 | | Vol. 11.29 – 4 August, 2020 |
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| In vitro and in vivo functional studies performed by silencing or overexpressing TET1 suggested that TET1 was able to suppress epithelial-mesenchymal transition and sensitize pancreatic ductal adenocarcinoma cells to 5FU and gemcitabine. RNA-seq, whole genome bisulfite sequencing and ChIP-seq were used to explore the TET1-associated pathway.
[Oncogene] |
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 | | PUBLICATIONSRanked by the impact factor of the journal |
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| Mouse and human islets were used in combination with confocal microscopy, electrophysiology, glucagon immunoassays, and fluorescent thallium flux assays to assess α-cell Ca2+ handling, Vm, KATP currents, and GCG secretion.
[Molecular Metabolism] |
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| IL-17F possessed similar pathogenic activities to IL-17A in mouse β-cell lines and islets and was likely to be a type 17 associated pathogenic factor in type 1 diabetes.
[Scientific Reports] |
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| Investigators found that overexpression of Go-Ichi-Ni-San 2 (GINS2) contributed to advanced clinical stage of pancreatic cancer and promoted epithelial–mesenchymal-transition in vitro and in vivo via specifically activating the ERK/MAPK signal pathway.
[Cancer Gene Therapy] |
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| Researchers evaluated the potential beneficial effects of DGAT1 inhibitors on pancreatic β-cells, and further verified their antidiabetic effects in db/db mice.
[Acta Pharmacologica Sinica] |
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| The therapeutic efficacy of LentiVIP was tested in a multiple low-dose STZ-induced animal model of type 1 diabetes. LentiVIP delivery into diabetic animals reduced hyperglycemia, improved glucose tolerance, and prevented weight loss.
[Gene Therapy] |
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| The authors found that metformin suppressed HNF4G activity via AMPK-mediated phosphorylation-coupled ubiquitination degradation and inhibited in vitro invasion and in vivo metastasis of pancreatic ductal adenocarcinoma cells with SMAD4 deficiency.
[Protein & Cell] |
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| Researchers demonstrated that hotspot mutant p53, p53-R273H, promoted cell scattering growth and migration via inhibiting the expression of Krupple-like factor 6 (KLF6), a Zinc finger transcription factor and a documented tumor suppressor.
[Cell Death & Disease] |
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| The authors discuss the important roles of mucins that lead to the lethality of pancreatic adenocarcinoma, particularly MUC1, MUC4, MUC5AC and MUC16 in disease progression, and present a comprehensive analysis of the clinical application of mucins and their promising roles in cancer treatment.
[Journal of Cellular and Molecular Medicine] |
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| Tyme Technologies, Inc. announced that the FDA has granted the company Orphan Drug Designation for its lead pipeline candidate, SM-88, as a potential treatment for patients with pancreatic cancer.
[TYME Inc.] |
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| Genprex, Inc. announced that Dr. George K. Gittes, MD of the University of Pittsburgh, was awarded a grant of $2.59 million from the NIH National Institute of Diabetes and Digestive and Kidney Diseases.
[Genprex Inc.] |
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| October 20 – October 21
Virtual |
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| | University of Miami Health System – Miami, Florida, United States |
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| | Cold Spring Harbor Laboratory – New York, New York, United States |
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| | Weill Cornell Medicine – New York, New York, United States |
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| | Cold Spring Harbor Laboratory – Long Island, New York, United States |
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| | Stanford Institute for Stem Cell Biology and Regenerative Medicine – Stanford, California, United States |
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