Tumor induction by an endogenous K-ras oncogene is highly dependent on cellular context.

By C. Guerra, Nieves Mijimolle, Alma Dhawahir, P. Dubus, M. Barradas, Manuel Serrano, V. Campuzano, M. Barbacid. Cancer Cell, 2003

595 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/264a1a473e21a13d1225a6a6e11fafce175b7212

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. R. DePinho
2. Manuel Serrano
3. Hans Clevers
4. N. Bardeesy
5. D. Tuveson
6. Alec C. Kimmelman
7. R. Vries
8. T. Jacks

In Oncology

1. Hans Clevers
2. D. Tuveson
3. T. Jacks
4. R. DePinho
5. M. Collado
6. Manuel Serrano
7. Giulia Biffi
8. D. Peeper

Citations in the corpus

• Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice. (2007, methodology): “…of cryosections (10 mm) (2–4 hr for tissues of Elas-tTA/tetO-Cre/Rosa26R mice and pancreata of tumor-bearing K-Ras+/LSLG12Vgeo;Elas-tTA/tetO-Cre animals and up to 48 hr for normal tissues of K-Ras+/LSLG12Vgeo;Elas-tTA/tetO-Cre mice) was carried out as previously described (Guerra et al., 2003).”
• Preinvasive and invasive ductal pancreatic cancer and its early detection in the mouse. (2003, background): “Nevertheless, we see the slowly progressive acquisitionregion of a mutated KRAS locus (Guerra et al., 2003).”
• Senescence in tumours: evidence from mice and humans (2010, background): “It is now well established that induction of senescence by oncogenic Ras in vitro occurs only when the oncogene is overexpressed, but not when the oncogene is expressed at its normal level”
• Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer (2014, unknown): “Activating mutations in KRAS are present in the majority of human PDAC cases, and genetically engineered mouse (GEM) models have substantiated critical roles of oncogenic Kras in driving tumor initiation and in enabling tumor progression along with deficiencies of P53, Ink4a/Arf, Smad4, and/or Pten ”
• Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma. (2003, background): “However, recent studies have shown that such a direct loop is not operative in response to endogenous—as opposed to overexpressed— levels of activated RAS (Guerra et al. 2003; D. Tuveson and T. Jacks, pers. comm.).”
• Hyperactive Ras in developmental disorders and cancer (2007, background): “In an elegant series of experiments, strains of mice were created that express an oncogenic Kras G12D or Kras G12V allele from the endogenous Kras locu”
• Organoid Models of Human and Mouse Ductal Pancreatic Cancer (2014, background): “…have been proposed for the development of PDA, with the pancreatic acinar cell hypothesized to be amajor contributor to PDA initiation (De La O et al., 2008; Gidekel Friedlander et al., 2009; Guerra et al., 2003; Habbe et al., 2008; Kopp et al., 2012; Morris et al., 2010; Sawey et al., 2007).”
• Genetics and biology of pancreatic ductal adenocarcinoma. (2006, background): “…by studies in mouse cells in which an activated K-RAS allele, expressed at physiological levels, provokes immortalization of fibroblasts in vitro and preneoplastic hyperplasias of the lung and GI track when activated in vivo (Jackson et al. 2001; Guerra et al. 2003; Tuveson et al. 2004).”
• The essence of senescence. (2010, background): “Subsequently, several groups reported that RAS and mutant RAF proteins act mitogenically or, conversely, drive cells into senescence as a function of increasing expression levels (Woods et al. 1997; Guerra et al. 2003; Deng et al. 2004; Tuveson et al. 2004; Sarkisian et al. 2007; Chen et al. 2009).”