Research Topics
Species | RONALD ANTHONY DEPINHOSummaryAffiliation: Harvard University Country: USA Publications
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Publications
A mouse plasma peptide atlas as a resource for disease proteomicsQing Zhang
Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA
Genome Biol 9:R93. 2008..A major finding from this study is the identification of novel isoforms and transcript variants not previously predicted from genome analysis...- The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesisDaniel R Carrasco
Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, and Department of Pathology, Brigham and Women s Hospital, Boston, MA 02115, USA
Cancer Cell 11:349-60. 2007..The similarities of this model with the human disease, coupled with documented frequent XBP-1s overexpression in human MM, serve to implicate XBP-1s dysregulation in MM pathogenesis... 
What drives intense apoptosis resistance and propensity for necrosis in glioblastoma? A role for Bcl2L12 as a multifunctional cell death regulatorAlexander H Stegh
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
Cell Cycle 7:2833-9. 2008....- The age of cancerR A DePinho
Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Nature 408:248-54. 2000..Further verification of the role of these effects should in turn lead to the design of effective therapeutics for the treatment and prevention of cancer in the aged... - Bcl2L12 inhibits post-mitochondrial apoptosis signaling in glioblastomaAlexander H Stegh
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
Genes Dev 21:98-111. 2007..Thus, Bcl2L12 contributes to the classical tumor biological features of GBM such as intense apoptosis resistance and florid necrosis, and may provide a target for enhanced therapeutic responsiveness of this lethal cancer... - Genetic analysis of Pten and Ink4a/Arf interactions in the suppression of tumorigenesis in miceMingjian James You
Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 99:1455-60. 2002..This study provides genetic evidence of collaboration between Pten and Ink4a/Arf in constraining the growth and oncogenic transformation of cultured cells and in suppressing a wide spectrum of tumors in vivo... - Up-regulation of c-Jun inhibits proliferation and induces apoptosis via caspase-triggered c-Abl cleavage in human multiple myelomaKlaus Podar
Jerome Lipper Multiple Myeloma Center, Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
Cancer Res 67:1680-8. 2007..Finally, our data suggest that this mechanism may not only be restricted to MM but may also be important in a broad range of malignancies including erythroleukemia and solid tumors... - Ink4a/Arf tumor suppressor does not modulate the degenerative conditions or tumor spectrum of the telomerase-deficient mouseChristine M Khoo
Department of Medical Oncology, Belfer Foundation Institute for Innovative Cancer Science, Dana Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 104:3931-6. 2007..These observations highlight the importance of genetic context in dictating whether telomere dysfunction promotes or suppresses age-related degenerative conditions as well as the rate of initiation and type of spontaneous cancers... - Telomerase extracurricular activitiesSandy Chang
Department of Medical Oncology, Dana-Farber Cancer Institute, Departments of Medicine and Genetics, Harvard Medical School, and Department of Pathology, Brigham and Women's Hospital, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 99:12520-2. 2002 - Take care of your chromosomes lest cancer take care of youRichard S Maser
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Cancer Cell 3:4-6. 2003.... - Telomeres and the DNA damage response: why the fox is guarding the henhouseRichard S Maser
Department of Medical Oncology, Dana Farber Cancer Institute, Departments of Medicine and Genetics, Harvard Medical School, Boston, MA 02115, USA
