2006
DOI: 10.1158/0008-5472.can-06-1495
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Abstract: Little is known about the mechanisms that underlie Brca1-associated ovarian tumorigenesis, mainly due to the lack of an appropriate experimental model. We developed genetically defined primary mouse ovarian surface epithelial (OSE) cell lines in which the loss of functional Brca1 and p53 recapitulates the events that are thought to occur in early ovarian cancer development in patients with Brca1 mutations. This system allows for the introduction of additional oncogenes that are thought to cooperate with the lo… Show more

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Cited by 110 publications
(121 citation statements)
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“…35 BRCA1-deficient mouse ovarian epithelial cells were also shown to have increased sensitivity to platinum. 36,37 Furthermore, it has been shown in breast cancer that BRCA1 functions as a differential modulator of chemotherapy-induced apoptosis in the presence of a range of cytotoxic agents. 5 Overexpression of BRCA1 in OC cells in vivo led to resistance to DNA-damaging agents including cisplatin, etoposide and doxorubicin.…”
Section: Discussionmentioning
confidence: 99%
“…35 BRCA1-deficient mouse ovarian epithelial cells were also shown to have increased sensitivity to platinum. 36,37 Furthermore, it has been shown in breast cancer that BRCA1 functions as a differential modulator of chemotherapy-induced apoptosis in the presence of a range of cytotoxic agents. 5 Overexpression of BRCA1 in OC cells in vivo led to resistance to DNA-damaging agents including cisplatin, etoposide and doxorubicin.…”
Section: Discussionmentioning
confidence: 99%
“…A subsequent systematic review by (Stordal et al 2009), revealed that BRCA1 was the mostly likely genetic player in this relationship. Cells with BRCA1 defects have reduced efficiency in repairing DNA adducts and show increased apoptosis in response to platinums conferring sensitivity (Foulkes 2006;Xing et al 2006). The response to taxanes, in BRCA1 deficient cells is reduced apoptosis conferring resistance (Lafarge et al 2001).…”
Section: Introductionmentioning
confidence: 99%
“…In one epidemiological study (Villeneuve et al, 1999), no instance of p53 loss was observed without simultaneous loss of BRCA1. To test this model in a more defined setting, Xing and Orsulic (Xing and Orsulic, 2006) generated a mouse model in which to study p53 and Brca1 interaction further. They observed that inactivation of Brca1 and p53 in mouse OSE cells of ovary explants did not lead to transformation unless the Myc oncogene is over expressed virally, while ClarkKnowles et al reported increased proliferation in mouse OSE cells deficient for Brca1 and p53 but no increase if Brca1 or p53 was inactivated independently (Clark-Knowles et al, 2006).…”
Section: Mutations In the P53 Pathwaymentioning
confidence: 99%