Dr. Ashworth received his . in biochemistry from the University College London in 1984. After his postdoctoral fellowship at the University College London and The Institute of Cancer Research (ICR), he joined the faculty of ICR, becoming the first Director of the Breakthrough Breast Cancer Research Center in 1999 and ICR’s Chief Executive Officer in 2011. In 2015, Dr. Ashworth joined the University of California San Francisco (UCSF) as President of the UCSF Helen Diller Family Comprehensive Cancer Center and Senior Vice President for cancer clinical services in UCSF Health. He is a Professor of Medicine in the Division of Hematology/Oncology, Department of Medicine, and E. Dixon Heise Distinguished Professor in Oncology. He is the co-director of UCSF’s Center for BRCA Research, which opened in 2016, and inaugural chair of the University of California Cancer Consortium that launched in September 2017. Dr. Ashworth’s pioneering research has shed light on some of the genetic changes that drive many inherited breast cancers, stimulated a new a field of research, and advanced the development of a novel class of “synthetic lethal” cancer therapies. His continuous focus on translating his laboratory finding to the clinic has paved the way for more personalized treatment options for patients with BRCA mutations, and will have a lasting impact for years to come.
The activation of gene transcription is a multistep process that is triggered by factors that recognize transcriptional enhancer sites in DNA . These factors work with co-activators to direct transcriptional initiation by the RNA polymerase II apparatus. The mediator of RNA polymerase II transcription subunit 1 protein is a subunit of the CRSP (cofactor required for SP1 activation) complex, which, along with TFIID , is required for efficient activation by SP1. This protein is also a component of other multisubunit complexes [., thyroid hormone receptor -(TR-) associated proteins that interact with TR and facilitate TR function on DNA templates in conjunction with initiation factors and cofactors]. It also regulates p53 -dependent apoptosis and it is essential for adipogenesis . This protein is known to have the ability to self-oligomerize.