Publications by authors named "Yupei Zhao"

Transcriptional dysregulation is a hallmark of cancer initiation and progression, driven by genetic and epigenetic alterations. Enhancer reprogramming has emerged as a pivotal driver of carcinogenesis, with cancer cells often relying on aberrant transcriptional programs. The advent of high-throughput sequencing technologies has provided critical insights into enhancer reprogramming events and their role in malignancy.

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Objective: To evaluate surgical impact on the overall survival (OS) of pancreatic neuroendocrine neoplasm (pNEN) with synchronous hepatic metastases (sHMs).

Methods: A total of 163 pNEN-sHM patients were recruited from 3 institutions in China, who were categorized into 3 groups: no resection, resection of the primary lesion, and resection of both primary and hepatic lesions (PHR). Cox regression was employed to evaluate surgical impact on the OS.

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Pancreatic cancer (PCa) has insidious onset, high malignancy and poor prognosis. Gemcitabine (GEM) is one of the first-line chemotherapy drugs for PCa. However, GEM resistance has always been a bottleneck problem leading to recurrence and death of PCa patients.

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The pancreas, an organ with dual functions, regulates blood glucose levels through the endocrine system by secreting hormones such as insulin and glucagon. It also aids digestion through the exocrine system by secreting digestive enzymes. Complex interactions and signaling mechanisms between the endocrine and exocrine functions of the pancreas play a crucial role in maintaining metabolic homeostasis and overall health.

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In this study, CO reacted with a curing agent through nucleophilic addition to form ammonium salts, enabling the stable capture and internal release of CO, which achieved gas-phase nucleation and foaming. Additionally, the introduction of wave-absorbing agents improved the absorption mechanism and promoted uniform foaming. This nucleation-free foaming process relies on the induced growth of gas nuclei and the synergistic effect of the wave-absorbing agents, effectively preventing the uneven foaming issues caused by traditional nucleating agents.

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Background: Pancreatic cancer is a highly aggressive neoplasm characterized by poor diagnosis. Amino acids play a prominent role in the occurrence and progression of pancreatic cancer as essential building blocks for protein synthesis and key regulators of cellular metabolism. Understanding the interplay between pancreatic cancer and amino acid metabolism offers potential avenues for improving patient clinical outcomes.

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Background: Pancreatic ductal adenocarcinoma (PDAC) is one of the most malignant tumors. Macrophages are abundant in the tumor microenvironment, making them an attractive target for therapeutic intervention. While current immunotherapies, including immune checkpoint inhibition (ICI) and chimeric antigen receptor T (CAR-T) cells, have shown limited efficacy in pancreatic cancer, a novel approach involving chimeric antigen receptor macrophages (CAR-M) has, although promising, not been explored in pancreatic cancer.

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Solvent effects play a critical role in solution polymerization, especially in free radical polymerization, where they influence both monomer-solvent interactions and the resulting polymer structure. In this study, polymethacrylimide (PMI) aerogels were synthesized via freeze-drying using dimethylformamide (DMF), dimethylacetamide (DMAc), and dimethyl sulfoxide (DMSO) as solvents. The effects of monomer reactivity ratios, monomer distribution, and solvent-monomer interactions on the shrinkage, bulk density, pore size, and compressive properties of the aerogels were investigated.

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Article Synopsis
  • This study investigates the link between the microbiome and metabolic substances in pancreatic ductal adenocarcinoma (PDAC) through an analysis of tissue samples from 105 patients over six years.
  • Findings reveal decreased microbial diversity in PDAC tumors compared to normal adjacent tissues, with specific opportunistic pathogens linked to poorer overall survival outcomes.
  • The metabolomic analysis identified 553 unique metabolites differentiating PDAC from normal tissues, suggesting that microbiota may influence PDAC development by modulating certain metabolic pathways.
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Pancreatic cancer is an extremely malignant tumor. PVT1 and MYC signaling has been considered as a therapeutic target recently. Nonetheless, the prognostic values and critical regulatory networks of PVT1-MYC duet in pancreatic cancer remain unclear.

