Masashi Narita's research focuses on understanding mechanisms of cellular response to the stresses, such as cellular senescence and apoptosis. Senescent cells cease to proliferate. The stability of this cell cycle arrest is critical for the tumour suppressive role of senescence, as some senescent cells persist within tissues for long periods (e.g. Naevi are benign tumours that cease proliferating, due to senescence arrest). However, not all senescent cells persist, but if they do, they can be harmful. Senescent cells are not inert, but rather actively communicate with their surroundings, influencing the microenvironment and potentially burdening the tissue. Hence senescent cells can also be cleared from the tissue, typically via activating an immune response. An imperfect clearance of senescent cells from the tissue microenvironment may promote cancer and degenerative disorders. In this framework, Masashi Narita's lab aim to answer the following questions: (1) How gene expression is regulated during senescence, compared with other stress responses; (2) how cell communication modulates senescence-associated phenotypes; (3) how senescence modulates tumour initiation; (4) how ageing contributes to tumorigenesis, and (5) why benign tumours are benign?