Carina R. Maier

TL;DR: It is shown that p53-deficient colon cancer cells exposed to tumor-like metabolic stress in spheroid culture activated the mevalonate pathway to promote the synthesis of ubiquinone, which was essential to maintain mitochondrial electron transport for respiration and pyrimidine synthesis in metabolically compromised environments.

TL;DR: It is shown that mTOR signaling and SREBP activity are sufficient to activate sapienate metabolism by increasing FADS2 expression, and targeting m TOR signaling can reduce sapienates metabolism in vivo.

TL;DR: In this paper, the authors used CRISPR/Cas9-mediated targeting of Trp53 and KRas in lung cancer patients to develop tumor models with similar morphology, marker expression and transcriptional profiles.

TL;DR: In this article, the deubiquitylase USP28 is recruited to sites of DNA damage in cisplatin-treated cells, which stabilizes ∆Np63.

TL;DR: This study reports that the deubiquitylase USP28 affects the FA DNA repair pathway during cisplatin treatment in SCC, thereby influencing therapy outcome, and presents a novel mechanism by which tumor cells, and in particular ΔNp63 expressing S CC, can be targeted to overcome chemotherapy resistance.