Project description:Gastric cancer is one of the leading causes of cancer mortality worldwide, and peritoneal metastasis is a hallmark of incurable advanced gastric cancer. The identification of molecular vulnerability for such conditions is imperative to improve the prognosis of gastric cancer. Here, we comprehensively analysed cancer cells purified from malignant ascitic fluid samples and their corresponding cell lines from 98 patients, through whole-genome sequencing, whole transcriptome sequencing, methylation analyses, and genome-wide enhancer analyses.
Project description:Gastric cancer is one of the leading causes of cancer mortality worldwide, and peritoneal metastasis is a hallmark of incurable advanced gastric cancer. The identification of molecular vulnerability for such conditions is imperative to improve the prognosis of gastric cancer. Here, we comprehensively analysed cancer cells purified from malignant ascitic fluid samples and their corresponding cell lines from 98 patients, through whole-genome sequencing, whole transcriptome sequencing, methylation analyses, and genome-wide enhancer analyses.
Project description:Gastric cancer is one of the leading causes of cancer mortality worldwide, and peritoneal metastasis is a hallmark of incurable advanced gastric cancer. The identification of molecular vulnerability for such conditions is imperative to improve the prognosis of gastric cancer. Here, we comprehensively analysed cancer cells purified from malignant ascitic fluid samples and their corresponding cell lines from 98 patients, through whole-genome sequencing, whole transcriptome sequencing, methylation analyses, and genome-wide enhancer analyses.
Project description:Gastric cancer is one of the most aggressive cancers and is the second leading cause of cancer death worldwide. Approximately 40% of global gastric cancer cases occur in China, with peritoneal metastasis being the prevalent form of recurrence and metastasis in advanced disease (>50%). Currently, there are limited clinical approaches for predicting and treatment of peritoneal metastasis, resulting in a 6- month average survival time. By comprehensive genome analysis will uncover the pathogenesis of peritoneal metastasis. Here we describe a comprehensive whole-genome and transcriptome sequencing analysis of one advanced gastric cancer case, including non-cancerous mucosa, primary cancer and matched peritoneal metastatic cancer. The peripheral blood is used as normal control.
Project description:LncRNA and mRNA expression profiling for 7 human gastric cancr samples (3 tumor tissues and 3 tumor lymph node and 1 normal tissue) We have completed the metastasis-related Long Noncoding RNA expression profiling data microarray analysis of the 7 human gastric cancer related samples
Project description:LncRNA and mRNA expression profiling for 7 human gastric cancr samples (3 tumor tissues and 3 tumor lymph node and 1 normal tissue) We have completed the metastasis-related Long Noncoding RNA expression profiling data microarray analysis of the 7 human gastric cancer related samples In the study presented here, a consecutively operated, well-defined cohort of three gastric cancer tissues and three metastatic lymph nodes tissues compared with the normal tissues and lymph nodes tissues, followed up more than five years, was used to acquire expression profiles of a total of 1942 lncRNA and 1976 mRNA, leading to the successful construction of supervised
Project description:Peritoneal metastasis (PM) has a suppressive tumor immune microenvironment (TIME), which limits the effects of immunotherapy. This study aims to investigate the immunomodulatory effects of intraperitoneal administration of IL-33 on PM-associated TIME. Immunocompetent mice were used to investigate the role of IL-33 in development of abdominal dissemination and host outcome. Murine (m) and human (h) gastric cancer cells were tested for their response to IL-33 by qRT-PCR, flow cytometry, and immunofluorescence. Survival was significantly prolonged in patients with high Il-33 mRNA expression. Intraperitoneal administration of IL-33 could induce the celiac inflammatory environment, activate immunologic effector cells and reverse the immunosuppressive tumor microenvironment, which delayed tumor progression and peritoneal metastasis of gastric cancer. Mechanistically, IL-33 could induce M2 polarization by activating p38-GATA-binding protein 3 (GATA3) signaling pathway. IL-33 combined with anti-CSF1R or p38 inhibitor to regulate tumor-associated macrophages (TAMs) showed synergistic anti-tumor effect. Intraperitoneal administration of IL-33 inducing local inflammatory milieu provided a novel approach for the treatment of metastatic peritoneal malignancies, which combined with TAMs reprogramming to reshape TIME could achieve better treatment efficacy.
Project description:HGSOC, the most aggressive form of OC, is characterized by insidious onset, rapid intraperitoneal spread and development of massive ascites. Peritoneal adhesion was considered as the first step of abdominal metastasis, underscoring that only tumor cells gain access to peritoneal adherence contribute to metastasis. Studies on ovarian cancer progression were mainly focused on the primary and metastatic tumor cells, while understanding of the ascitic tumor cells is limited. We hypothesized that uncovering the gene expression profiles of ascitic tumor cells from high grade serous ovarian cancer patients will allow us to understand more specifically their unique phenotype which mediates the peritoneal adhesion. In this study, gene expression profiling was completed for 15 magnetic sorted tumor cells samples from matched primary tumors, ascites and metastases of 5 high grade serous ovarian cancer patients. By comparing the expression data from ascitic tumor cells with primary and metastasis tumor cells, we identified a set of differential expressed genes in ovarian ascitic tumor cells advantageous for peritoneal adhesion and metastasis. Further study revealed that ascites microenvironment modulated the ascitic tumor cells phenotype and contributed to ovarian cancer dissemination through facilitating CAFs in formation of compact spheroids with ascitic tumor cells. We used microarrays to profile the expression of 15 matched tumor cells samples in order to identify molecular alteration between primary tumor cells, ascitic tumor cells and metastatic tumor cells in high grade serous ovarian cancer.
Project description:Metastasis associated 1 family, member 2 (MTA2) gene is classified to metastasis associated gene family. We have previously reported that MTA2 gene was overexpressed in gastric cancer tissues, correlating with tumor invasion, lymph node metastasis, and advanced TNM stage. MTA2 knockdown significantly inhibited gastric cancer cell invasion and metastasis. Yet, its molecular mechanisms are still unclear. The aim of this study is to investigate the molecular mechanisms of MTA2 in regulating malignant behaviors of gastric cancer. This experiment captures the expression data between BGC-823/NC and BGC-823/MTA2, SGC-7901/NC and SGC-7901/shMTA2 cells using Whole human genome microarray 4×44K (Design ID: 014850, Agilent technologies).