients, and validated in data from the TCGA database. The effect of MECP2 expression on survival was also investigated.MECP2 was significantly increased at both mRNA and protein levels in GC compared with paracancerous tissues. MECP2 positive expression was significantly correlated with the TNM stages, histological types, and lymph node metastasis status, but was not correlated with sex or age. Significantly shorter overall survival and disease-free survival was observed in MECP2 positive GC cases compared with the MECP2 negative cases. Univariate and multivariate analyses showed that gender, histological type, lymph node metastasis, and MECP2 expression were independent prognostic factors of GC.The dysregulated expression of MECP2 in GC and its correlation to clinicopathological parameters indicate that MECP2 may regulate the development of GC.

MiR-182-5p improves the viability, mitosis, migration, and invasion ability of human gastric cancer cells by down-regulating RAB27A.

We investigated the effect of miR-182-5p on the viability, proliferation, invasion, and migration ability of human gastric cells by regulating the expression of RAB27A. Real-time PCR assay was used to detect the expression of miR-182-5 and RAB27A in human gastric carcinoma tissues, para-carcinoma tissues, and different cell lines. Western blotting was also used to determine the RAB27A expression in both tissues and cell lines. We chose the HGC-27 cell line as experiment subject as it demonstrated the highest miR-182-5p level. HGC-27 cells were transfected with different vectors and the cell viability, mitosis, invasion, and migration ability were measured through MTT assay, flow cytometry (FCM) analysis, Transwell assay, and wound healing assay. In comparison with the normal tissues, miR-182-5p is expressed at a higher level in gastric cancer (GC) tissues, while RAB27A is expressed at a lower level in cancerous tissues. The down-regulation of miR-182-5p and up-regulation of RAB27A can significantly decrease the viability, migration, invasion, and mitosis of HGC-27 cells. The target relationship between miR-182-5p and RAb27A was confirmed through a dual-luciferase reporter gene assay and Western blot assay. miR-182-5p enhances the viability, mitosis, migration, and invasion of human GC cells by down-regulating RAB27A.

PD-001 - Interference of PG2 TATA BOX region with the serum PG2 level in gastric cancer

PD-001 - Interference of PG2 TATA BOX region with the serum PG2 level in gastric cancer

Long non-coding RNA HOXA transcript at the distal tip as a biomarker for gastric cancer.

A long non-coding RNA named HOXA transcript at the distal tip (HOTTIP) has been reported to be significantly increased in several cancers, including hepatocellular cancer, pancreatic cancer and lung cancer. However, the clinical value of HOTTIP expression in gastric cancer remains unknown. The present study aimed to investigate HOTTIP expression levels in gastric cancer and to elucidate its clinical significance. Reverse transcription polymerase chain reaction was used to assess the expression level of HOTTIP in gastric cancer cell lines and tissues. In a cohort of 94 patients with gastric cancer, HOTTIP expression was significantly lower in cancer tissues compared with the normal adjacent tissues. In addition, receiver operating characteristic (ROC) curve analysis was performed to evaluate the diagnostic value of HOTTIP in gastric cancer, and the area under the ROC curve was 0.767. In conclusion, the results of the present study indicated that HOTTIP may be a predictive biomarker for gastric cancer.

Serum IL-33 level is a predictor of progression-free survival after chemotherapy.

This study aimed to evaluate the association between of serum IL-33 (sIL-33) level in gastric cancer (GC) patients and progression-free survival (PFS). A total of 62 patients with advanced GC and 32 healthy subjects were enrolled. sIL-33 level was detected in pre-chemotherapy patients, post-chemotherapy patients and healthy subjects, respectively. sIL-33 levels were 131.9 (95% CI 105.9-184.9) pg/mL, 95.1 (95% CI 70.8-140.2) pg/mL and 95.7 (95% CI 73.3-114.3) pg/mL in pre-chemotherapy patients, post-chemotherapy patients and controls, respectively. The sIL-33 level in pre-chemotherapy patients was significantly higher than that in both post-chemotherapy patients and controls (P < 0.001 and P < 0.001, respectively). There was no statistically significant difference between the sIL-33 levels in post-chemotherapy patients and controls (P > 0.05). PFS in patients with the decline extent > 30.1% (median PFS not reached) was statistically significant longer than that (median PFS 7 months, 95% CI 1.569 - 12.431) in patients with the decline extent ≤ 30.1% (P = 0.003). The decline extent of sIL-33 level (> 30.1%) was associated with longer PFS (P = 0.006). Distant metastasis was associated with the decline extent of sIL-33 level (P = 0.034). The decline extent of sIL-33 after chemoresistance could be regarded as a predictor of the PFS of GC patients.