期刊名称：ANNUAL REVIEW OF CANCER BIOLOGY
 期刊简介(About the journal)
投稿须知(Instructions to Authors)
编辑部信息(Editorial Board)
About the journal
The Annual Review of Cancer Biology reviews a range of subjects in cancer research that represent important and emerging areas in the field. With recent advances in our understanding of the basic mechanisms of cancer development and the translation of an increasing number of these findings into the clinic in the form of targeted treatments for the disease, the Annual Review of Cancer Biology is divided into three broad themes: Cancer Cell Biology, Tumorigenesis and Cancer Progression, and Translational Cancer Science.
Instructions to Authors
Editorial Board
Editorial Committee
Tyler Jacks, Co-Editor
Dr. Tyler Jacks is a world leader in the field of cancer genetics and is known for his ground-breaking work on the development of genetically-engineered mouse models of cancer (GEMMs). Over the course of his academic career, he has published over 200 peer- reviewed papers along with numerous review articles and book chapters. Dr. Jacks graduated magna cum laude with a BA in Biology in 1983 from Harvard College before becoming a graduate student in the laboratory of Dr. Harold Varmus at the University of California, San Francisco, where he showed that ribosomal frameshifting during translation gives rise to the gag-pol protein of the Rous sarcoma virus, HIV-1 virus and mouse mammary tumor virus. He went on to demonstrate that a stem-loop structure and RNA sequence making up the frameshift site are required for efficient frameshifting in vitro. In 1998, Dr. Jacks returned to Cambridge, Massachusetts, to join Dr. Robert Weinberg’s group as a post-doctoral fellow at the Whitehead Institute, where he developed several GEMMs, including the Rb, p53 and Nf1 mice. In 1992, Dr. Jacks became an assistant professor in the MIT Department of Biology and a member of the MIT Center for Cancer Research, which became the Koch Institute for Integrative Cancer Research at MIT in 2011. Currently, he is the David H. Koch Professor of Biology, Director of the Koch Institute for Integrative Cancer Research at MIT and an Investigator at the Howard Hughes Medical Institute.
The Jacks lab has focused on developing new methods for the construction and characterization of GEMMs of human cancer. His group has produced GEMMs with constitutive and conditional mutations in several tumor suppressor genes, oncogenes, and genes involved in cell cycle control and apoptosis. Using these strains, the laboratory has developed models of various human tumor syndromes and cancer types, including Li-Fraumeni Syndrome, neurofibromatosis type 1, astrocytoma, retinoblastoma, pancreatic cancer, invasive colon cancer, soft tissue sarcoma, endometriosis, ovarian cancer and lung adenocarcinoma. These GEMMS have been used to examine the mechanism of tumor initiation and progression, to uncover the molecular, genetic and biochemical relationship to the human diseases, as tools to study response and resistance to chemotherapy, and to explore methods in molecular imaging and early detection of cancer. His laboratory has also extensively studied human tumor-derived cells, determined protein function in these cells, and related gene expression patterns in human cancers to their studies in mouse models. Novel pathways and processes that are critical for the progression of cancer have been discovered during these investigations.
In recent years, the Jacks lab has moved into the burgeoning area of tumor immunology and utilizing GEMMs to understand the interactions between the immune system and cancer. In particular, the lab has developed a mouse model of lung adenocarcinoma that harbors mutations in the Kras and p53 genes and that also expresses model T cell antigens, which serve as targets for tumor-specific T cells and stimulate anti-tumor immune responses. These models offer a unique platform for investigating how anti-tumor immune responses shape tumor gene expression, and importantly how tumor evasion mechanisms contribute to the development of advanced disease. Moreover, they are invaluable preclinical models for testing immunotherapeutics, as single agents, or in combinations with traditional or targeted therapies.
