Research Topics
Genomes and Genes
| Julien SageSummaryAffiliation: Stanford University Country: USA Publications
Research Grants
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Detail Information
Publications
RB's original CIN?Julien Sage
Department of Pediatrics, Stanford University, Stanford, California 94305, USA
Genes Dev 24:1329-33. 2010..Here we discuss how transcriptional and post-transcriptional mechanisms under the control of the RB pathway ensure accurate progression through mitosis, thereby preventing cancer development...- The retinoblastoma tumor suppressor and stem cell biologyJulien Sage
Department of Pediatrics, Department of Genetics, Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford Cancer Institute, Stanford, California 94305, USA
Genes Dev 26:1409-20. 2012.... 
Making young tumors old: a new weapon against cancer?Julien Sage
Stanford University School of Medicine, CA 94305, USA
Sci Aging Knowledge Environ 2005:pe25. 2005..Thus, senescence may act as a key tumor suppressor mechanism in young tumors in vivo...- p107 in the public eye: an Rb understudy and moreStacey E Wirt
Departments of Pediatrics and Genetics, Stanford Medical School, Stanford, CA 94305, USA
Cell Div 5:9. 2010..In this review, we identify the unique and overlapping functions of p107 during the cell cycle, differentiation, and tumorigenesis... - Notch signaling inhibits hepatocellular carcinoma following inactivation of the RB pathwayPatrick Viatour
Department of Genetics, Department of Pediatrics, Stanford University, Stanford, CA, USA Department of Medical Chemistry, University of Liege, B 4000 Liege, Belgium
J Exp Med 208:1963-76. 2011..The level of Notch activity is also able to predict survival of HCC patients, suggesting novel means to diagnose and treat HCC... - G1 arrest and differentiation can occur independently of Rb family functionStacey E Wirt
Department of Pediatrics, Stanford Medical School, Stanford, CA 94305, USA
J Cell Biol 191:809-25. 2010.... - A crucial requirement for Hedgehog signaling in small cell lung cancerKwon Sik Park
Department of Pediatrics, Stanford University, Stanford, California, USA
Nat Med 17:1504-8. 2011.... - Functional interactions between retinoblastoma and c-MYC in a mouse model of hepatocellular carcinomaLouis A Saddic
Department of Pediatrics, Stanford University, Stanford, California, United States of America
PLoS ONE 6:e19758. 2011..Thus, loss of RB function does not provide a proliferative advantage to c-MYC-expressing HCC cells but the RB and c-MYC pathways may cooperate to control the polyploidy of mature hepatocytes... - Regulation of RB transcription in vivo by RB family membersDeborah L Burkhart
Department of Pediatrics, Stanford Medical School, 269 Campus Drive, CCSR1215, Stanford, CA 94305, USA
Mol Cell Biol 30:1729-45. 2010..These experiments identify novel regulatory feedback mechanisms within the RB pathway in mammalian cells... - Keeping an eye on retinoblastoma control of human embryonic stem cellsJamie F Conklin
Department of Pediatrics, Stanford Medical School, Stanford, California 94305, USA
J Cell Biochem 108:1023-30. 2009..Here we review what is known about the expression and function of members of the RB pathway in hESCs and discuss areas of interest in this field... - Tandem E2F binding sites in the promoter of the p107 cell cycle regulator control p107 expression and its cellular functionsDeborah L Burkhart
Departments of Pediatrics and Genetics, Stanford Medical School, Stanford, California, United States of America
PLoS Genet 6:e1001003. 2010..These experiments also suggest novel therapeutic strategies to increase the p107 levels in tumor cells... - PDGF signalling controls age-dependent proliferation in pancreatic β-cellsHainan Chen
Department of Developmental Biology, Stanford University School of Medicine, Stanford, California 94305, USA
Nature 478:349-55. 2011..The discovery of a conserved pathway controlling age-dependent β-cell proliferation indicates new strategies for β-cell expansion... - Characterization of the cell of origin for small cell lung cancerKwon Sik Park
Department of Genetics, Stanford University, Palo Alto, CA, USA
Cell Cycle 10:2806-15. 2011..In addition, mice in which Rb and p53 are deleted in a variety of non-neuroendocrine lung epithelial cells did not develop SCLC. These data indicate that SCLC likely arises from neuroendocrine cells in the lung... - Loss of p130 accelerates tumor development in a mouse model for human small-cell lung carcinomaBethany E Schaffer
Department of Pediatrics, Stanford Medical School, Stanford, California 94305 5149, USA
Cancer Res 70:3877-83. 2010..These findings indicate that p130 plays a key tumor suppressor role in SCLC. Rb/p53/p130-mutant mice provide a novel preclinical mouse model to identify novel therapeutic targets against SCLC... - Transient inactivation of Rb and ARF yields regenerative cells from postmitotic mammalian muscleKostandin V Pajcini
Baxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA
Cell Stem Cell 7:198-213. 2010..These results show that differentiation of mammalian cells is reversed by inactivation of Arf and Rb and support the hypothesis that Arf evolved at the expense of regeneration... 
