Publications by authors named "Yin Xinpeng"

Obesity is a significant risk factor for various cancers, including pancreatic cancer (PC), but the underlying mechanisms are still unclear. In our study, pancreatic ductal epithelial cells were cultured using serum from human subjects with diverse metabolic statuses, revealing that serum from patients with obesity alters inflammatory cytokine signaling and ferroptosis, where a mutual enhancement between interleukin 34 (IL-34) expression and ferroptosis defense was observed in these cells. Notably, oncogenic KRAS amplified their interaction and this leads to the initiation of pancreatic ductal adenocarcinoma (PDAC) in diet-induced obese mice via macrophage-mediated immunosuppression.

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Article Synopsis
  • The study examines the interactions between the endocrine and exocrine components of the pancreas during the development of pancreatic ductal adenocarcinoma (PDAC), highlighting that the role of endocrine cells in this process has not been thoroughly explored.
  • Using advanced techniques like single-cell and spatial transcriptome sequencing, researchers discovered significant changes in pancreatic endocrine cells, particularly an increase in pancreatic polypeptide-positive cells, as cancer progresses.
  • The findings suggest a mechanism where PDAC cells can induce the transformation of pancreatic α and β cells into dual-function cells, which may contribute to cancer development, indicating a complex interplay between endocrine and exocrine cells in the tumor microenvironment.
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Objective: Pancreatic cancer is one of the most aggressive malignancies, a robust prognostic signature and novel biomarkers are urgently needed for accurate stratification of the patients and optimization of clinical decision-making.

Methods: A list of bioinformatic analysis were applied in public dataset to construct an immune-related signature. Furthermore, the most pivotal gene in the signature was identified.

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Previous work based on Graph Convolutional Networks (GCNs) has shown promising performance in 3D skeleton-based motion recognition. We believe that the 3D skeleton-based motion recognition problem can be explained as a modeling task of dynamic skeleton-based graph construction. However, existing methods fail to model human poses with dynamic correlations between human joints, ignoring the information contained in the skeleton structure of the non-connected relationship during human motion modeling.

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Article Synopsis
  • Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with limited treatment options, and the phenomenon of entosis—where cells consume other cells—may play a role in its progression.
  • Research showed that entosis is linked to worse patient outcomes and occurs more often in liver metastases compared to primary tumors, with specific genes like NET1 being associated with this aggressive behavior.
  • The study suggests that entosis contributes to the development of a dangerous subpopulation of PDAC cells, which could help inform future therapeutic strategies and serve as molecular markers for diagnosing poor prognosis.
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Pancreatic cancer (PC), a highly lethal malignancy, commonly exhibits metabolic reprogramming that results in therapeutic vulnerabilities. Nevertheless, the mechanisms underlying the impacts of aberrant cholesterol metabolism on PC development and progression remain elusive. In this study, we found that squalene epoxidase (SQLE) is a crucial mediator of cholesterol metabolism in PC growth.

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The prevalence of obesity and diabetes mellitus (DM) has been consistently increasing worldwide. Sharing powerful genetic and environmental features in their pathogenesis, obesity amplifies the impact of genetic susceptibility and environmental factors on DM. The ectopic expansion of adipose tissue and excessive accumulation of certain nutrients and metabolites sabotage the metabolic balance via insulin resistance, dysfunctional autophagy, and microbiome-gut-brain axis, further exacerbating the dysregulation of immunometabolism through low-grade systemic inflammation, leading to an accelerated loss of functional β-cells and gradual elevation of blood glucose.

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Research on obesity- and diabetes mellitus (DM)-related carcinogenesis has expanded exponentially since these two diseases were recognized as important risk factors for cancers. The growing interest in this area is prominently actuated by the increasing obesity and DM prevalence, which is partially responsible for the slight but constant increase in pancreatic cancer (PC) occurrence. PC is a highly lethal malignancy characterized by its insidious symptoms, delayed diagnosis, and devastating prognosis.

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Article Synopsis
  • * While treatments for obesity and DM can lower the risk of developing PC, some medications might actually increase the likelihood of pancreatic cancer.
  • * Monitoring blood glucose levels and weight changes could help identify pancreatic cancer early in patients with obesity and DM, allowing for better intervention opportunities and improved survival rates.
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Introduction: Previous studies have investigated the prognostic significance of glycolysis markers in pancreatic cancer; however, conclusions from these studies are still controversial.

Methods: PubMed, Embase, and Web of Science were systematically searched to investigate the prognostic role of glycolysis markers in pancreatic cancer up to May 2022. Pooled hazard ratios (HRs) with 95% confidence intervals (CIs) related to overall survival (OS), disease free survival (DFS), recurrence-free survival (RFS), and distant metastasis-free survival (DMFS) were calculated using the STATA 12.

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The incidence of metabolism-related diseases like obesity and type 2 diabetes mellitus has reached pandemic levels worldwide and increased gradually. Most of them are listed on the table of high-risk factors for malignancy, and metabolic disorders systematically or locally contribute to cancer progression and poor prognosis of patients. Importantly, adipose tissue is fundamental to the occurrence and development of these metabolic disorders.

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Pancreatic cancer is one of the most serious health issues in developed and developing countries, with a 5-year overall survival rate currently <9%. Patients typically present with advanced disease due to vague symptoms or lack of screening for early cancer detection. Surgical resection represents the only chance for cure, but treatment options are limited for advanced diseases, such as distant metastatic or locally progressive tumors.

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Background: Pancreatic cancer (PC) is a highly malignant tumor featured with high intra-tumoral heterogeneity and poor prognosis. Cell-in-cell (CIC) structures have been reported in multiple cancers, and their presence is associated with disease progression. Nonetheless, the prognostic values and biological functions of CIC-related genes in PC remain poorly understood.

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Pancreatic cancer (PC) is a highly lethal and aggressive disease with its incidence and mortality quite discouraging. A robust prognostic signature and novel biomarkers are urgently needed for accurate stratification of the patients and optimization of clinical decision-making. Since the critical role of immune microenvironment in the progression of PC, a prognostic signature based on seven immune-related genes was established, which was validated in The Cancer Genome Atlas (TCGA) training set, TCGA testing set, TCGA entire set and GSE71729 set.

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