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Article Synopsis
  • * Researchers identified CALB2 as a key protein that is highly expressed in cancer-associated fibroblasts (CAFs) and cancer cells, which is linked to worse patient outcomes and an immunosuppressive tumor microenvironment.
  • * The findings revealed that CALB2, in conjunction with hypoxia, promotes an inflammatory fibroblast phenotype that enhances cancer cell migration and growth, indicating its potential role in PDAC metastasis and the development of inflammation-targeted treatments.
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Pancreatic cancer, a highly fatal malignancy, is predicted to rank as the second leading cause of cancer-related death in the next decade. This highlights the urgent need for new insights into personalized diagnosis and treatment. Although molecular subtypes of pancreatic cancer were well established in genomics and transcriptomics, few known molecular classifications are translated to guide clinical strategies and require a paradigm shift.

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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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Pancreatic cancer remains one of the most lethal malignant diseases. Gemcitabine-based chemotherapy is still one of the first-line systemic treatments, but chemoresistance occurs in the majority of patients. Recently, accumulated evidence has demonstrated the role of the tumour microenvironment in promoting chemoresistance.

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Amino acid metabolism plays a pivotal role in tumor microenvironment, influencing various aspects of cancer progression. The metabolic reprogramming of amino acids in tumor cells is intricately linked to protein synthesis, nucleotide synthesis, modulation of signaling pathways, regulation of tumor cell metabolism, maintenance of oxidative stress homeostasis, and epigenetic modifications. Furthermore, the dysregulation of amino acid metabolism also impacts tumor microenvironment and tumor immunity.

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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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  • Pancreatic neuroendocrine tumors (PanNETs) show a wide range of invasiveness, and existing genomic knowledge sheds some light on this variability, especially between different types like insulinomas and other PanNET variants.
  • Researchers used a 2D classification system based on RNA sequencing of PanNETs from both mouse models and humans to categorize these tumors primarily into benign insulinomas and various invasive subtypes.
  • By integrating the 2D classification, specific mutation status (DAXX/ATRX), and tumor size, they identified a subset of PanNETs with low recurrence risk, helping to clarify the complexity of these tumors and enhance their prognostic evaluation.
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Glucocorticoids (GCs), a class of hormones secreted by the adrenal glands, are released into the bloodstream to maintain homeostasis and modulate responses to various stressors. These hormones function by binding to the widely expressed GC receptor (GR), thereby regulating a wide range of pathophysiological processes, especially in metabolism and immunity. The role of GCs in the tumor immune microenvironment (TIME) of lung cancer (LC) has been a focal point of research.

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Cancer cells rewire metabolism to sculpt the immune tumor microenvironment (TME) and propel tumor advancement, which intricately tied to post-translational modifications. Histone lactylation has emerged as a novel player in modulating protein functions, whereas little is known about its pathological role in pancreatic ductal adenocarcinoma (PDAC) progression. Employing a multi-omics approach encompassing bulk and single-cell RNA sequencing, metabolomics, ATAC-seq, and CUT&Tag methodologies, we unveiled the potential of histone lactylation in prognostic prediction, patient stratification and TME characterization.

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Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy with a poor prognosis and limited therapeutic options. Research on the tumor microenvironment (TME) of PDAC has propelled the development of immunotherapeutic and targeted therapeutic strategies with a promising future. The emergence of single-cell sequencing and mass spectrometry technologies, coupled with spatial omics, has collectively revealed the heterogeneity of the TME from a multiomics perspective, outlined the development trajectories of cell lineages, and revealed important functions of previously underrated myeloid cells and tumor stroma cells.

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Introduction: Intraductal papillary mucinous neoplasm (IPMN) is an important precursor lesion of pancreatic cancer. Systemic inflammatory parameters are widely used in the prognosis prediction of cancer; however, their prognostic implications in IPMN with associated invasive carcinoma (IPMN-INV) are unclear. This study aims to explore the prognostic value of systemic inflammatory parameters in patients with IPMN-INV.

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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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Pancreatic ductal adenocarcinoma (PDAC) is a highly malignant neoplasm characterized by a poor prognosis and limited therapeutic strategy. The PDAC tumor microenvironment presents a complex heterogeneity, where neutrophils emerge as the predominant constituents of the innate immune cell population. Leveraging the power of single-cell RNA-seq, spatial RNA-seq, and multi-omics approaches, we included both published datasets and our in-house patient cohorts, elucidating the inherent heterogeneity in the formation of neutrophil extracellular traps (NETs) and revealed the correlation between NETs and immune suppression.

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