Scientists demonstrated that NR5A2 acted as a negative prognostic biomarker in PDAC. NR5A2 silencing inhibited the proliferation and migration abilities of pancreatic cancer cells in vitro and in vivo.
[Cell Death Discovery]
The authors explored the possible beneficial effects of vitexin on high glucose-induced cytotoxicity in pancreatic β-cells. The INS-1 pancreatic β-cell line was used in this study.
[Archives of Physiology and Biochemistry]
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Investigators analyzed the role of Cox6a2 in pancreatic β-cell function and its pathophysiological significance in diabetes mellitus.
[Biochemical and Biophysical Research Communications]
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Nagai, Y., Matsuoka, T., Shimo, N., Miyatsuka, T., Miyazaki, S., Tashiro, F., Miyazaki, J., Katakami, N., & Shimomura, I. (2021). Glucotoxicity-induced suppression of Cox6a2 expression provokes β-cell dysfunction via augmented ROS production. Biochemical and Biophysical Research Communications, 556, 134–141. https://doi.org/10.1016/j.bbrc.2021.03.148 Cite
Cultured pancreatic stellate cells were found to secrete high levels of activin A resulting in PDAC cell migration that was abolished by anti-activin A neutralizing antibody.
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Mancinelli, G., Torres, C., Krett, N., Bauer, J., Castellanos, K., McKinney, R., Dawson, D., Guzman, G., Hwang, R., Grimaldo, S., Grippo, P., & Jung, B. (2021). Role of stromal activin A in human pancreatic cancer and metastasis in mice. Scientific Reports, 11(1), 7986. https://doi.org/10.1038/s41598-021-87213-y Cite
The authors engineered a high affinity soluble human leukemia inhibitory factor (LIF) receptor decoy that sequestered human LIF and inhibited its signaling as a therapeutic strategy.
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Hunter, S. A., McIntosh, B. J., Shi, Y., Sperberg, R. A. P., Funatogawa, C., Labanieh, L., Soon, E., Wastyk, H. C., Mehta, N., Carter, C., Hunter, T., & Cochran, J. R. (2021). An engineered ligand trap inhibits leukemia inhibitory factor as pancreatic cancer treatment strategy. Communications Biology, 4(1), 1–13. https://doi.org/10.1038/s42003-021-01928-2 Cite
Investigators provided evidence that a member of the human Schlafen (SLFN) family of proteins, SLFN5, is overexpressed in human PDAC. Targeted deletion of SLFN5 resulted in decreased PDAC cell proliferation and suppressed PDAC tumorigenesis in in vivo PDAC models.
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Fischietti, M., Eckerdt, F., Blyth, G. T., Arslan, A. D., Mati, W. M., Oku, C. V., Perez, R. E., Lee-Chang, C., Kosciuczuk, E. M., Saleiro, D., Beauchamp, E. M., Lesniak, M. S., Verzella, D., Sun, L., Fish, E. N., Yang, G.-Y., Qiang, W., & Platanias, L. C. (2021). Schlafen 5 as a novel therapeutic target in pancreatic ductal adenocarcinoma. Oncogene, 1–14. https://doi.org/10.1038/s41388-021-01761-1 Cite
The University of Texas MD Anderson Cancer Center and TriSalus Life Sciences®, announced a strategic research collaboration to evaluate the treatment of tumors of the pancreas and liver by integrating interventional delivery of SD-101, an investigational toll-like receptor 9 agonist, in combination with checkpoint inhibition immunotherapy.
[TriSalus Life Sciences]
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Provention Bio, Inc. has announced that the company received a notification from the FDA, stating that, as part of its ongoing review of the company’s Biologic License Application for teplizumab for the delay or prevention of clinical type 1 diabetes, the FDA has identified deficiencies that preclude discussion of labeling and post-marketing requirements/commitments at this time.
[Provention Bio, Inc.]
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The authors report dynamic metabolic reprogramming in immortalized human non-cancerous pancreatic ductal epithelial cells.
[Cancer Gene Therapy]
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Suzuki, T., Kishikawa, T., Sato, T., Takeda, N., Sugiura, Y., Seimiya, T., Sekiba, K., Ohno, M., Iwata, T., Ishibashi, R., Otsuka, M., & Koike, K. (2021). Mutant KRAS drives metabolic reprogramming and autophagic flux in premalignant pancreatic cells. Cancer Gene Therapy, 1–14. https://doi.org/10.1038/s41417-021-00326-4 Cite
Investigators showed that inhibiting serpinB13, a cathepsin L protease inhibitor expressed in the pancreatic epithelium, caused in vitro and in vivo cleavage of the extracellular domain of Notch1.
[Science Translational Medicine]
Using in vitro and in vivo pancreatic cancer models, scientists showed that IDO1 expression was highly context dependent, influenced by attachment-independent growth and the canonical activator IFNγ.
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Newman, A. C., Falcone, M., Uribe, A. H., Zhang, T., Athineos, D., Pietzke, M., Vazquez, A., Blyth, K., & Maddocks, O. D. K. (2021). Immune-regulated IDO1-dependent tryptophan metabolism is source of one-carbon units for pancreatic cancer and stellate cells. Molecular Cell, 0(0). https://doi.org/10.1016/j.molcel.2021.03.019 Cite