DNA Repair (Amst) 3:979-88. 2004..Here, we review recent work defining the roles for DSB repair machinery in telomere maintenance and in response to telomere dysfunction... - PLAGL2 regulates Wnt signaling to impede differentiation in neural stem cells and gliomasHongwu Zheng
Belfer Institute for Applied Cancer Science, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Cancer Cell 17:497-509. 2010..The identification of PLAGL2 as a glioma oncogene highlights the importance of a growing class of cancer genes functioning to impart stem cell-like characteristics in malignant cells... - Connecting chromosomes, crisis, and cancerRichard S Maser
Department of Adult Oncology, Dana-Farber Cancer Institute, Harvard Medical School, 44 Binney Street, M413, Boston, MA 02115, USA
Science 297:565-9. 2002..A greater understanding of telomere-induced crisis and the cell's crisis management mechanisms should guide the rational development of new therapeutics for cancer and other disorders... - Obligate roles for p16(Ink4a) and p19(Arf)-p53 in the suppression of murine pancreatic neoplasiaNabeel Bardeesy
Department of Adult Oncology, Dana Farber Cancer Institute, National Cancer Institute, Bethesda, Maryland, USA
Mol Cell Biol 22:635-43. 2002..This genetically defined model provides insights into the molecular pathogenesis of SCA and serves as a platform for dissection of cell-specific programs of epithelial tumor suppression... - Cooperative interactions of p53 mutation, telomere dysfunction, and chronic liver damage in hepatocellular carcinoma progressionParaskevi A Farazi
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Cancer Res 66:4766-73. 2006..Thus, this study supports a model that, in the face of chronic liver damage, attenuated p53 function and telomere-induced chromosomal instability play critical and cooperative roles in the progression of hepatocellular carcinoma... - Constitutive telomerase expression promotes mammary carcinomas in aging miceSteven E Artandi
Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street M413, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 99:8191-6. 2002..These data indicate that enforced mTERT expression can promote the development of spontaneous cancers even in the setting of ample telomere reserve... - Bcl2L12-mediated inhibition of effector caspase-3 and caspase-7 via distinct mechanisms in glioblastomaAlexander H Stegh
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 105:10703-8. 2008..Thus, alphaB-crystallin is a Bcl2L12-induced oncoprotein that enables Bcl2L12 to block the activation of both effector caspases via distinct mechanisms, thereby contributing to GBM pathogenesis and its hallmark biological properties... - mTORC1-dependent and -independent regulation of stem cell renewal, differentiation, and mobilizationBoyi Gan
Department of Medical Oncology, Belfer Foundation Institute for Innovative Cancer Science, Dana Farber Cancer Institute, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 105:19384-9. 2008..Thus, TSC1 is a critical regulator of HSC self-renewal, mobilization, and multilineage development and executes these actions via both mTORC1-dependent and -independent pathways... - Telomere dysfunction provokes regional amplification and deletion in cancer genomesSandy Chang
Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA
Cancer Cell 2:149-55. 2002..This model provides a platform for discovery of genes responsible for the major cancers affecting aged humans... - Telomere dysfunction and Atm deficiency compromises organ homeostasis and accelerates ageingKWOK KIN WONG
Department of Adult Oncology, Dana Farber Cancer Institute Boston, Massachusetts 02115, USA
Nature 421:643-8. 2003.... - p53: good cop/bad copNorman E Sharpless
Department of Adult Oncology, Dana-Farber Cancer Institute, Department of Medicine and Genetics, Harvard Medical School, Boston, MA 02115, USA
Cell 110:9-12. 2002..By extension, this relationship implies that therapies aimed to reduce cancer and postpone aging, and thereby increase longevity, will necessarily work either upstream or downstream, but not on the level of, p53... 
