Editorial Board

The content of this site is guided by the contribution of our Editorial Board members, who have played pivotal roles in advancing our understanding of apoptosis both as a driver of cancer and as a potential target for cancer therapy.


Avi Ashkenazi, PhD

Senior Staff Scientist and Director, Molecular Oncology Department, Genentech, Inc., South San Francisco

Avi Ashkenazi trained and completed his PhD at the Hebrew University of Jerusalem, Israel. He completed postdoctoral research in the Department of Hormone Research at the University of California, San Francisco and in the Department of Molecular Biology at Genentech, Inc., where he studied the molecular biology and biochemistry of novel muscarinic acetylcholine receptors. Dr Ashkenazi joined Genentech, Inc. in 1989 as a Scientist, becoming a Staff Scientist in the Molecular Oncology Department in 1999. He was appointed Director of the Molecular Oncology Department in 2005 and Senior Staff Scientist in 2006. His research is focused on the biologic roles of the tumor necrosis factor ligand and receptor gene superfamilies in the regulation of apoptosis and immunity, and their potential utility as agents or targets for the treatment of cancer and/or autoimmune disease. His laboratory independently discovered Apo2L/TRAIL and its receptors, elucidated their apoptosis signaling mechanisms, and is currently assessing their potential for cancer therapy.

Dr Ashkenazi is a world-renowned leader in the study of apoptosis and has received several honors and awards, including First Prize, the Boehringer Ingelheim Award in 1988. He is a member of the Board of Trustees of the Israel Cancer Research Fund and of the American Association for Cancer Research's Laboratory Research Awards Committee. Dr Ashkenazi has co-authored more than 100 publications in peer-reviewed scientific and medical journals, has presented more than 75 talks at scientific and medical conferences, has co-edited a book on antibody fusion proteins, and is a named inventor on over 25 issued patents. He is a member of the editorial boards of several international peer-reviewed journals, including Cancer Biology and Therapy, Cell Death and Differentiation, Current Biology, the Journal of Biological Chemistry, and Nature Reviews Cancer: Highlights.

 

Gerard Evan, PhD, FRS

Gerard Evan was born and raised in London, UK and received his MA in Biochemistry from the University of Oxford in 1977. He then moved to the Medical Research Council (MRC) Laboratory of Molecular Biology at the University of Cambridge, where he gained a PhD in Molecular Immunology in 1981 using monoclonal antibodies to define immunologic targets on tumor cells. He was first an MRC Traveling Fellow and later a UK Science Research Council Postdoctoral Fellow in the laboratory of J Michael Bishop at the University of California San Francisco (UCSF) from 1982 to 1984. There he developed an abiding interest in the molecular mechanisms of cell growth and cell death, focusing particularly on elucidating the biology of the enigmatic Myc protein — a powerful engine of cell proliferation that is aberrantly expressed in most human cancers. In 1988 he was recruited to the Imperial Cancer Research Fund (ICRF) Laboratories in London and appointed Napier Professor of the Royal Society in 1996. In 2001, Dr Evan was the Eppley Visiting Professor of Cancer Research at the University of Nebraska, Omaha and a Visiting Professor of the Norwegian Academy of Sciences; in 2002 he was Visiting Professor at the European Cancer Genetics School in Italy and, in 2003, Visiting Professor at the National University of Singapore. He is a member of the European Molecular Biology Organization, a Fellow of the UK Academy of Medical Sciences, and a Fellow of the Royal Society of London. Dr Evan's research is focused on understanding the processes responsible for genesis and maintenance of cancers (in particular, cancers of the pancreas, colon, brain, skin, and liver). In 1992, he made the unexpected and counter-intuitive discovery that mutations that drive cancer cell proliferation also drive the contradictory pathway of cell suicide and proposed that this coupling of opposing pathways is a central innate tumor suppressive mechanism built into all human cells. Only when this coupling fails can cancers emerge and, by inference, re-instatement of the defective cell suicide pathway would lead to the rapid and specific demise of cancer cells. Understanding the molecular mechanisms that underlie the cell suicide machinery and how it can be manipulated therapeutically are the overarching aims of his laboratory.

 

Herbert Hurwitz, MD

Herbert Hurwitz completed his medical training at Thomas Jefferson University in Philadelphia and began his career with a residency in Internal Medicine at the Michael Reese Hospital in Chicago. In 1992, he became a Clinical Fellow in Oncology at The Johns Hopkins Oncology Center in Baltimore, where he also obtained a masters degree in clinical investigation. Dr Hurwitz is actively involved in clinical trials of new anticancer drugs, in particular, anti-angiogenic agents, drug combinations, and radiotherapy-containing regimens and has a particular, interest in gastrointestinal cancer. Dr Hurwitz was the principal investigator on the pivotal bevacizumab trial, which led to the approval of bevacizumab in the treatment of metastatic colorectal cancer. His work currently focuses on the mechanism of resistance, sensitivity, and toxicity for anti-angiogenic agents. His research also includes the potential role of apoptotic signaling pathways in for the treatment of cancer.

Dr Hurwitz has authored or co-authored more than 50 publications in peer-reviewed scientific and medical journals and often presents at national and international scientific and professional gatherings. He is a member of the American Association for Cancer Research and the American Society of Clinical Oncology.