Biliary HMGB1 levels and biochemical indices in the assessment of acute obstructive septic cholangitis combined with septic shock.

Background: Acute Obstructive Septic Cholangitis (AOSC) is a serious infectious disease of the biliary system. It is prone to develop into septic shock without prompt management.

Methods: Bile was collected from 71 AOSC patients (45 AOSC without septic shock, 26 AOSC with septic shock) during biliary drainage and on days 1 and 3 postoperatively.

-induced promotes the malignant progression of pancreatic neuroendocrine neoplasms through -mediated lipid metabolism.

N6-methyladenosine (m6A) is considered the most prevalent RNA epigenetic regulator in cancer. FTO, an m6A demethylase, has been implicated in contributing to the progression of various cancers by up-regulating the expression of multiple oncogenes. However, studies exploring its impact on lipid metabolism in cancer, especially in pNENs, remain scarce.

Hypoxia drives CBR4 down-regulation promotes gastroenteropancreatic neuroendocrine tumors via activation mammalian target of rapamycin mediated by fatty acid synthase.

Hypoxia has been highly proven a hallmark of tumor micro-environment, promoting the malignant phenotypes, playing a crucial role from tumor initiation, progression, invasion, and intravasation to metastatic dissemination and outgrowth. Increasing evidence also showed that hypoxia mediated the abnormal lipid metabolism in cancer by regulating various oncogenic signal pathways. However, it is still unclear but attractive how hypoxia specifically functioned and changed the condition of the tumor micro-environment.

Hypoxia exosome derived CEACAM5 promotes tumor-associated macrophages M2 polarization to accelerate pancreatic neuroendocrine tumors metastasis via MMP9.

Exosomes play significant roles in the communications between tumor cells and tumor microenvironment. However, the specific mechanisms by which exosomes modulate tumor development under hypoxia in pancreatic neuroendocrine tumors (pNETs) are not well understood. This study aims to investigate these mechanisms and made several important discoveries.

Hypoxia upregulating ACSS2 enhances lipid metabolism reprogramming through HMGCS1 mediated PI3K/AKT/mTOR pathway to promote the progression of pancreatic neuroendocrine neoplasms.

Background: Pancreatic neuroendocrine neoplasms (pNENs) are relatively rare. Hypoxia and lipid metabolism-related gene acetyl-CoA synthetase 2 (ACSS2) is involved in tumor progression, but its role in pNENs is not revealed. This study showed that hypoxia can upregulate ACSS2, which plays an important role in the occurrence and development of pNENs through lipid metabolism reprogramming.

Serum Lipid Level in Evaluating Chinese Pancreatic Neuroendocrine Neoplasms: A Retrospective Study.

Background: Pancreatic neuroendocrine neoplasms (p-NENs) are relatively rare and highly heterogeneous. Dyslipidemia may be related to the risk of developing p-NENs, although dyslipidemia in patients with p-NENs is rarely reported. In this study, the clinical characteristics of p-NENs patients with different lipid levels and their prognostic value in p-NENs patients were evaluated.

ALKBH5 enhances lipid metabolism reprogramming by increasing stability of FABP5 to promote pancreatic neuroendocrine neoplasms progression in an m6A-IGF2BP2-dependent manner.

The process of post-transcriptional regulation has been recognized to be significantly impacted by the presence of N6-methyladenosine (m6A) modification. As an m6A demethylase, ALKBH5 has been shown to contribute to the progression of different cancers by increasing expression of several oncogenes. Hence, a better understanding of the key targets of ALKBH5 in cancer cells could potentially lead to the development of new therapeutic targets.

FABP5 regulates lipid metabolism to facilitate pancreatic neuroendocrine neoplasms progression via FASN mediated Wnt/β-catenin pathway.

Pancreatic neuroendocrine neoplasms (pNENs) are among the most frequently occurring neuroendocrine neoplasms (NENs) and require targeted therapy. High levels of fatty acid binding protein 5 (FABP5) are involved in tumor progression, but its role in pNENs remains unclear. We investigated the mRNA and protein levels of FABP5 in pNEN tissues and cell lines and found them to be upregulated.

Orlistat Induces Ferroptosis in Pancreatic Neuroendocrine Tumors by Inactivating the MAPK Pathway.

Orlistat is an antiobesity drug approved by the US Food and Drug Administration (FDA) with potential antitumor activity against a few malignant tumors, however, whether orlistat affects the progression of pancreatic neuroendocrine tumors (pNETs) remains unknown. Protein and mRNA levels of FASN were measured using western blotting (WB) and qRT-PCR. The effects of FASN and orlistat on cell proliferation were examined using CCK-8, colony formation, and EdU assays.

Novel insights into the interplay between m6A modification and programmed cell death in cancer.

N6-methyladenosine (m6A) methylation, the most prevalent and abundant RNA modification in eukaryotes, has recently become a hot research topic. Several studies have indicated that m6A modification is dysregulated during the progression of multiple diseases, especially in cancer development. Programmed cell death (PCD) is an active and orderly method of cell death in the development of organisms, including apoptosis, autophagy, pyroptosis, ferroptosis, and necroptosis.

Development and validation of prognostic nomograms for patients with colon neuroendocrine neoplasms.

Background: Colon neuroendocrine neoplasms (NENs) have one of the poorest median overall survival (OS) rates among all NENs. The American Joint Committee on Cancer (AJCC) tumor-node-metastasis (TNM) staging system-currently the most commonly used prediction model-has limited prediction accuracy because it does not include parameters such as age, sex, and treatment. The aim of this study was to construct nomograms containing various clinically important parameters to predict the prognosis of patients with colon NENs more accurately.

Associations of serum glucagon levels with glycemic variability in type 1 diabetes with different disease durations.

Purpose: Glucagon has been recognized as a pivotal factor implicated in the pathophysiology ofdiabetes. The purpose of this study is to investigate the dynamic secretion levels of serum glucagon (GLA) in patients with type 1 diabetes mellitus (T1DM) with different courses of disease, and to analyze its correlation with blood glucose fluctuation.

Methods: This observational study included 55 T1DM patients and divided into 3 groups according to the courses of disease.