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Articles by Denada Dibra
"Triple-Negative Breast Tumors Are Dependent on Mutant p53 for Growth a" by Denada Dibra, Sydney M Moyer et al.
Abstract The TP53 tumor suppressor gene is mutated early in the majority of patients with triple-negative breast cancer (TNBC). The most frequent TP53 alterations are missense mutations that contribute to tumor aggressiveness. We developed an autochthonous somatic K14-Cre driven TNBC mouse model with p53R172H and p53R245W mutations in which mutant p53 can be toggled on and off genetically while leaving the tumor microenvironment intact and wild-type for p53.
"p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-drive" by Denada Dibra, Mihai Gagea et al.
Abstract Obesity is a significant global health concern. Non-alcoholic fatty liver disease and non-alcoholic steatohepatitis (NASH) are common risk factors for hepatocellular carcinoma (HCC) and are closely associated with metabolic comorbidities, including obesity and diabetes. The TP53 tumor suppressor is the most frequently mutated gene in liver cancers, with half of these alterations being missense mutations.
"Mutant p53 Protects Triple-Negative Breast Adenocarcinomas From Ferrop" by Denada Dibra, Shunbin Xiong et al.
The TP53 tumor suppressor gene is mutated early in most of the patients with triple-negative breast cancer (TNBC). The most frequent TP53 alterations are missense mutations that contribute to tumor aggressiveness. Here, we used an autochthonous somatic TNBC mouse model, in which mutant p53 can be toggled on and off genetically while leaving the tumor microenvironment intact and wild-type for p53 to identify physiological dependencies on mutant p53.
p53R172H and p53R245W Hotspot Mutations Drive Distinct Transcriptomes in Mouse Mammary Tumors Through a Convergent Transcriptional Mediator
Aggressive breast cancers harbor TP53 missense mutations. Tumor cells with TP53 missense mutations exhibit enhanced growth and survival through transcriptional rewiring. To delineate how TP53 mutations in breast cancer contribute to tumorigenesis and progression in vivo, we created a somatic mouse model driven by mammary epithelial cell-specific expression of Trp53 mutations.
Mutant p53 protects triple-negative breast adenocarcinomas from ferroptosis in vivo
Research Article CANCER Denada Dibra https://orcid.org/0000-0003-4764-4965, Shunbin Xiong, [...] , Sydney M. Moyer https://orcid.org/0000-0002-2911-4058, Adel K. El-Naggar, [...] , Yuan Qi https://orcid.org/0000-0001-9718-7593, Xiaoping Su https://orcid.org/0000-0003-1824-943X, Elisabeth K.
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