Alexandria P Eiken, Audrey L Smith, Sydney A Skupa, Elizabeth Schmitz, Sandeep Rana, Sarbjit Singh, Siddhartha Kumar, Jayapal Reddy Mallareddy, Aguirre A de Cubas, Akshay Krishna, Achyuth Kalluchi, M Jordan Rowley, Christopher R D'Angelo, Matthew A Lunning, R Gregory Bociek, Julie M Vose, Amarnath Natarajan, Dalia El-Gamal
Chronic lymphocytic leukemia (CLL) cell survival and growth is fueled by the induction of B-cell receptor (BCR) signaling within the tumor microenvironment (TME) driving activation of NF-κB signaling and the unfolded protein response (UPR). Malignant cells have higher basal levels of UPR posing a unique therapeutic window to combat CLL cell growth using pharmacological agents that induce accumulation of misfolded proteins. Frontline CLL therapeutics that directly target BCR signaling such as Bruton-tyrosine kinase (BTK) inhibitors (e...
April 30, 2024: Cancer Res Commun