Retracted: Inhibition of nuclear factor κb activity by genistein is mediated via Notch‐1 signaling pathway in pancreatic cancer cells

Abstract

This article has been retracted at the request of: Editor‐in‐Chief and Author ‘Inhibition of nuclear factor κb activity by genistein is mediated via Notch‐1 signaling pathway in pancreatic cancer cells’, by Wang, Z., Zhang, Y., Banerjee, S., Li, Y. and Sarkar, F. H. The above article and associated erratum, published online on 11 November 2005 and 6 February 2014, respectively, in Wiley Online Library (http://wileyonlinelibrary.com), have been retracted by agreement between the authors, the journal Editor‐in‐Chief, Professor Peter Lichter, and Wiley Periodicals, Inc. In addition to what was corrected in the erratum, a university investigation involving the first and the corresponding author determined that several figures in this paper were re‐used, mislabeled, manipulated, or duplicated while processing/compiling the final figures assembled from the original data sources. Therefore, the authors are retracting the paper in its entirety although they maintain that these issues did not affect the major conclusions. They apologize for any inconvenience this may have caused. Reference Wang, Z., Zhang, Y., Banerjee, S., Li, Y. and Sarkar, F. H. (2006), Inhibition of nuclear factor κb activity by genistein is mediated via Notch‐1 signaling pathway in pancreatic cancer cells. Int. J. Cancer, 118:1930–1936. doi:10.1002/ijc.21589; corrected by Erratum: Inhibition of nuclear factor κb activity by genistein is mediated via Notch‐1 signaling pathway in pancreatic cancer cells. Int. J. Cancer, 134: E3. doi: .

Genistein selectively potentiates arsenic trioxide‐induced apoptosis in human leukemia cells via reactive oxygen species generation and activation of reactive oxygen species‐inducible protein kinases (p38‐MAPK, AMPK)

“…Actually, the 14 hr treatment period is shorter than the genistein treatments generally used by other authors to down-regulate the steady-state activity of NF-jB, or prevent its activation by stressing agents. [20][21][22]24,48 Moreover, while in other works genistein was used in combination with stressing treatments that activated NF-jB, 21,22,24 ATO does not stimulate NF-jB in leukemia cells, as observed in the present experiments and also reported in preceding studies. 42,49 By contrast, the pro-oxidant action of genistein may adequately explain its capacity to potentiate ATO toxicity in leukemia cells.…”

Significance of Notch1-signaling Pathway in Human Pancreatic Development and Carcinogenesis

“…The GSIs being tested to treat pancreatic cancers include MK0752 (Merck) and RO04929097 (Roche/Genentech). Recent literature also indicates that both Notch1 and Notch 2 are important members involved in pancreatic carcinogenesis 11, 13–15 .…”

RNAi-mediated knockdown of Notch-1 leads to cell growth inhibition and enhanced chemosensitivity in human breast cancer

“…Down-regulation of Notch-1 was found to cause apoptosis in adult T-ALL and pancreatic cancer (17,18). Yet there is discrepancy about the effect of down-regulation of Notch-1 on human breast cancer.…”