Cellular mechanisms of tumour suppression by the retinoblastoma geneDeborah L Burkhart
Cancer Biology Program, Stanford University School of Medicine, Stanford, California 94305, USA
Nat Rev Cancer 8:671-82. 2008..However, we still do not know the identity of the cell types in which RB normally prevents cancer initiation in vivo, and the specific functions of RB that suppress distinct aspects of the tumorigenic process are poorly understood...- Inactivating all three rb family pocket proteins is insufficient to initiate cervical cancerMyeong Kyun Shin
McArdle Laboratory for Cancer Research, University of Wisconsin School of Medicine and Public Health, Madison, WI 53706, USA
Cancer Res 72:5418-27. 2012..These findings strongly argue that the oncogenic properties of HPV-16 E7 in human cervical carcinogenesis may involve disruption of E7 binding proteins beyond simply the pRb family members... - Hematopoietic stem cell quiescence is maintained by compound contributions of the retinoblastoma gene familyPatrick Viatour
Department of Pediatrics, Stanford Medical School, Stanford, CA 94305, USA
Cell Stem Cell 3:416-28. 2008..The presence of a single p107 allele is sufficient to largely rescue these defects. Thus, Rb family members collectively maintain HSC quiescence and the balance between lymphoid and myeloid cell fates in the hematopoietic system... - Structure and function of the thymic microenvironmentNancy Ruth Manley
Department of Genetics, Coverdell Center, 500 DW Brooks Drive, University of Georgia, Athens, GA 30602, USA
Front Biosci 16:2461-77. 2011..This review will summarize the current state of understanding of the composition and organization of thymic microenvironments and the mechanisms that promote their proper development and function... - MicroRNA programs in normal and aberrant stem and progenitor cellsChristopher P Arnold
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305, USA
Genome Res 21:798-810. 2011..Together, these analyses reveal the miRNA programs that may control key processes in normal and aberrant stem and progenitor cells, setting the foundations for dissecting post-transcriptional regulatory networks in stem cells... - Methylation of the retinoblastoma tumor suppressor by SMYD2Louis A Saddic
Departments of Pediatrics, Stanford University, Stanford, California 94305, USA
J Biol Chem 285:37733-40. 2010..These results support the idea that a code of post-translational modifications exists for RB and helps guide its functions in mammalian cells... - miR than meets the eyeJulien Sage
Department of Pediatrics, Stanford University, Stanford, California 94305, USA
Genes Dev 25:1663-7. 2011..These experiments identify the RB/miR-17~92/p21 axis as a critical regulator of retinoblastoma tumorigenesis and potentially many other cancers... - Newly identified aspects of tumor suppression by RBPatrick Viatour
Department of Genetics, Stanford University, Stanford, CA 94305, USA
Dis Model Mech 4:581-5. 2011..In particular, we discuss the pro- and anti-tumorigenic roles of RB during the early stages of cancer, as well as the importance of the RB pathway in stem cells and cell fate decisions... - The role of the retinoblastoma/E2F1 tumor suppressor pathway in the lesion recognition step of nucleotide excision repairPatrick S Lin
Department of Medicine, Division of Oncology, Stanford University School of Medicine, Stanford, CA 94305 5151, United States
DNA Repair (Amst) 8:795-802. 2009..Our study identifies a novel E2F1 gene target and further supports the growing body of evidence that the Rb/E2F1 tumor suppressor pathway is involved in the regulation of the DNA lesion recognition step of nucleotide excision repair... - Discovery and preclinical validation of drug indications using compendia of public gene expression dataMarina Sirota
