Pancreatic Cancer
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(FIVE YEARS 20178)



2021 ◽  
Vol 144 ◽  
pp. 112325
Cheng Wang ◽  
Baojun Huang ◽  
Linxiao Sun ◽  
Xi Wang ◽  
Baofeng Zhou ◽  

2021 ◽  
Vol 158 ◽  
pp. 36-37
Eduard Jonas ◽  
Jessica Lindemann ◽  
Marc Bernon ◽  
Jake Krige

2021 ◽  
Vol 13 (10) ◽  
pp. 1263-1287
Sonia Perales ◽  
Carolina Torres ◽  
Cristina Jimenez-Luna ◽  
Jose Prados ◽  
Joaquina Martinez-Galan ◽  

Yizhen Pang ◽  
Long Zhao ◽  
Qihang Shang ◽  
Tinghua Meng ◽  
Liang Zhao ◽  

Kihak Lee ◽  
Hyo Jae Oh ◽  
Min-Su Kang ◽  
Sinae Kim ◽  
Sehee Ahn ◽  

2021 ◽  
Yongjie Li ◽  
Min Zeng ◽  
Ting Wang ◽  
Feng Jiang

Abstract Pancreatic cancer is a malignant tumor of digestive system with high fatality rate, and its prognosis is very poor. Type Ⅴ collagen α3 (COL5A3) is highly expressed in a variety of tumor tissues, but its prognostic value and immune infiltration in pancreatic cancer are still unclear. Therefore, we evaluated the prognostic role of COL5A3 in pancreatic cancer and its correlation with immune infiltration. The transcriptional expression profiles of COL5A3 in pancreatic cancer and normal tissues were downloaded from the Cancer Genome Atlas (TCGA). In the GEO (Gene expression omnibus) dataset (GSE16515), we compared the expression of COL5A3 in normal and tumor tissues. The expression of COL5A3 protein was evaluated by the human protein atlas (THPA). The effect of COL5A3 on survival was evaluated by Kaplan-Meier method. Receiver operating characteristic (ROC) curve was used to distinguish pancreatic cancer from paracancerous normal tissues. Protein-protein interaction (PPI) network was constructed by the STRING. Use the "ClusterProfiler" package for functional enrichment analysis. Tumor immune estimation resource (TIMER) and tumor-immune system interaction database (TISIDB) were used to determine the relationship between COL5A3 mRNA expression and immune infiltration. Compared with normal tissues, COL5A3 is highly expressed in pancreatic cancer tissues. The high expression of COL5A3 is related to the poor clinicopathological features and poor prognosis of pancreatic cancer. Kaplan-Meier survival analysis showed that the prognosis of pancreatic cancer patients with high expression of COL5A3 was worse than that of patients with low expression of COL5A3. ROC curve shows that COL5A3 has high sensitivity and specificity in the diagnosis of pancreatic cancer. Correlation analysis showed that the expression of COL5A3 mRNA was related to immune cell infiltration. This study reveals for the first time that COL5A3 may be a new prognostic biomarker related to immune infiltration and provide a new target for the diagnosis and treatment of pancreatic cancer.

2021 ◽  
Vol 27 (38) ◽  
pp. 6387-6398
Stephen Safe ◽  
Rupesh Shrestha ◽  
Kumaravel Mohankumar ◽  
Marcell Howard ◽  
Erik Hedrick ◽  

2021 ◽  
Charles P Hinzman ◽  
Shivani Bansal ◽  
Yaoxiang Li ◽  
Anton Iliuk ◽  
Michael Girgis ◽  

Although cancer-derived extracellular vesicles (cEVs) are thought to play a pivotal role in promoting cancer progression events, their precise effect on neighboring normal cells is unknown. In this study, we investigated the impact of pancreatic cancer ductal adenocarcinoma (PDAC) derived EVs on recipient non-tumorigenic pancreatic normal epithelial cells upon internalization. We show that PDAC cEVs increase the proliferation and invasive capability of treated normal cells. We further demonstrate that cEVs induce endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) in treated normal pancreatic epithelial cells within 24 hours. Subsequently, these cells release several inflammatory cytokines. Leveraging a layered multi-omics approach, we analyzed EV cargo from a panel of 6 PDAC and 2 normal pancreas cell lines, using multiple EV isolation methods. We found that cEVs were enriched for an array of biomolecules which can induce or regulate ER stress and the UPR, including palmitic acid, sphingomyelins, metabolic regulators of tRNA charging and proteins which regulate trafficking and degradation. We further show that palmitic acid, at doses relevant to those found in cEVs, is sufficient to induce ER stress in normal pancreas cells. These results suggest that cEV cargo packaging may be designed to disseminate proliferative and invasive characteristics upon internalization by distant recipient normal cells, hitherto unreported. This study is among the first to highlight a major role for PDAC cEVs to induce stress in treated normal pancreas cells that may modulate a systemic response leading to altered phenotypes. For the first time, our study implicates cEV transported palmitic acid as a potential driver in this process. These findings highlight the importance of EVs in mediating disease etiology and open potential areas of investigation toward understanding the role of cEV lipids in promoting cell transformation in the surrounding microenvironment.

Neoplasma ◽  
2021 ◽  
Rongrong Huang ◽  
Gaoyong Liao ◽  
Meifeng Gao ◽  
Yu Ou

2021 ◽  
Xin Chen ◽  
Weifan Zhang ◽  
Rujuan Liu ◽  
Zeen Zhu ◽  
Mengyuan Gong ◽  

Abstract Background: Low responsiveness to chemotherapy is an important cause of poor prognosis in pancreatic cancer. Smoking is a high-risk factor for pancreatic cancer and its resistance to gemcitabine; however, the underlying mechanisms remain unclear. 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is the main metabolite of tobacco burning and has been shown to be associated with cancer development and chemoresistance, but in pancreatic cancer, its mechanism remains poorly understood.Methods: The effect of NNK on pancreatic cancer cell viability was confirmed by using Cell Counting Kit-8 and colony formation assays. Stem cell sphere formation assays and western blotting/qPCR measurements of stemness-related molecules were used to detect pancreatic cancer cell stemness. The pancreatic cancer autophagy status was evaluated by immunofluorescence staining of LC3 and western blotting/qPCR analysis of autophagy-related molecules.Results: NNK promoted stemness and gemcitabine resistance in pancreatic cancer cell lines. Furthermore, NNK intervention increased autophagy and changed the expression levels of autophagy-related markers, which preliminarily confirmed the activation of autophagy by NNK. Finally, the results showed that NNK-promoted stemness, and gemcitabine resistance was activated by the autophagy pathway, which was mediated by the β2AR-Akt signalling pathway.Conclusions: Autophagy induced by activating the NNK-induced β2AR-Akt signalling pathway promoted stemness and gemcitabine resistance in pancreatic cancer cells.

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