Searching for the novel tumour biomarkers is pressing for gastric cancer diagnostication and prognostication. The serum specimens from patients diagnosed with locally advanced gastric carcinoma before operation and 4 week after surgery were collected, respectively, and serum proteome profiling was conducted by liquid chromatography–mass spectrometry (MS)/MS. Fifty‐five proteins were identified to be up‐regulated and 16 proteins were down‐regulated, and these differentially expressed proteins participated in various biological processes. Serum levels of SOX3, one of down‐regulated proteins, in stomach cancer patients were higher than in healthy controls. SOX3 levels in cancer tissues were remarkably related to tumour differentiation, lymph node metastasis, primary tumour invasion and pTNM (pathological TNM) stage. Analysis with The Cancer Genome Atlas database indicated that SOX3 level and pTNM stage were the independent risk factors for the patient survival and that the overall survival was negatively associated with the SOX3 levels. Loss‐of‐function showed that SOX3 promoted gastric cancer cell invasion and migration in vitro and in vivo. SOX3 silence inhibits the expression of MMP9, and SOX3 is responsible for MMP9 expression transcriptionally. Our study highlights the potentiality of the paired pre‐ and post‐operation serum proteome signatures for the detection of biomarkers and reveals that SOX3 may serve as a candidate prognosis marker for gastric cancer.

Background The dysregulated long non-coding RNA (lncRNA) small nucleolar RNA host genes ( SNHGs ) have been demonstrated to be involved in gastric carcinogenesis and progression; however, the role of SNHG17 in gastric carcinoma remains to be investigated. We aimed to ascertain the expression of SNHG17 in gastric carcinoma tissues and cell lines, and to investigate its mechanistic role in this malignancy. Methods The expression levels of SNHG17 , P15 , P16 , P18 , P19 and cyclin dependent kinases-4 (CDK4) were determined by real-time quantitative polymerase chain reaction (RT-qPCR) and/or western blotting in human gastric cancer tissues and cell lines. Correlations between SNHG17 levels and clinicopathological features were evaluated. siRNAs were used to silence SNHG17 in cell lines, and then Cell Counting Kit-8, colony formation, and transwell migration assays were used to assess proliferation, clonogenic potential, and migration, respectively. Flow cytometry was used to analyze cell cycle distributions and apoptosis. In vivo tumorigenicity was evaluated using xenografts in nude mice. Results Analysis of The Cancer Genome Atlas (TCGA) database revealed that SNHG17 expression was remarkably higher in gastric carcinoma tissues than normal stomach mucosae (P=4.85×10 −10 ). We confirmed that SNHG17 was overexpressed in gastric cancer tissues (P<0.0001) and cell lines (P<0.01) compared with corresponding noncancerous tissues and gastric epithelial cell line, respectively. Furthermore, SNHG17 levels in tumor tissues were associated with lymph node metastasis (P=0.0006), pTNM stage (P=0.0061), and lymphovascular invasion (P=0.0005), but were not associated with overall survival (OS) (P=0.888). Loss-of-function studies indicated that SNHG17 promoted gastric carcinoma cell proliferation in vitro and in vivo (P<0.01), and that SNHG17 enhanced gastric cancer cell migration (P<0.01). Mechanistically, we found that SNHG17 inhibited P15 and P16 , and enhanced CDK4 expression, resulting in a G0/G1 cell cycle arrest, and that SNHG17 inhibited cell apoptosis. Conclusions These preliminary findings highlight the role of SNHG17 in gastric cancer, and suggest that it may be a novel indicator and/or a potential therapeutic target for diagnosing and/or treating gastric cancer.

Objective: To evaluate the survival outcomes of patients who underwent conversion surgery for metastatic pancreatic ductal adenocarcinoma (mPDAC) after neoadjuvant therapy (NAT) and to identify potential candidates that may benefit from this treatment strategy. Background: The role and eligibility population of conversion surgery for mPDAC remains controversial in the era of NAT. Methods: A consecutive cohort of patients diagnosed with mPDAC and treated with NAT followed by conversion surgery between 2019 and 2021 were confirmed from a prospective database maintained by the Department of Pancreatic Hepatobiliary Surgery of Changhai Hospital. In accordance with residual metastases and technical resectability after NAT, patients were classified as the complete pathological response of metastases (ypM0) resection group, residual metastases (ypM1) resection group, and exploration group. Median overall survival (mOS) was calculated using the Kaplan-Meier method, uni- and multivariable cox regression was performed to identify clinicopathological predictors of OS. Results: A total of 244 patients with mPDAC were identified from the prospective database, with 19 (7.8%) patients who underwent ypM0 resection, 22 (9.0%) underwent ypM1 resection, and 23 (9.4%) underwent explorative laparotomy. The mOS was 32.6 months for ypM0 resected patients, 15.1 months for ypM1 resected patients, and 13.4 months for those who underwent explorative laparotomy (P < .001). Univariable and multivariable Cox regression analyses confirmed that ypM0 resection, normalization of preoperative CA19-9 levels, and continued adjuvant therapy were independent prognostic factors of conversion surgery for mPDAC after NAT. Subgroup analyses revealed that oligometastases and continued adjuvant therapy were associated with improved prognosis in the ypM1 resection group. Conclusion: In patients with mPDAC who underwent NAT followed by conversion surgery, the complete pathological response of metastases, normalization of preoperative CA19-9 levels, and continued adjuvant therapy were independent risk factors for prognosis. Patients with residual oligometastases after treatment were expected to prolong survival through resection. These patients may benefit from conversion surgery and should be potential candidates for this treatment strategy.