Division of Systems Medicine, Department of Pediatrics, Stanford University School of Medicine, 251 Campus Drive, Stanford, CA 94305 5415, USA
Sci Transl Med 3:96ra77. 2011..This computational method provides a systematic approach for repositioning established drugs to treat a wide range of human diseases... - GFP reporter mice for the retinoblastoma-related cell cycle regulator p107Deborah L Burkhart
Department of Pediatrics and Genetics, Cancer Biology Program, Stanford Medical School, Stanford, California, USA
Cell Cycle 7:2544-52. 2008..Thus, p107 BAC-eGFP transgenic mice serve as a useful tool to identify distinct cell types in which p107 is expressed and may have key functions in vivo, and to characterize changes in cellular networks accompanying Rb deficiency... - IQGAP1 scaffold-kinase interaction blockade selectively targets RAS-MAP kinase-driven tumorsKatherine L Jameson
1 Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California, USA 2 Program in Cancer Biology, Stanford University School of Medicine, Stanford, California, USA 3
Nat Med 19:626-30. 2013..Scaffold-kinase interaction blockade acts by a mechanism distinct from direct kinase inhibition and may be a strategy to target overactive oncogenic kinase cascades in cancer... - The RB family is required for the self-renewal and survival of human embryonic stem cellsJamie F Conklin
Department of Pediatrics, Stanford Medical School, Stanford, California 94305, USA
Nat Commun 3:1244. 2012..These experiments indicate that a homeostatic level of RB activity is essential for the self-renewal and the survival of human embryonic stem cells... - Cyclin C makes an entry into the cell cycleJulien Sage
Departments of Pediatrics and Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA
Dev Cell 6:607-8. 2004..In an article published recently in Cell, Ren and Rollins investigate mechanisms controlling the G0/G1 transition in quiescent cells and identify new cyclin C/Cdk3 complexes as key regulators of cell cycle reentry in human cells... - C/EBPbeta cooperates with RB:E2F to implement Ras(V12)-induced cellular senescenceThomas Sebastian
Laboratory of Protein Dynamics and Signaling, NCI Frederick, Frederick, MD 21702 1201, USA
EMBO J 24:3301-12. 2005..C/EBPbeta is therefore a novel component of the RB:E2F-dependent senescence program activated by oncogenic stress in primary cells... - Recapitulation of the effects of the human papillomavirus type 16 E7 oncogene on mouse epithelium by somatic Rb deletion and detection of pRb-independent effects of E7 in vivoScott J Balsitis
McArdle Laboratory for Cancer Research, University of Wisconsin Medical School, 1400 University Avenue, Madison, WI 53706, USA
Mol Cell Biol 23:9094-103. 2003..These findings indicate that inactivation of the Rb pathway can largely account for E7's phenotypes at an early age, but that pRb-independent activities of E7 are detectable in vivo... - Acute mutation of retinoblastoma gene function is sufficient for cell cycle re-entryJulien Sage
Instituto de Biologia Molecular y Celular del Cancer, CSIC Universidad de Salamanca, 37007 Salamanca, Spain
Nature 424:223-8. 2003..Thus, the use of conditional knockout strategies might refine our understanding of gene function and help to model human cancer more accurately...
Research Grants
- The RB Gene Family in Cancer InitiationJulien Sage; Fiscal Year: 2010..These studies will further provide the foundation for the detection and treatment of early stages of human cancer. ..
- The RB Gene Family in Cancer InitiationJulien Sage; Fiscal Year: 2009..These studies will further provide the foundation for the detection and treatment of early stages of human cancer. ..