Dr. Jacks has received numerous awards and honors for his contributions to the study of cancer genetics including the AACR Outstanding Achievement Award, the Amgen Award from the American Society of Biochemistry and Molecular Biology, the Chestnut Hill Award for Excellence in Medical Research, the Paul Marks Prize for Cancer Research, the Hope Funds for Cancer Research Award for Excellence and the Sergio Lombroso Award in Cancer Research. He was also a 2013 honoree of the MGH Cancer Center’s One Hundred celebration. Dr. Jacks served both as Chair and Member of the National Cancer Advisory Board at the National Cancer Institute as well as a member on the Board of Directors of the American Association for Cancer Research (AACR), where he was elected President of the organization in 2009. Dr. Jacks was also elected to the National Academy of Sciences, the Institute of Medicine of the National Academies, the American Academy of Arts and Sciences and the inaugural class of Fellows of the AACR Academy. Dr. Jacks serves on the Board of Directors of Thermo and Amgen. He is also a co-founder of T2 Biosystems and Dragonfly Therapeutics, and serves as an advisor to several other companies. In 2015, he was the recipient of the Killian Award, the highest honor the MIT faculty can bestow upon one of its members. He is currently serving as director of the Blue Ribbon Panel for the National Cancer Moonshot Initiative, a working group of the National Cancer Advisory Board that provides expert advice to the task force lead by former Vice-President Biden.
Charles L. Sawyers, Co-Editor
Charles L. Sawyers received a BA from Princeton University in 1981 and an MD from Johns Hopkins University School of Medicine in 1985, followed by an internal medicine residency at the University of California, San Francisco. He became a Howard Hughes Medical Institute investigator in 2002 while at the University of California, Los Angeles, and then moved to Memorial Sloan Kettering in 2006, where he currently serves as the Chair of the Human Oncology and Pathogenesis Program.
Dr. Sawyers studies mechanisms of cancer drug resistance with an eye toward developing novel therapies. He co-discovered the antiandrogen drug enzalutamide that was approved by the FDA in 2012 for the treatment of advanced prostate cancer. He shared the 2009 Lasker~DeBakey Clinical Medical Research Award for the development of the ABL kinase inhibitor imatinib for patients with chronic myeloid leukemia and the second-generation ABL inhibitor dasatinib to overcome imatinib resistance. He received the 2013 Breakthrough Prize in Life Sciences, the 2013 Taubman Prize for Excellence in Translational Medical Science, and the 2015 BBVA Knowledge Award in Biomedicine.
Dr. Sawyers is a member of the National Academy of Sciences, the National Academy of Medicine, and the American Academy of Arts and Sciences. He is past president of the American Association for Cancer Research (AACR) and the American Society of Clinical Investigation, was appointed to the National Cancer Advisory Board by President Obama, and has served on the Board of Directors of Novartis since 2013. He also serves as Steering Committee Chair of AACR Project GENIE, an international consortium of cancer centers that share genomic and clinical data from patients treated at their respective clinical sites.
Scott A. Armstrong, Committee Member
Scott A. Armstrong, MD, PhD, became the Chairman of the Department of Pediatric Oncology at Dana-Farber Cancer Institute in July 2016. He also serves as Associate Chief of the Division of Hematology/Oncology at Boston Children’s Hospital. He was previously the Director of the Center for Epigenetics Research at Memorial Sloan Kettering Cancer Center and Professor of Pediatrics at the Weill Cornell Medical College. Dr. Armstrong earned his medical degree and his PhD from University of Texas Southwestern Medical School in 1996. After internship and residency training with the Boston Combined Residency Program (BCRP) at Boston Medical Center and Boston Children’s Hospital, he completed a hematology/oncology fellowship at the Dana-Farber/Boston Children’s Cancer and Blood Disorders Center. The major focus of his career has been on delineating the biology of childhood cancers and the development of new therapeutic approaches for children with cancer. His research program has focused on the mechanisms of leukemia development and the relationship between leukemia and normal hematopoietic stem cells. He continues to direct a vigorous research program that focuses on development of new therapeutics that target chromatin based mechanisms, and he is actively involved in the development and translation of a number of new small molecule approaches that likely will be tested in clinical trials in the near future.
