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]
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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
Researchers found that regenerating family member 4 (Reg4) knockdown significantly impaired pancreatic regeneration after pancreatitis.
[Journal of Cellular Physiology]
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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]
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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
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]
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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.
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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