Synergistic tumor suppressor activity of BRCA2 and p53 in a conditional mouse model for breast cancer

By J. Jonkers, R. Meuwissen, H. Gulden, H. Peterse, M. A. Valk, A. Berns. Nature Genetics, 2001

1,106 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/f757247f9c79bc2c93b9d1a1223deffdd3c3ee81

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Citations in the corpus

Mutant p53 drives invasion by promoting integrin recycling. (2009, methodology): “For intestinal tumorigenesis experiments, AhCre, Apc580 s (referred to as Apcfl) (Sansom et al., 2004), p53fl (Jonkers et al., 2001), and Lox stop lox p53R172H (Olive et al., 2004) alleles were used.”
P53 and Pten control neural and glioma stem/progenitor cell renewal and differentiation (2008, positive): “To explore the role of p53 and Pten in glioma, we utilized the hGFAP-Cre transgene 5, 6 to delete p53 alone or in combination with Pten in all CNS lineages using conditional p53 7 and Pten alleles (Supplementary Fig.”
Mutant p53 drives metastasis and overcomes growth arrest/senescence in pancreatic cancer (2010, methodology): “mouse strains have been previously described (8, 12, 20, 22, 29, 41, 42).”
Homologous recombination and human health: the roles of BRCA1, BRCA2 and associated proteins (2015, background): “Mice deleted for the BRC-encoding exon 11 in the germline are inviable, whereas somatic exon 11 deletion causes tumor development (Jonkers et al. 2001).”
Gata-3 is an essential regulator of mammary-gland morphogenesis and luminal-cell differentiation (2007, background): “Initially, keratin 14 (K14)–cre;Gata-3 f/f mice were analysed, in which the K14 promoter drives excision not only in the skin, but also in luminal and myoepithelial cells of the mammary glan”
High sensitivity of BRCA1-deficient mammary tumors to the PARP inhibitor AZD2281 alone and in combination with platinum drugs (2008, methodology): “Brca1 / ;p53 / mammary tumors were generated in K14cre;Brca1F/F;p53F/F mice, genotyped, and orthotopically transplanted into syngeneic wild-type mice as described (12, 13, 34).”
Somatic inactivation of E-cadherin and p53 in mice leads to metastatic lobular mammary carcinoma through induction of anoikis resistance and angiogenesis. (2006, methodology): “Blotting and hybridization was performed as described (Jonkers et al., 2001).”
p53 target genes sestrin1 and sestrin2 connect genotoxic stress and mTOR signaling. (2008, neutral): “Using hepatocyte-specific p53 knockout mice created by crossing p53 F/F mice (Jonkers et al., 2001) with Alb-Cre mice (Postic et al., 1999), we confirmed that induction of Sesn2 and p21 Waf1 by DEN was p53 dependent (Figure S6H).”