Linking functional decline of telomeres, mitochondria and stem cells during ageingErgun Sahin
Belfer Institute for Applied Cancer Science, Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Nature 464:520-8. 2010....- Impaired processing of DNA photoproducts and ultraviolet hypermutability with loss of p16INK4a or p19ARFPapri Sarkar-Agrawal
Department of Dermatology, Boston University School of Medicine, Boston, MA 02118, USA
J Natl Cancer Inst 96:1790-3. 2004..These results may further explain why INK4a/ARF mutations predispose to malignant melanoma, a UV-induced tumor... - How disruption of cell cycle regulating genes might predispose to sun-induced skin cancerThomas M Rünger
Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts 02118, USA
Cell Cycle 4:643-5. 2005..Differences in the apoptotic response to ultraviolet light between melanocytes and keratinocytes might explain why INK4a/ARF mutations predispose to malignant melanoma, but not to keratinocyte-derived skin cancers... - FoxOs are lineage-restricted redundant tumor suppressors and regulate endothelial cell homeostasisJi Hye Paik
Department of Medical Oncology, Dana Farber Cancer Institute, Brigham and Women s Hospital, and Harvard Medical School, Boston, MA 02115, USA
Cell 128:309-23. 2007..Functional studies validated Sprouty2 and PBX1, among others, as FoxO-regulated mediators of endothelial cell morphogenesis and vascular homeostasis... - Olig2-regulated lineage-restricted pathway controls replication competence in neural stem cells and malignant gliomaKeith L Ligon
Department of Pediatric Oncology, Dana Farber Cancer Institute and Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
Neuron 53:503-17. 2007..Our findings identify an Olig2-regulated lineage-restricted pathway critical for proliferation of normal and tumorigenic CNS stem cells... - FoxOs are critical mediators of hematopoietic stem cell resistance to physiologic oxidative stressZuzana Tothova
Division of Hematology, Department of Medicine, Brigham and Women s Hospital, and Department of Genetics, Harvard Medical School, Boston, MA 02115, USA
Cell 128:325-39. 2007..Thus, FoxO proteins play essential roles in the response to physiologic oxidative stress and thereby mediate quiescence and enhanced survival in the HSC compartment, a function that is required for its long-term regenerative potential... - mSin3-associated protein, mSds3, is essential for pericentric heterochromatin formation and chromosome segregation in mammalian cellsGregory David
Departments of Medical Oncology, Medicine, and Genetics, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
Genes Dev 17:2396-405. 2003.... - Targeting EGFR induced oxidative stress by PARP1 inhibition in glioblastoma therapyMasayuki Nitta
Department of Radiation Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, United States of America
PLoS ONE 5:e10767. 2010..These observations suggest that oxidative stress secondary to EGFR hyper-activation necessitates increased cellular reliance on PARP1 mediated BER, and offer critical insights into clinical trial design... - A genome-wide screen reveals functional gene clusters in the cancer genome and identifies EphA2 as a mitogen in glioblastomaFenghua Liu
Department of Neurological Surgery, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA
Cancer Res 66:10815-23. 2006..This novel genome-wide approach greatly expanded the list of target genes in glioblastoma and represents a powerful new strategy to identify the upstream determinants of tumor phenotype in a range of human cancers... - Pancreatic LKB1 deletion leads to acinar polarity defects and cystic neoplasmsAram F Hezel
MGH Cancer Center, Simches Research Building, CPZN 4216, 185 Cambridge St, Boston, MA 02114, USA
Mol Cell Biol 28:2414-25. 2008..These genetic studies provide in vivo evidence of a key role for LKB1 in the establishment of epithelial cell polarity that is vital for pancreatic acinar cell function and viability and for the suppression of neoplasia... - Coactivation of receptor tyrosine kinases affects the response of tumor cells to targeted therapiesJayne M Stommel
Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
Science 318:287-90. 2007..Thus, effective GBM therapy may require combined regimens targeting multiple RTKs... - Glioma oncoprotein Bcl2L12 inhibits the p53 tumor suppressorAlexander H Stegh
Belfer Institute for Applied Cancer Science, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
Genes Dev 24:2194-204. 2010..Thus, Bcl2L12 is a multifunctional protein that contributes to intense therapeutic resistance of GBM through its ability to operate on two key nodes of cytoplasmic and nuclear signaling cascades... - Smad4 is dispensable for normal pancreas development yet critical in progression and tumor biology of pancreas cancerNabeel Bardeesy
Massachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA
Genes Dev 20:3130-46. 2006.... - High-resolution genomic profiles of human lung cancerGiovanni Tonon
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 102:9625-30. 2005..Integrated DNA-RNA analyses identified WHSC1L1 and TPX2 as two candidates likely targeted for amplification in both pancreatic ductal adenocarcinoma and non-small-cell lung cancer... - Telomere dysfunction promotes genome instability and metastatic potential in a K-ras p53 mouse model of lung cancerSamanthi A Perera
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Carcinogenesis 29:747-53. 2008..Furthermore, these findings clearly demonstrate (in an in vivo model system) the dual nature of telomere shortening as both a tumor-suppressive and tumor-promoting mechanism in lung cancer, dependent on p53 status... - Identification of a PTEN-regulated STAT3 brain tumor suppressor pathwayNuria de la Iglesia
Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA
Genes Dev 22:449-62. 2008..These findings indicate that STAT3 plays opposing roles in glial transformation depending on the genetic background of the tumor, providing the rationale for tailored therapeutic intervention in glioblastoma... - Marked genomic differences characterize primary and secondary glioblastoma subtypes and identify two distinct molecular and clinical secondary glioblastoma entitiesElizabeth A Maher
Center for Neuro-Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Cancer Res 66:11502-13. 2006..We conclude that glioblastoma is composed of at least three distinct molecular subtypes, including novel subgroups of secondary glioblastoma, which may benefit from different therapeutic strategies... - Alu elements mediate MYB gene tandem duplication in human T-ALLJennifer O'Neil
Department of Pediatric Oncology, Belfer Foundation Institute for Innovative Cancer Science, Dana Farber Cancer Institute, Boston, MA 02115, USA
J Exp Med 204:3059-66. 2007..We conclude that Alu-mediated MYB tandem duplication occurs at low frequency during normal thymocyte development and is clonally selected during the molecular pathogenesis of human T-ALL... - Suppression of ovarian follicle activation in mice by the transcription factor Foxo3aDiego H Castrillon
Department of Medical Oncology, Dana Farber Cancer Institute, and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA
Science 301:215-8. 2003.... - Genomic alterations link Rho family of GTPases to the highly invasive phenotype of pancreas cancerAlec C Kimmelman
Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 105:19372-7. 2008..Like RIOK3, PAK4 promotes pancreas ductal cell motility and invasion. Together, the genomic and functional profiles establish the Rho family GTP-binding proteins as integral to the hallmark invasive nature of this lethal disease... - The age of cancer: telomeres, checkpoints, and longevityRonald A Depinho
Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA
J Clin Invest 111:S9-14. 2003 - Telomere-based crisis: functional differences between telomerase activation and ALT in tumor progressionSandy Chang
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
Genes Dev 17:88-100. 2003.... - LKB1 (XEEK1) regulates Wnt signalling in vertebrate developmentOlga Ossipova
Department of Cancer Biology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Nat Cell Biol 5:889-94. 2003..These studies show that LKB1/XEEK1 is required for Wnt-beta-catenin signalling in frogs and mammals and provides novel insights into its role in vertebrate developmental patterning and carcinogenesis... - Loss of the Lkb1 tumour suppressor provokes intestinal polyposis but resistance to transformationNabeel Bardeesy
Department of Adult Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
Nature 419:162-7. 2002..Together, our data rationalize several features of PJS polyposis--notably its peculiar histopathological presentation and limited malignant potential--and place Lkb1 in a distinct class of tumour suppressors... - Common and distinct genomic events in sporadic colorectal cancer and diverse cancer typesEric S Martin
Department of Medical Oncology, Belfer Institute for Innovative Cancer Science, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Cancer Res 67:10736-43. 2007.... - mTORC1 signaling governs hematopoietic stem cell quiescenceBoyi Gan
Department of Medical Oncology, Dana Farber Cancer Institute and Department of Medicine and Genetics, Harvard Medical School, Boston, Massachusetts, USA
Cell Cycle 8:1003-6. 2009..Further pharmacological approaches show that PTEN, TSC1 and PML regulate HSC maintenance through mTORC1. mTORC1-mediated cell growth regulatory circuits thus play a critical role in the regulation of HSC quiescence... - p53 and Pten control neural and glioma stem/progenitor cell renewal and differentiationHongwu Zheng
Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
Nature 455:1129-33. 2008.... - PI3 kinase signals BCR-dependent mature B cell survivalLakshmi Srinivasan
Program of Cellular and Molecular Medicine, Children s Hospital, and Immune Disease Institute, Harvard Medical School, Boston, MA 02115, USA
Cell 139:573-86. 2009.... - Molecular diversity of astrocytes with implications for neurological disordersRobert M Bachoo
Department of Medical Oncology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 101:8384-9. 2004.... - Stromal biology of pancreatic cancerGerald C Chu
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA, USA
J Cell Biochem 101:887-907. 2007..Such knowledge may be used to understand the evolution and biology of this lethal cancer and may convert these insights into new points of therapeutic intervention... - FoxOs cooperatively regulate diverse pathways governing neural stem cell homeostasisJi Hye Paik
Department of Medical Oncology, Belfer Institute for Applied Cancer Science, Harvard Medical School, Boston, MA 02115, USA
Cell Stem Cell 5:540-53. 2009..Thus, the FoxO family coordinately regulates diverse genes and pathways to govern key aspects of NSC homeostasis in the mammalian brain... - Differential impact of telomere dysfunction on initiation and progression of hepatocellular carcinomaParaskevi A Farazi
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Cancer Res 63:5021-7. 2003.... - Epidermal growth factor receptor and Ink4a/Arf: convergent mechanisms governing terminal differentiation and transformation along the neural stem cell to astrocyte axisRobert M Bachoo
Center for Neuro-Oncology, Boston, Massachusetts 02115, USA
Cancer Cell 1:269-77. 2002..These data support the view that dysregulation of specific genetic pathways, rather than cell-of-origin, dictates the emergence and phenotype of high-grade gliomas... - Inactivation of hepatic Foxo1 by insulin signaling is required for adaptive nutrient homeostasis and endocrine growth regulationXiaocheng C Dong
Howard Hughes Medical Institute, Division of Endocrinology, Children s Hospital Boston, Karp Family Research Laboratories, 300 Longwood Avenue, Harvard Medical School, Boston, MA 02115, USA
Cell Metab 8:65-76. 2008.... - DNA-dependent protein kinase catalytic subunit is not required for dysfunctional telomere fusion and checkpoint response in the telomerase-deficient mouseRichard S Maser
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Mol Cell Biol 27:2253-65. 2007.... - A genetic screen for candidate tumor suppressors identifies RESTThomas F Westbrook
Howard Hughes Medical Institute, Department of Genetics, Harvard Partners Center for Genetics and Genomics, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA
Cell 121:837-48. 2005..These results implicate REST as a human tumor suppressor and provide a novel approach to identifying candidate genes that suppress the development of human cancer... - p16(Ink4a) interferes with Abelson virus transformation by enhancing apoptosisZohar Sachs
Department of Pathology, Sackler School of Graduate Biomedical Sciences, Tufts University School of Medicine, Boston, Massachusetts 02111, USA
J Virol 78:3304-11. 2004..These results indicate that both products of the Ink4a/Arf locus influence Ab-MLV transformation and reveal that in addition to its well-recognized effects on the cell cycle, p16(Ink4a) can suppress transformation by inducing apoptosis... - Both p16(Ink4a) and the p19(Arf)-p53 pathway constrain progression of pancreatic adenocarcinoma in the mouseNabeel Bardeesy
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 103:5947-52. 2006.... - High-resolution genomic profiles define distinct clinico-pathogenetic subgroups of multiple myeloma patientsDaniel R Carrasco
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA
Cancer Cell 9:313-25. 2006.... - The tumor suppressor LKB1 kinase directly activates AMP-activated kinase and regulates apoptosis in response to energy stressReuben J Shaw
Department of Systems Biology, Harvard Medical School, and Division of Signal Transduction, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA
Proc Natl Acad Sci U S A 101:3329-35. 2004..The role of LKB1/AMPK in the survival of a subset of genetically defined tumor cells may provide opportunities for cancer therapeutics... - Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinomaAndrew J Aguirre
Department of Medical Oncology, Dana Farber Cancer Institute and Department of Genetics, Harvard Medical School, Boston, MA 02115, USA
