Dr. Mendelsohn's studies have been focused on nuclear receptor signaling. She was a post-doc in the Chambon Lab in Strasbourg, France, where she generated retinoic acid (Rar) receptor knockout mice, and characterized the phenotypes in mouse models. She subsequently began working on the urinary tract, defining the molecular and cellular role of retinoids in the kidney, ureter and bladder during development and during adult homeostasis, using a dominant negative RaraDN model to inactivate RA-signaling in distinct cell types.
More recently, her lab has been focused on the role of Pparg, a second member of the nuclear receptor superfamily in bladder formation, regeneration and cancer with the goal of identifying cellular and molecular changes that lead to bladder cancer using mouse models, organoids and cell culture. Recent studies from the Mendelsohn lab show that activating mutations in Pparg (VP16;Pparg) can drive luminal subtype bladder cancer formation in mice by controlling cell type specification of urothelial progenitors These Pparg-induced tumors are immune cold which is typical of human papillary luminal tumors which may be linked to loss of Nfkb expression. Nfkb is a major regulator of the immune response and its activity is suppressed by Pparg most likely via interactions at the Rela promoter. The lab is currently pursuing these observations, with the aim of identifying Pparg binding sites and down-stream transcriptional targets that are altered during tumor formation.
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Saturday, May 14, 2022
10:05 AM – 10:35 AM