CDK4/6 Inhibition Induces Senescence and Enhances Radiation Response by Disabling DNA Damage Repair in Oral Cavity Squamous Cell Carcinoma.

Purpose: HPV(-) OCSCC resists radiation treatment. The gene, encoding p16INK4A, is commonly disrupted in OCSCC. p16 inhibits CDK4/CDK6, leading to cell cycle arrest, but the biological sequelae of CDK4/6 inhibition in OCSCC remains understudied.

The recent and future health burden of the U.S. mobile sector apportioned by source.

Mobile sources emit particulate matter as well as precursors to particulate matter (PM) and ground-level ozone, pollutants known to adversely impact human health. This study uses source-apportionment photochemical air quality modeling to estimate the health burden (expressed as incidence) of an array of PM- and ozone-related adverse health impacts, including premature death, attributable to 17 mobile source sectors in the US in 2011 and 2025. Mobile sector-attributable air pollution contributes a substantial fraction of the overall pollution-related mortality burden in the U.

Palbociclib Renders Human Papilloma Virus-Negative Head and Neck Squamous Cell Carcinoma Vulnerable to the Senolytic Agent Navitoclax.

We demonstrate that inhibition of cyclin-dependent kinases 4/6 (CDK4/6) leads to senescence in human papillomavirus (HPV)-negative (-) head and neck squamous cell carcinoma (HNSCC), but not in HPV-positive (+) HNSCC. The BCL-2 family inhibitor, navitoclax, has been shown to eliminate senescent cells effectively. We evaluated the efficacy of combining palbociclib and navitoclax in HPV HNSCC.