Somatic activation of the K-ras oncogene causes early onset lung cancer in mice

By L. Johnson, Kim L. Mercer, D. Greenbaum, R. Bronson, D. Crowley, D. Tuveson, T. Jacks. Nature, 2001

1,217 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/361a20ab478f9bccf83f404099a96c5ce1dbe581

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Citations in the corpus

Recent insights into the function of autophagy in cancer (2016, background): “Spontaneous non-small-cell lung cancer (NSCLC) arises following Kras activation through a stepwise progression from hyperplasia to adenoma to adenocarcinoma, associated with spontaneous mutation in p53 (Jackson et al. 2001; Johnson et al. 2001).”
Environment impacts the metabolic dependencies of Ras-driven non-small cell lung cancer (2016, background): “…allele in somatic cells and initiates primarily low grade lung adenomas that progress to invasive adenocarcinomas over the period of 6–8 months (Johnson et al., 2001), 2) Intratracheal delivery of adenoviral Cre (Ad5-CMV-Cre) to the lungs of animals harboring conditional KrasLSL-G12D/+;…”
Modulation of K-ras-dependent lung tumorigenesis by microRNA-21 (2010, neutral): “Unlike K-ras;p53 / compound mutant mice (Johnson et al., 2001), we did not observe an increased tumor spectrum or increased metastasis in the CAGmiR-21;K-rasmutant mice.”
Analysis of lung tumor initiation and progression using conditional expression of oncogenic K-ras. (2001, methodology): “noprecipitation were performed as described in Johnson et al. (1997).”
A gene expression signature associated with "K-Ras addiction" reveals regulators of EMT and tumor cell survival. (2009, background): “K-ras mutations occur most frequently in adenocarcinomas of the lung, pancreas, and colon, and mutational activation of K-Ras in these tissues is sufficient to initiate neoplasia in mice (Aguirre et al., 2003; Haigis et al., 2008; Johnson et al., 2001).”
Tumor induction by an endogenous K-ras oncogene is highly dependent on cellular context. (2003, methodology): “transformation by ras oncogenes requires abrogation of cellular senescence programs, for instance by mutation of the P53 or Several in vivo models expressing K-ras oncogenes have been recently described (Fisher et al., 2001; Jackson et al., INK4a tumor suppressor pathways. Here, we show that express”
Hexokinase 2 is required for tumor initiation and maintenance and its systemic deletion is therapeutic in mouse models of cancer (2013, methodology): “To test whether systemic ablation of HK2 can reverse tumorigenesis in vivo, we used the KRasLA2-G12D NSCLC mouse model, in which lung tumors are developed with an early onset and complete penetrance (Johnson et al., 2001).”
Guidelines for the welfare and use of animals in cancer research (2010, background): “…Mutant Trp53 Pancreas-specific K-rasG12D+Ink4a/Arf deficiency or combined withTrp53R172H Metastatic lung cancer Metastatic pancreatic cancer (Johnson et al, 2001) (Aguirre et al, 2003; Hingorani et al, 2005) AML1/ETO or MLL fusion proteins AML AML (Zuber et al, 2009) MYCN…”
LKB1 modulates lung cancer differentiation and metastasis (2007, neutral): “Only point mutation or deletion 8 of 80 (10) 4 of 42 (10) 1 of 22 (5) 13 of 144 (9) Only single-copy loss by MLPA 11 of 80 (14) 2 of 42 (5) 1 of 22 (5) 14 of 144 (10) Homozygous mutation or deletion 8{ of 80 (10) 2 of 42 (5) 0 of 22 (0) 10 of 144 (7) Total 27 of 80 (34) 8 of 42 (19) 2 of 22 (9) 37 o”
Induction and apoptotic regression of lung adenocarcinomas by regulation of a K-Ras transgene in the presence and absence of tumor suppressor genes. (2001, background): “Our results, those of Johnson et al. (2001), and similar results from a K-Ras-based model produced by A. Berns and his colleagues (Meuwissen et al. 2001) raise the possibility that mutant K-Ras, even at physiologically normal or subnormal levels (Table 1), is sufficient to drive proliferation in at…”