Share This Author
Pancreatic carcinoma cells induce fibrosis by stimulating proliferation and matrix synthesis of stellate cells.
Pancreatic stellate cells strongly support tumor growth in the nude mouse model and the increased deposition of connective tissue in pancreatic carcinoma is the result of a paracrine stimulation of pancreatic stllate cells by carcinoma cells.
Sulfasalazine: a potent and specific inhibitor of nuclear factor kappa B.
It is demonstrated that sulfasalazine is a potent and specific inhibitor of NF-kappaB activation, and thus may explain some of the known biological properties of sulf asalazine.
Transforming growth factor beta1 treatment leads to an epithelial-mesenchymal transdifferentiation of pancreatic cancer cells requiring extracellular signal-regulated kinase 2 activation.
Cross-talk with the Ras-MEK-ERK-signaling cascade appears to be essential for mediating these effects of TGF-beta1, which led to a reversible and time-dependent epithelial-mesenchymal transdifferentiation in T GF-beta-responsive pancreatic cancer cell lines.
p300 Acts as a Transcriptional Coactivator for Mammalian Notch-1
A novel domain is identified in Notch-1-IC, the EP domain, which is indispensable for full transcriptional activation, and this transactivation domain is localized adjacent to the ankyrin repeats of Notch, 1-IC.
Sphingosylphosphorylcholine regulates keratin network architecture and visco-elastic properties of human cancer cells
It is shown that incubation of human epithelial tumour cells with SPC induces a perinuclear reorganization of intact keratin 8–18 filaments, which may facilitate biological phenomena that require a high degree of elasticity, such as squeezing of cells through membranous pores during metastasis.
StellaTUM: current consensus and discussion on pancreatic stellate cell research
Members of the Pancreatic Star Alliance discuss and consolidate current knowledge to outline and delineate areas of consensus or otherwise (eg, with regard to methodological approaches) and, more importantly, to identify essential directions for future research.
Mitogenic and antiapoptotic role of constitutive NF‐κB/Rel activity in pancreatic cancer
- S. Liptay, C. Weber, L. Ludwig, M. Wagner, G. Adler, R. Schmid
- BiologyInternational journal of cancer
- 20 July 2003
The data demonstrate that an EGF‐R/Ras/PI3 kinase/Akt/IKK‐dependent pathway contributes to constitutive NF‐κB/Rel activity in pancreatic cancer.
Cloning of a gene highly overexpressed in cancer coding for a novel KH-domain containing protein
It is speculated that koc may assume a role in the regulation of tumour cell proliferation by interfering with transcriptional and or posttranscriptional processes, however, the precise role of koc in human tumour cells is unknown and remains to be elucidated.
Overexpression of c‐myc in pancreatic cancer caused by ectopic activation of NFATc1 and the Ca2+/calcineurin signaling pathway
It is demonstrated that ectopic activation of NFATc1 and the Ca2+/calcineurin signaling pathway is an important mechanism of oncogenic c‐myc activation in pancreatic cancer.
NF-κB2 Is a Putative Target Gene of Activated Notch-1 via RBP-Jκ
Detailed examination of Rep-κB–DNA interaction revealed the sequence requirements for binding to be almost identical to those of recombination signal binding protein Jκ (RBP-Jκ), the mammalian homolog of the protein encoded by Drosophila suppressor of hairless [Su(H].