Publications by authors named "Beidi Wang"

To explore the association between exposure to polycyclic aromatic hydrocarbons (PAHs) and endometriosis risk. Data were obtained from the 2003-2006 National Health and Nutrition Examination Survey database. Urinary concentrations of PAHs were divided into quartiles, and weighted multivariate logistic regression, restricted cubic spline, and subgroup analyses were performed.

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Background: PD-1 inhibitors have been approved for the first-line treatment of patients with advanced gastric cancer, gastroesophageal junction cancer, or esophageal adenocarcinoma. However, the results of several clinical trials are not entirely consistent, and the dominant population of first-line immunotherapy for advanced gastric/gastroesophageal junction cancer still needs to be precisely determined.

Objective: This objective of this study is to evaluate the efficacy of anti-PD-1/PD-L1 therapy in advanced gastric/gastroesophageal junction adenocarcinoma patients through a systematic review and meta-analysis of relevant clinical trials.

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Background & Aims: Gastric cancer (GC) is a major cancer type characterized by high heterogeneity in both tumor cells and the tumor immune microenvironment (TIME). One intractable GC subtype is gastric signet-ring cell carcinoma (GSRCC), which is associated with poor prognosis. However, it remains unclear what the GSRCC TIME characteristics are and how these characteristics may contribute to clinical outcomes.

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Endometriosis is a gynaecological condition characterized by the growth of endometrium-like tissues within and outside of the pelvic cavity. Recent studies have demonstrated that aberrant infiltration of M2 macrophages is mainly responsible for the establishment of endometriotic lesions. A growing body of evidence shows that glycolysis and lactate accumulation have great impact on the regulation of immunomicroenvironment.

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Article Synopsis
  • Researchers developed an 18-immune-related long non-coding RNA (IRLP) signature for gastric cancer (GC) using data from The Cancer Genome Atlas (TCGA), demonstrating strong prognostic predictive power with AUC values of 0.77, 0.86, and 0.80.
  • The IRLP signature serves as an independent prognostic factor, outperforming traditional TNM staging in predicting patient outcomes, and highlighted differences in immune cell infiltration between high-risk and low-risk groups.
  • Molecular experiments indicated that the lncRNA LINC01082 plays a role in the progression of gastric cancer, suggesting further areas of study in GC development.
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Background: The incidence rate of adenocarcinoma of the oesophagogastric junction (AEG) has significantly increased over the past decades, with a steady increase in morbidity. The aim of this study was to explore a variety of clinical factors to judge the survival outcomes of AEG patients.

Methods: We first obtained the clinical data of AEG patients from the Surveillance, Epidemiology, and End Results Program (SEER) database.

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Study Question: How is the activation of estrogen receptor β (ERβ) in endometriotic stromal cells (ESCs) involved in macrophage recruitment to promote the pathogenesis of endometriosis?

Summary Answer: ERβ modulates the production of C-C motif chemokine ligand 2 (CCL2) via nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling in ESCs and thus recruits macrophages to ectopic lesions to promote pathogenesis.

What Is Known Already: Macrophages are mainly recruited to the peritoneal cavity to promote the pathogenesis of endometriosis. Recent studies have demonstrated that ERβ plays an important role in the progression of endometriosis through modulating apoptosis and inflammation.

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As a component of p53-dependent lncRNA (long non-coding RNA), PANDAR (the promoter of CDKN1A antisense DNA damage activated RNA) participates in the epigenetic regulation in human cancer. However, the involvement of PANDAR in cancer chemoresistance is unknown. In this study, we report that PANDAR serves as a negative regulator of cisplatin sensitivity in human ovarian cancer via PANDAR-SRFS2-p53 feedback regulation in nuclear.

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Long non-coding RNA colon cancer-associated transcript 2 (CCAT2) is dysregulated in a variety of types of human cancer. However, the role of CCAT2 in epithelial ovarian carcinoma (EOC) remains largely unknown. The aim of this study is to investigate the effect of CCAT2 on epithelial-mesenchymal transition (EMT) and related molecular mechanisms in epithelial ovarian cancer cells.

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Long non-coding RNA CCAT2 (colon cancer-associated transcript 2) is dysregulated in varieties of human tumors. However, the role of CCAT2 in epithelial ovarian carcinoma (EOC) is not yet known clearly. The aim of this study is to investigate the effects of CCAT2 on proliferation and invasion of EOC cells and the potential mechanisms by which CCAT2 functions.

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Background: Cervical cancer is one of the most common malignant tumours of the female reproductive system, ranking second only to breast cancer in morbidity worldwide. Essential features of the progression of cervical cancer are invasion and metastasis, which are closely related to disease prognosis and mortality rate. At the present time there is no effective method to evaluate cancer invasion and metastasis before surgery.

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The present study investigated the underlying role of growth arrest-specific transcript 5 (GAS5) in epithelial ovarian cancer (EOC), which is the main cause of death in women with malignant tumor of the genital system. In vivo GAS5 expression in 60 EOC specimens was evaluated by quantitative reverse transcription (qRT)-PCR, which was used to study the differences of GAS5 expression between EOC tissues and normal ovarian epithelium. In vitro GAS5 overexpression was applied to discover the biological functions in EOC cell lines.

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Tannic acid (TA) has been associated with anticancer functions in multiple tumor types both in vitro and in vivo. However, its effect on ovarian carcinoma cells has not been investigated, and its underlying anticancer mechanism(s) remain unclear. In this study, the effects of TA alone and in combination with cisplatin were evaluated using ovarian carcinoma cell lines.

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