Global Increase of p16INK4a in APC-Deficient Mouse Liver Drives Clonal Growth of p16INK4a-Negative Tumors

Repository of the Max Delbrück Center for Molecular Medicine (MDC) in the Helmholtz Association http://edoc.mdc-berlin.de/14379 Global increase of p16INK4a in APC-deficient mouse liver drives clonal growth of p16INK4a negative tumors

p16INK4a suppresses BRCA1-deficient mammary tumorigenesis

Senescence prevents the proliferation of genomically damaged, but otherwise replication competent cells at risk of neoplastic transformation. p16INK4A (p16), an inhibitor of CDK4 and CDK6, plays a critical role in controlling cellular senescence in multiple organs. Functional inactivation of p16 by gene mutation and promoter methylation is frequently detected in human breast cancers. However, d...

Oval cell proliferation in p16INK4a expressing mouse liver is triggered by chronic growth stimuli

Terminal differentiation requires molecules also involved in aging such as the cell cycle inhibitor p16(INK4a). Like other organs, the adult liver represents a quiescent organ with terminal differentiated cells, hepatocytes and cholangiocytes. These cells retain the ability to proliferate in response to liver injury or reduction of liver mass. However, under conditions which prevent mitotic act...

Study of Rest as a Negative Regulator of P16ink4a

iii Dedication To God, who has blessed me with a wonderful family and amazing opportunities. To my family who has shown me unconditional love and support. You have been my stability, my rock, and my biggest fans. You have been there every step of the way and have picked me back up when I felt like giving up. You have shown me that together, we are unbreakable. To my parents who have been my str...

p16INK4a Expression in Porokeratosis

Vol. 29, No. 3, 2017 373 Received February 5, 2016, Revised May 16, 2016, Accepted for publication June 27, 2016 Corresponding author: Masutaka Furue, Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashiku, Fukuoka 812-8582, Japan. Tel: 81-92-642-5581, Fax: 81-92-642-5600, E-mail: [email protected] This is an Open Access arti...