Julien Sage
Academic Appointments
- Associate Professor, Pediatrics - Cancer Biology
- Member, Bio-X
- Member, Child Health Research Institute
- Member, Stanford Cancer Institute
- Associate Professor, Genetics
Key Documents
Contact Information
- Academic Offices
Personal Information EmailAlternate Contact Joel Schaefer Grants Coordinator Email Tel Work (650) 724-9246
Professional Overview
Administrative Appointments
- Member, Institute for Stem Cell Biology and Regenerative Medicine (2006 - present)
Honors and Awards
- Harriet and Mary Zelencik Scientist in Children's Cancer and Blood Diseases, Lucille Packard Foundation for Children's Health (Since 2013)
- Morgridge Faculty Scholar, Lucille Packard Foundation for Children's Health (2008-2013)
- Scholar Award, Leukemia and Lymphoma Society (2009-2014)
- Scholar Award, Damon Runyon Cancer Research Foundation (2005-2008)
Professional Education
| B.S.: | Ecole Normale Superieure, France, Biology (1993) |
| Ph.D.: | Nice University, France, Biology (1998) |
Graduate & Fellowship Program Affiliations
Internet Links
Scientific Focus
Current Research Interests
The accumulation of genetic and epigenetic alterations transforms normal cells into cancer cells. But how does cancer initiate? In the hierarchy from stem cells to terminally differentiated cells present in adult tissues, what cell types have the potential to act as target cells for cancer? And how do these mutant cells become cancer stem cells? Key issues in the cancer field are to identify the target cells for cancer initiation and to determine the nature and consequences of cancer-initiating lesions.
To address these basic questions, we study the mechanisms of action of the retinoblastoma (RB) tumor suppressor gene. RB is a potent tumor suppressor that is mutated in a broad range of human tumors. RB has been implicated in the control of multiple cellular processes, including cell cycle progression, senescence, cell death, chromatin structure, chromosomal stability and cellular differentiation.
A focus of the lab is to identify the cell of origins of various cancers and to determine what function(s) of RB and its two family members p107 and p130 are critical for tumor suppression. In particular, our data indicate that altering the function of RB family members in adult stem cells initiate cancer in several organs and tissues and we are actively investigating the mechanisms underlying these observations.
Because of the role of RB in the control of proper embryonic development and differentiation, and because of accumulating evidence that RB family members interact with chromatin remodeling factors, a second focus of the lab is to investigate the role of RB in embryonic stem cells (from mice and humans) as well as during the reprogramming of iPS cells and during regeneration using the flatworm Schmidtea mediterranea as a model organism. We are particularly interested in investigating links between the basic cell cycle machinery and factors involved in cellular reprogramming as well as lineage fate decisions.
Publications
- IQGAP1 scaffold-kinase interaction blockade selectively targets RAS-MAP kinase-driven tumors. Nat Med. 2013; (5): 626-30
- Inactivation of the RB family prevents thymus involution and promotes thymic function by direct control of Foxn1 expression. J Exp Med. 2013; (6): 1087-97
- The RB family is required for the self-renewal and survival of human embryonic stem cells. Nat Commun. 2012: 1244
- The retinoblastoma tumor suppressor and stem cell biology. Genes Dev. 2012; (13): 1409-20
- A crucial requirement for Hedgehog signaling in small cell lung cancer. Nat Med. 2011; (11): 1504-8
- Discovery and preclinical validation of drug indications using compendia of public gene expression data. Sci Transl Med. 2011; (96): 96ra77
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