Scopus Publication Detail
The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in Scopus. This abstract is what is used to create the fingerprint of the publication.
Boning Gao; Adi F Gazdar; John D Minna; Jerry W Shay; Yang Xie; Hao Tang)
Molecular Cancer Research. 2013;11(6):638-650.Abstract
We used CDK4/hTERT - immortalized normal human bronchial epithelial cells (HBEC) from several individuals to study lung cancer pathogenesis by introducing combinations of common lung cancer oncogenic changes (p53, KRAS, and MYC) and followed the stepwise transformation of HBECs to full malignancy. This model showed that: (i) the combination of five genetic alterations (CDK4, hTERT, sh-p53, KRAS, and c-MYC) is sufficient for full tumorigenic conversion of HBECs; (ii) genetically identical clones of transformed HBECs exhibit pronounced differences in tumor growth, histology, and differentiation; (iii) HBECs from different V12 individuals vary in their sensitivity to transformation by these oncogenic manipulations; (iv) high levels of KRAS are required for full malignant transformation of HBECs, however, prior loss of p53 function is required to prevent oncogene-induced senescence; (v) overexpression of c-MYC greatly enhances malignancy but only in the context of sh-p53+KRAS V12; (vi) growth of parental HBECs in serum-containing medium induces differentiation, whereas growth of oncogenically manipulated HBECs in serum increases in vivo tumorigenicity, decreases tumor latency, produces more undifferentiated tumors, and induces epithelial-to-mesenchymal transition (EMT); (vii) oncogenic transformation of HBECs leads to increased sensitivity to standard chemotherapy doublets; (viii) an mRNA signature derived by comparing tumorigenic versus nontumorigenic clones was predictive of outcome in patients with lung cancer. Collectively, our findings show that this HBEC model system can be used to study the effect of oncogenic mutations, their expression levels, and serum-derived environmental effects in malignant transformation, while also providing clinically translatable applications such as development of prognostic signatures and drug response phenotypes. © 2013 American Association for Cancer Research.
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
Daniel T. Starczynowski; William W. Lockwood; Sophie Deléhouzée; Raj Chari; Joanna Wegrzyn; Megan Fuller; Ming-Sound Tsao; Stephen Lam; Adi F. Gazdar; Wan L. Lam; et al.Journal of Clinical Investigation. 2011;121(10):4095-4105.
Noriaki Sunaga; David S. Shames; Luc Girard; Michael Peyton; Jill E. Larsen; Hisao Imai; Junichi Soh; Mitsuo Sato; Noriko Yanagitani; Kyoichi Kaira; et al.Molecular Cancer Therapeutics. 2011;10(2):336-346.
Julian Carretero; Takeshi Shimamura; Klarisa Rikova; Autumn L. Jackson; Matthew D. Wilkerson; Christa L. Borgman; Matthew S. Buttarazzi; Benjamin A. Sanofsky; Kate L. McNamara; Kathleyn A. Brandstetter; et al.Cancer Cell. 2010;17(6):547-559.
Appears in this Document