Commitment and Oncogene-Induced Plasticity of Human Stem Cell-Derived Pancreatic Acinar and Ductal Organoids

Scientists report induction of human pluripotent stem cells toward pancreatic ductal and acinar organoids that recapitulate properties of the neonatal exocrine pancreas.
[Cell Stem Cell]
Huang, L., Desai, R., Conrad, D. N., Leite, N. C., Akshinthala, D., Lim, C. M., Gonzalez, R., Muthuswamy, L. B., Gartner, Z., & Muthuswamy, S. K. (2021). Commitment and oncogene-induced plasticity of human stem cell-derived pancreatic acinar and ductal organoids. Cell Stem Cell, 0(0). https://doi.org/10.1016/j.stem.2021.03.022 Cite
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Reg4 Regulates Pancreatic Regeneration Following Pancreatitis via Modulating the Notch Signaling

Researchers found that regenerating family member 4 (Reg4) knockdown significantly impaired pancreatic regeneration after pancreatitis.
[Journal of Cellular Physiology]
Dai, J., He, Y., Jiang, M., Niu, M., Li, B., Wu, Z., Bao, J., Wen, L., Wang, X., & Hu, G. (n.d.). Reg4 regulates pancreatic regeneration following pancreatitis via modulating the Notch signaling. Journal of Cellular Physiology, n/a(n/a). https://doi.org/https://doi.org/10.1002/jcp.30397 Cite
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MECOM Permits Pancreatic Acinar Cell Dedifferentiation Avoiding Cell Death under Stress Conditions

The authors applied a non-genetic lineage tracing method of human pancreatic exocrine acinar and duct cells that allowed cell-type-specific gene expression profiling by RNA sequencing.
[Cell Death & Differentiation]
Backx, E., Wauters, E., Baldan, J., Van Bulck, M., Michiels, E., Heremans, Y., De Paep, D. L., Kurokawa, M., Goyama, S., Bouwens, L., Jacquemin, P., Houbracken, I., & Rooman, I. (2021). MECOM permits pancreatic acinar cell dedifferentiation avoiding cell death under stress conditions. Cell Death & Differentiation, 1–15. https://doi.org/10.1038/s41418-021-00771-6 Cite
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Neddylation Pathway Alleviates Chronic Pancreatitis by Reducing HIF1α-CCL5-Dependent Macrophage Infiltration

Scientists demonstrated that global inactivation of neddylation pathway by MLN4924 significantly exacerbated chronic pancreatitis. The increased M2 macrophage infiltration, mediated by the upregulated chemokine ligand 5 (CCL5), was responsible for the enhanced pancreatitis-promoting activity of MLN4924.
[Cell Death & Disease]
Lin, Y., Chen, Y., Feng, W., Hua, R., Zhang, J., Huo, Y., Jiang, H., Yin, B., & Yang, X. (2021). Neddylation pathway alleviates chronic pancreatitis by reducing HIF1α-CCL5-dependent macrophage infiltration. Cell Death & Disease, 12(3), 1–11. https://doi.org/10.1038/s41419-021-03549-3 Cite
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Protectin D1 Decreases Pancreatitis Severity in Mice by Inhibiting Neutrophil Extracellular Trap Formation

Scientists showed that protectin D1 (PD1) ameliorates acute pancreatitis by decreasing early infiltration of neutrophils into the pancreas and neutrophil extracellular traps formation through peptidylarginine deiminase 4.
[International Immunopharmacology]
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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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