A study by researchers from the Florida campus of The Scripps Research Institute (TSRI) implicate Notch 1 as a critical effector in K-ras-driven lung adenocarcinoma and as a regulator of p53 at a post-translational level.
In the study, supported by the National Institutes of Health(NIH) was published the August 13, 2013 online edition of the journal Cancer Research. [1]
These findings directly provide important clinical insights into the correlation between Notch 1 activity and the poor prognosis of NSCLC patients who carry the non-mutated form of the p53 gene. ?If you look at lung cancer patient populations, Notch signaling alone isn?t a prognostic indicator, but if you look at p53-positive patients it is,” Josehen Kissil, Ph.D, (Photo) Associate Professor at the Department of Cancer Biology, The Scripps Research Institute, Florida Campus, and the lead scientists of the study, explained.
In an earlier and unrelated study, scientists found that activated Notch 1 substitutes for RAS activation synergistically with Myc in the development of NSCLC.[2]
For more information:
[1] Licciulli S, Avila JL, Hanlon L, Troutman S, Cesaroni M, Kota S, Keith B, et al. Notch1 is required for Kras-induced lung adenocarcinoma and controls tumor cell survival via p53.Cancer Res. 2013 Aug 13. [Epub ahead of print][Article][PubMed]
[2] Allen TD, Rodriguez EM, Jones KD, Bishop JM. Activated Notch1 induces lung adenomas in mice and cooperates with Myc in the generation of lung adenocarcinoma.Cancer Res. 2011 Sep 15;71(18):6010-8. doi: 10.1158/0008-5472.CAN-11-0595. Epub 2011 Jul 29. [Article][PubMed]
Photo: Joseph Kissi, Ph.D, Associate Professor at the Department of Cancer Biology, The Scripps Research Institute, Florida Campus. Photo Courtesy: The Scripps Research Institute (TSRI).
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