Laura D. Attardi, Committee Member
Laura Attardi is Professor of Radiation Oncology in the Radiation and Cancer Biology Department at Stanford University. She is also Professor of Genetics, a Member of Bio-X, a Member, Maternal & Child Health Research Institute (MCHRI), and a Member of the Stanford Cancer Institute. The observations that the p53 gene is mutated in at least half of all human cancers of a wide variety of types and that p53 null mice develop cancer at 100% frequency together underscore the critical role for p53 in tumor suppression. Wild-type p53 is a cellular stress sensor, responding to diverse insults such as DNA damage, hyperproliferative signals, and hypoxia by inducing growth arrest or apoptosis, responses thought to be important to tumor suppression. At the molecular level, p53 acts a transcription factor that activates gene expression programs to induce these different responses. Interestingly, in its capacity as a cellular stress sensor, p53 also plays physiological roles beyond tumor suppression as well as causing certain pathological effects. For example, p53 plays beneficial roles such as promoting fertility, and can promote detrimental phenotypes in certain situations such as the side effects of cancer therapies or developmental diseases. The overarching goal of our research is to better define the mechanisms by which the p53 protein promotes different responses in different settings, ranging from tumor suppression to responses to chemotherapeutics, using the mouse as an in vivo model system, with the ultimate goal of gaining insight that may facilitate clinical advances in diagnosis, prognostication and therapy. We utilize a combination of mouse genetic, cell biological, biochemical, and genomic approaches to address understand how p53 acts mechanistically. We hope to decipher the transcriptional networks responsible for mediating p53 functions in different contexts, an understanding that will help us understand how to best promote the beneficial and minimize the detrimental effects of p53 in the clinic.
Hans Clevers, Committee Member
Dr. Clevers is a professor of molecular genetics, a geneticist, physician, and medical researcher who was the first to identify stem cells in the intestine and is one of the world's leading researchers on normal stem cells and their potential for regenerative therapy. From 1991-2002, Dr. Clevers was Professor in Immunology at the University Utrecht and, since 2002, Professor in Molecular Genetics. From 2002-2012, he was director of the Hubrecht Institute in Utrecht. He is currently President of the Royal Netherlands Academy of Arts and Sciences.
Dr. Clevers has been a member of the Royal Netherlands Academy of Arts and Sciences since 2000 and a member of the American Academy of Arts and Sciences since 2012. He is the recipient of numerous awards, including the Dutch Spinoza Award in 2001, the Swiss Louis Jeantet Prize in 2004, the Memorial Sloan-Kettering Katharine Berkan Judd Award in 2005, the Israeli Rabbi Shai Shacknai Memorial Prize in 2006, the Dutch Josephine Nefkens Prize for Cancer Research and the German Meyenburg Cancer Research Award in 2008, the Dutch Cancer Society Award in 2009, the United European Gastroenterology Federation (UEGF) Research Prize in 2010, the German Ernst Jung-Preis für Medizin in 2011, the French Association pour la Recherche sur le Cancer (ARC) Léopold Griffuel Prize and the Heineken Prize in 2012 and the Breakthrough Prize in Life Sciences in 2013. He obtained an ERC Advanced Investigator grant in 2008. He is Chevalier de la Legion d'Honneur since 2005 and Knight in the Order of the Netherlands Lion since 2012.
Eric H. Rubin, Committee Member
Dr. Rubin has focused on cancer drug development for over 20 years. His research efforts focused on mechanisms of resistance to DNA topoisomerase-targeting drugs and his laboratory cloned a novel topoisomerase I- and p53-interacting tumor suppressor gene, TOPORS. In 2008 Dr. Rubin was recruited to Merck as Vice-President, Oncology Clinical Research. He led the development of the antiPD-1 antibody pembrolizumab, which was the first anti-PD-1 therapy approved in the U.S., and in the identification of the significant activity of this antibody across several additional cancer types. In his current role he oversees oncology early development and translational research activities at Merck. Dr. Rubin has authored over 100 original, peer-reviewed publications and book chapters related to oncology translational research, clinical trials and drug development. He is a deputy editor for Clinical Cancer Research. Dr. Rubin obtained his medical degree from the University of South Florida and completed residency at Yale-New Haven Hospital.
Jeffrey Settleman, Committee Member
Jeffrey Settleman, PhD, Distinguished Principal Investigator and Head of Oncology, Research at Calico. His current research is largely focused on molecularly targeted cancer therapeutics, personalized cancer medicine, and epigenetic mechanisms of drug resistance. He is especially interested in developing a better understanding of the nature of dynamic fluctuation of phenotypic states within tumor cell subpopulations, and the role the consequent heterogeneity plays in tumor evolution, response to drug treatment, and other stressful exposures.
