Nuclear IL-33/SMAD Signaling Axis Promotes Cancer Development in Chronic Inflammation

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.
[EMBO Journal]
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
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Dynamic Regulation of Expression of KRAS and Its Effectors Determines the Ability to Initiate Tumorigenesis in Pancreatic Acinar Cells

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.
[Cancer Research]
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
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A Gene–Environment-Induced Epigenetic Program Initiates Tumorigenesis

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.
[Nature]
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
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The EGFR-HSF1 Axis Accelerates the Tumorigenesis of Pancreatic Cancer

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]
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
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FDA Authorizes Marketing of New Device Designed To Remove Dead Pancreatic Tissue

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.
[FDA]
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The Expression Profile and Textural Characteristics of C595-Reactive MUC1 in Pancreatic Ductal Adenocarcinoma for Targeted Radionuclide Therapy

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.
[Cancers]
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
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Pancreas-Specific SNAP23 Depletion Prevents Pancreatitis by Attenuating Pathological Basolateral Exocytosis and Formation of Trypsin-Activating Autolysosomes

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.
[Autophagy]
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
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Concerted Cell and In Vivo Screen for Pancreatic Ductal Adenocarcinoma (PDA) Chemotherapeutics

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.
[Scientific Reports]
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
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Shared Extracellular Vesicle miRNA Profiles of Matched Ductal Pancreatic Adenocarcinoma Organoids and Blood Plasma Samples Show the Power of Organoid Technology

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]
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
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EMC6 Regulates Acinar Apoptosis via APAF1 in Acute and Chronic Pancreatitis

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]
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
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Hic-5 Is Required for Activation of Pancreatic Stellate Cells and Development of Pancreatic Fibrosis in Chronic Pancreatitis

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.
[Scientific Reports]
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
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