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Sarah Francoz

Researcher at Free University of Brussels

Publications -  14
Citations -  2242

Sarah Francoz is an academic researcher from Free University of Brussels. The author has contributed to research in topics: Mdm2 & MDMX. The author has an hindex of 11, co-authored 14 publications receiving 2063 citations. Previous affiliations of Sarah Francoz include Flanders Institute for Biotechnology & Ghent University.

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Inactivation of the p53 pathway in retinoblastoma

TL;DR: It is shown that the tumour surveillance pathway mediated by Arf, MDM2, MDMX and p53 is activated after loss of RB1 during retinogenesis, providing evidence that the p53 pathway is inactivated in retinoblastoma and that this cancer does not originate from intrinsically death-resistant cells as previously thought.
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Keeping p53 in check: essential and synergistic functions of Mdm2 and Mdm4.

TL;DR: This work presents a novel and scalable approach to gene expression engineering that allows for real-time annotation of gene expression changes in response to cancerigenicity and shows promise in finding novel and efficient treatments for cancer.
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Amplification of Mdmx (or Mdm4) directly contributes to tumor formation by inhibiting p53 tumor suppressor activity

TL;DR: It is shown that retrovirus-mediated Mdmx overexpression allows primary mouse embryonic fibroblast immortalization and leads to neoplastic transformation in combination with HRasV12, and this results make Hdmx a new putative drug target for cancer therapy.
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c-Raf, but Not B-Raf, Is Essential for Development of K-Ras Oncogene-Driven Non-Small Cell Lung Carcinoma

TL;DR: Results indicate that c-Raf plays a unique role in mediating K-Ras signaling and makes it a suitable target for therapeutic intervention.
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Mdm4 and Mdm2 cooperate to inhibit p53 activity in proliferating and quiescent cells in vivo

TL;DR: A p53 knock-in allele is combined, in which p53 is silenced by a transcriptional stop element flanked by loxP sites, with the mdm2- and mdm4-null alleles, which allows Cre-mediated conditional p53 expression in tissues in vivo and cells in vitro lacking Mdm2, Mdm4, or both.