David Sekula

TL;DR: RA-induced cyclin D1 proteolysis is highlighted as a mechanism signaling growth inhibition at G1 active in the prevention of human bronchial epithelial cell transformation.

TL;DR: It is demonstrated that retinoids promote ubiquitination and degradation of cyclin D1 during retinoid-induced differentiation of human embryonal carcinoma cells and that all-trans-retinoic acid (RA) treatment strongly implicates RA-mediated degradation of cycling D1 as a means of coupling induced differentiation and cell cycle control of human embryos.

TL;DR: UBE1L is proposed as a direct pharmacological target that overcomes oncogenic effects of PML/RARα by triggering its degradation and signaling apoptosis in APL cells.

TL;DR: Findings indicate how effective chemoprevention prevents carcinogenic transformation of bronchial epithelial cells when repair of genomic damage does not select against EGFR overexpressing cells.

TL;DR: The degradation of cyclin D1 is a candidate intermediate marker for effective retinoid-mediated cancer chemoprevention in the aerodigestive tract and is investigated as a common chemopsrevention signal in normal and neoplastic human bronchial epithelial cells.