Dr. Settleman was a postdoctoral fellow at the Whitehead Institute for Biomedical Research at M.I.T. in Bob Weinberg’s laboratory, before joining the Harvard School of Medicine faculty in 1992. During his 18 years on the Harvard faculty, he was named the Laurel Schwartz Professor of Oncology, he served as Director of the Center for Molecular Therapeutics and Scientific Director of the Massachusetts General Hospital Cancer Center, and led the Cancer Cell Biology program of the Dana Farber Harvard Cancer Center. From 2010-2015, he was the Senior Director of Discovery Oncology at Genentech, before moving to Calico in 2015.
Kevin M. Shannon, Committee Member
Dr. Kevin M. Shannon is Roma and Marvin Auerback Distinguished Professor in Pediatric Molecular Oncology in the Department of Pediatrics at UCSF. He is a physician-scientist whose research program focuses on hematopoietic growth control, genetic mechanisms underlying leukemogenesis, aberrant Ras signaling in human developmental disorders and cancer, mouse cancer modeling, and molecular therapeutics. He served as Director of the UCSF Medical Scientist Training Program (MSTP) from 2006-2012. He has been a research mentor for medical students, graduate students, and post-doctoral scholars, including six post-doctoral scholars who received “K” series awards from the NCI.
Karen Vousden, Committee Member
Karen Vousden is Cancer Research UK's Chief Scientist and a Group Leader at the Francis Crick Institute, where her work focuses on tumour suppressors. Tumour suppressors usually act to protect us from cancer. A protein called p53 was one of the first to be identified in our cells, and we now know it’s faulty or not working properly in the majority of cancers. Following the discovery of p53 in the 1970s, Professor Karen Vousden helped uncover how p53 works and how it is controlled, including identifying the molecule that sends p53 to the cellular dustbin, called MDM2.
But there are still many unanswered questions about the role of p53 in cancer. Professor Vousden and her team at The Francis Crick Institute in London are studying how p53 normally works to stop tumours forming, and how these protective effects are lost in cancers. She is also leading investigations looking into how different faulty versions of p53 help to drive cancer, and exploring whether losing this crucial molecule leaves weaknesses in cancer cells that could be exploited to destroy them.
Professor Vousden’s work on understanding this important tumour suppressor will be vital in helping develop new treatment approaches. As changes in p53 are found in almost all cancers, these treatments could improve survival in many different cancer types.
Eileen White, Committee Member
Dr. Eileen White received a BS from Rensselaer Polytechnic Institute and a PhD in Biology from SUNY Stony Brook in the Department of Dr. Arnold J. Levine. She was a Damon Runyon Postdoctoral fellow in the laboratory of Dr. Bruce Stillman at Cold Spring Harbor Laboratory. There she discovered that one of the oncogenes of the DNA tumor virus adenovirus encoded an inhibitor of programmed cell death or apoptosis (E1B 19K) that was a viral homologue of the human bcl-2 oncogene. She went on to establish that oncogene activation that deregulates cell growth also activates apoptosis, and that inhibition of apoptosis promotes cancer and treatment resistance. These findings revealed roles for the p53 tumor suppressor in activating apoptosis and suppressing cancer and for the Bcl-2-related anti-apoptotic proteins blocking apoptosis and promoting cancer.
She is currently the Deputy Director and Associate Director for Basic Science at the Rutgers Cancer Institute of New Jersey and Distinguished Professor of Molecular Biology and Biochemistry at Rutgers University. Dr. White has served on the Board of Scientific Counselors of the National Cancer Institute and the Board of Directors of the American Association for Cancer Research. She has received a MERIT Award from the NCI, an Investigatorship from the Howard Hughes Medical Institute, and the Red Smith Award from the Damon Runyon Cancer Research Foundation. Dr. White is an elected Fellow of the American Society of Microbiology (ASM) and of the American Association for the Advancement of Science. Dr. White has been or is a member of the Scientific Review Boards for the Starr Cancer Consortium and the Cancer Prevention Research Institute of Texas.
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