Julien Sage

Honors and Awards

• Scholar Award, Damon Runyon Cancer Research Foundation (2005-2008)
• Scholar Award, Leukemia and Lymphoma Society (2009-2014)

Professional Education

• B.S., Ecole Normale Superieure, France Biology (1993)
• Ph.D., Nice University, France Biology (1998)

Postdoctoral Advisees

• Ursula Ehmer, Kwon-Sik Park, Patrick Viatour

Graduate & Fellowship Program Affiliations

• Cancer Biology
• Genetics
• Pediatrics

Web Site Links

• http://www.stanford.edu/group/sage/

Research Interests

The accumulation of alterations can transform a normal cell into tumor cells. Despite the vast amount of knowledge gained in the last 30 years, cancer is now the first cause of death in the United States. Some key aspects of current basic cancer research include deciphering the molecular circuits controlling cellular proliferation, understanding and detecting the earlier stages of tumor development, and comprehending the interactions between tumor cells and their host.

Our research focuses on the retinoblastoma tumor suppressor gene (RB). RB is found mutated in a broad range of human tumors, including familial retinoblastoma and carcinomas of the lung, breast, liver, bladder, and prostate. RB normally works as a transcriptional regulator that controls the expression of programs of genes controlling cell cycle progression, cellular differentiation, and cell survival. Our goal is to take advantage of the central role of RB in cell cycle control and tumorigenesis in order to address basic issues in cancer.

Specifically, we have accumulated evidence that RB and its two family members p107 and p130 play a critical role in stem cell populations, both during embryonic development and in adult organs and tissues. We use mouse genetics and RNA interference tools to explore how RB, p107, and p130 control self-renewal, proliferation, and cell fate decisions in stem cell populations and how the control of stem cell functions by RB family genes normally suppresses cancer and ensures proper homeostasis in the organism.

Publications

• The retinoblastoma gene Rb and its family member p130 suppress lung adenocarcinoma induced by oncogenic K-Ras. Ho VM,  Schaffer BE, Karnezis AN, Park KS, Sage J.  Oncogene.  2009; 28 (10): 1393-9
• Keeping an eye on retinoblastoma control of human embryonic stem cells. Conklin JF,  Sage J.  J Cell Biochem.  2009;
• Cellular mechanisms of tumour suppression by the retinoblastoma gene. Burkhart DL,  Sage J.  Nat Rev Cancer.  2008; 8 (9): 671-82
• GFP reporter mice for the retinoblastoma-related cell cycle regulator p107. Burkhart DL,  Viatour P, Ho VM, Sage J.  Cell Cycle.  2008; 7 (16): 2544-52
• Hematopoietic stem cell quiescence is maintained by compound contributions of the retinoblastoma gene family. Viatour P,  Somervaille TC, Venkatasubrahmanyam S, Kogan S, McLaughlin ME, Weissman IL, Butte AJ, Passegué E, Sage J.  Cell Stem Cell.  2008; 3 (4): 416-28
• Acute mutation of retinoblastoma gene function is sufficient for cell cycle re-entry. Sage J,  Miller AL, Pérez-Mancera PA, Wysocki JM, Jacks T.  Nature.  2003; 424 (6945): 223-8
• Targeted disruption of the three Rb-related genes leads to loss of G(1) control and immortalization. Sage J,  Mulligan GJ, Attardi LD, Miller A, Chen S, Williams B, Theodorou E, Jacks T.  Genes Dev.  2000; 14 (23): 3037-50