Interleukin (IL)‐33 was highly expressed in the skin and pancreatic epithelial cells in chronic inflammation, leading to a markedly repressed Smad6 expression as well as dramatically upregulated p‐SMAD2/3 and p‐SMAD1/5 in the epithelial cells.
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Nuclear IL‐33/SMAD signaling axis promotes cancer development in chronic inflammation | The EMBO Journal. (n.d.). Retrieved February 23, 2021, from https://www.embopress.org/doi/abs/10.15252/embj.2020106151 Cite
The authors revealed that control of the expression of KRAS and its effectors regulated the sensitivity of acinar cells to transformation by oncogenic Kras mutations.
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Assi, M., Achouri, Y., Loriot, A., Dauguet, N., Dahou, H., Baldan, J., Libert, M., Fain, J. S., Guerra, C., Bouwens, L., Barbacid, M., Lemaigre, F. P., & Jacquemin, P. (2021). Dynamic regulation of expression of KRAS and its effectors determines the ability to initiate tumorigenesis in pancreatic acinar cells. Cancer Research. https://doi.org/10.1158/0008-5472.CAN-20-2976 Cite
Researchers showed that the combination of Kras mutation and tissue damage promoted a unique chromatin state in the pancreatic epithelium that distinguished neoplastic transformation from normal regeneration and was selected for throughout malignant evolution.
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Alonso-Curbelo, D., Ho, Y.-J., Burdziak, C., Maag, J. L. V., Morris, J. P., Chandwani, R., Chen, H.-A., Tsanov, K. M., Barriga, F. M., Luan, W., Tasdemir, N., Livshits, G., Azizi, E., Chun, J., Wilkinson, J. E., Mazutis, L., Leach, S. D., Koche, R., Pe’er, D., & Lowe, S. W. (2021). A gene–environment-induced epigenetic program initiates tumorigenesis. Nature, 1–7. https://doi.org/10.1038/s41586-020-03147-x Cite
Investigators clarified the mechanisms on early activation of heat shock factor 1 (HSF1) and its role in the pancreatic cancer tumorigenesis.
[Journal of Experimental & Clinical Cancer Research]
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Qian, W., Chen, K., Qin, T., Xiao, Y., Li, J., Yue, Y., Zhou, C., Ma, J., Duan, W., Lei, J., Han, L., Li, L., Shen, X., Wu, Z., Ma, Q., & Wang, Z. (2021). The EGFR-HSF1 axis accelerates the tumorigenesis of pancreatic cancer. Journal of Experimental & Clinical Cancer Research, 40(1), 25. https://doi.org/10.1186/s13046-020-01823-4 Cite
The FDA authorized marketing of the EndoRotor System to resect and remove necrotic tissue for patients with walled-off pancreatic necrosis, a potentially deadly condition which can occur several weeks after an episode of severe acute pancreatitis, often requiring tissue removal.
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Scientists determined the feasibility of Mucin 1 (MUC1)-based targeted radionuclide therapy for PDAC, by evaluating the expression profile of MUC1 in different pancreatic cells and tissues using the C595 antibody.
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Hull, A., Li, Y., Bartholomeusz, D., Hsieh, W., Escarbe, S., Ruszkiewicz, A., & Bezak, E. (2021). The Expression Profile and Textural Characteristics of C595-Reactive MUC1 in Pancreatic Ductal Adenocarcinoma for Targeted Radionuclide Therapy. Cancers, 13(1), 61. https://doi.org/10.3390/cancers13010061 Cite
In vitro pancreatitis induction by supraphysiological cholecystokinin (CCK) or ethanol plus low-dose CCK were used to assess SNAP23-KD effects on exocytosis and autophagy.
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Dolai, S., Takahashi, T., Qin, T., Liang, T., Xie, L., Kang, F., Miao, Y.-F., Xie, H., Kang, Y., Manuel, J., Winter, E., Roche, P. A., Cattral, M. S., & Gaisano, H. Y. (2020). Pancreas-specific SNAP23 depletion prevents pancreatitis by attenuating pathological basolateral exocytosis and formation of trypsin-activating autolysosomes. Autophagy, 0(0), 1–14. https://doi.org/10.1080/15548627.2020.1852725 Cite
Cultured primary PDA cells expressed Rgs16::GFP in response to cytotoxic drugs. A histone deacetylase inhibitor, TSA, stimulated Rgs16::GFP expression in PDA primary cells, potentiated gemcitabine and JQ1 cytotoxicity in cell culture, and Gem + TSA + JQ1 inhibited tumor initiation and progression in vivo.
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Layeghi-Ghalehsoukhteh, S., Pal Choudhuri, S., Ocal, O., Zolghadri, Y., Pashkov, V., Niederstrasser, H., Posner, B. A., Kantheti, H. S., Azevedo-Pouly, A. C., Huang, H., Girard, L., MacDonald, R. J., Brekken, R. A., & Wilkie, T. M. (2020). Concerted cell and in vivo screen for pancreatic ductal adenocarcinoma (PDA) chemotherapeutics. Scientific Reports, 10(1), 20662. https://doi.org/10.1038/s41598-020-77373-8 Cite
Researchers showed that the miRNA cargo of extracellular vesicles (EVs) from pancreatic ductal adenocarcinoma organoids largely differs among patients. However, they detected a common set of EV miRNAs that were present in matched organoids and blood plasma samples of individual patients.
[Cellular and Molecular Life Sciences]
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Zeöld, A., Sándor, G. O., Kiss, A., Soós, A. Á., Tölgyes, T., Bursics, A., Szűcs, Á., Harsányi, L., Kittel, Á., Gézsi, A., Buzás, E. I., & Wiener, Z. (2020). Shared extracellular vesicle miRNA profiles of matched ductal pancreatic adenocarcinoma organoids and blood plasma samples show the power of organoid technology. Cellular and Molecular Life Sciences. https://doi.org/10.1007/s00018-020-03703-8 Cite
Potential regulatory proteins in pancreatitis were identified by proteomic screen using pancreatic tissues of PRSS1Tg AP mice. Adenoviral shRNA-mediated knockdown of identified proteins, followed by functional assays was performed to validate their roles.
[Cell Death & Disease]
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Tan, J., Cao, R., Zhou, L., Zhou, Z., Chen, H., Xu, J., Chen, X., Jin, Y., Lin, J., Qi, Z., Zeng, J., Li, S., Luo, M., Hu, G., Jin, J., & Zhang, G. (2020). EMC6 regulates acinar apoptosis via APAF1 in acute and chronic pancreatitis. Cell Death & Disease, 11(11), 1–13. https://doi.org/10.1038/s41419-020-03177-3 Cite
Mechanistically, Hic-5 knock down significantly inhibited the TGF-β/Smad2 signaling pathway, resulting in reduced collagen production and α-smooth muscle actin expression in the activated pancreatic stellate cells.
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Gao, L., Lei, X.-F., Miyauchi, A., Noguchi, M., Omoto, T., Haraguchi, S., Miyazaki, T., Miyazaki, A., & Kim-Kaneyama, J. (2020). Hic-5 is required for activation of pancreatic stellate cells and development of pancreatic fibrosis in chronic pancreatitis. Scientific Reports, 10(1), 19105. https://doi.org/10.1038/s41598-020-76095-1 Cite