Genes Dev 17:3112-26. 2003..This faithful mouse model may permit the systematic analysis of genetic lesions implicated in the human disease and serve as a platform for the identification of early disease markers and for the efficient testing of novel therapies... - Stem-cell ageing modified by the cyclin-dependent kinase inhibitor p16INK4aViktor Janzen
Center for Regenerative Medicine, Massachusetts General Hospital, Harvard Medical School, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Nature 443:421-6. 2006..Inhibition of p16INK4a may ameliorate the physiological impact of ageing on stem cells and thereby improve injury repair in aged tissue... - Direct transcriptional activation of promyelocytic leukemia protein by IFN regulatory factor 3 induces the p53-dependent growth inhibition of cancer cellsTae Kyung Kim
The Laboratory of Cell Growth and Function Regulation, Division of Biotechnology, College of Life Sciences and Biotechnology, School of Medicine, Korea University, Anam Dong, Seongbuk gu, Seoul 136 713, South Korea
Cancer Res 67:11133-40. 2007.... - LKB1 signaling in mesenchymal cells required for suppression of gastrointestinal polyposisPekka Katajisto
Genome Scale Biology Program and Institute of Biomedicine, Biomedicum Helsinki, 00014 University of Helsinki, Finland
Nat Genet 40:455-9. 2008..We also noted TGFbeta signaling defects in polyps of individuals with PJS, suggesting that the identified stromal-derived mechanism of tumor suppression is also relevant in PJS... - A Foxo/Notch pathway controls myogenic differentiation and fiber type specificationTadahiro Kitamura
Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York, USA
J Clin Invest 117:2477-85. 2007..Notch/Foxo1 cooperation may integrate environmental cues through Notch with metabolic cues through Foxo1 to regulate progenitor cell maintenance and differentiation... - STAT3 is a negative regulator of granulopoiesis but is not required for G-CSF-dependent differentiationChien Kuo Lee
Department of Pathology, Kaplan Comprehensive Cancer Center, New York University School of Medicine, 10016, USA
Immunity 17:63-72. 2002.... - The role of Ink4a/Arf in ErbB2 mammary gland tumorigenesisMark D'Amico
Department of Oncology, Lombardi Cancer Center, Georgetown University, Washington, D C 20007, USA
Cancer Res 63:3395-402. 2003..In view of the important role of Ink4a/Arf in response to chemotherapy, these transgenic mice may provide a useful model for testing breast tumor therapies... - Walking the telomere plank into cancerKwok-Kin Wong
J Natl Cancer Inst 95:1184-6. 2003 - Keeping telomerase in its placeRichard S Maser
Nat Med 8:934-6. 2002 - Telomeres, stem cells, senescence, and cancerNorman E Sharpless
Department of Medicine and Genetics, Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599 8212, USA
J Clin Invest 113:160-8. 2004..g., p16(INK4a)-Rb, ARF-p53, and the telomere) have evolved to ward against this possibility. These beneficial antitumor pathways, however, appear also to limit the stem cell life span, thereby contributing to aging... - The differential impact of p16(INK4a) or p19(ARF) deficiency on cell growth and tumorigenesisNorman E Sharpless
Department of Medicine, Lineberger Cancer Center, CB 7295, The University of North Carolina School of Medicine, Chapel Hill, NC 27599 7295, USA
Oncogene 23:379-85. 2004.... - Endogenous oncogenic K-ras(G12D) stimulates proliferation and widespread neoplastic and developmental defectsDavid A Tuveson
Abramson Family Cancer Research Institute, Abramson Cancer Center and Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104 USA
Cancer Cell 5:375-87. 2004..Our results suggest that endogenous oncogenic ras is sufficient to initiate transformation by stimulating proliferation, while further genetic lesions may be necessary for progression to frank malignancy... - Cancer chromosomes in crisisRonald A Depinho
Nat Genet 36:932-4. 2004.... - Absence of telomerase and shortened telomeres have minimal effects on skin and pancreatic carcinogenesis elicited by viral oncogenesDavid Argilla
Department of Biochemistry and Biophysics, Diabetes Center, and Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA 94143, USA
Cancer Cell 6:373-85. 2004.... - Block of T cell development in P53-deficient mice accelerates development of lymphomas with characteristic RAG-dependent cytogenetic alterationsBrian B Haines
Center for Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
Cancer Cell 9:109-20. 2006..These findings provide genetic evidence that block of lymphocyte development at stages with RAG endonuclease activity can provoke lymphomagenesis on a background with deficient DNA damage responses... - Elevated telomere-telomere recombination in WRN-deficient, telomere dysfunctional cells promotes escape from senescence and engagement of the ALT pathwayPurnima R Laud
Department of Molecular Genetics, University of Texas, The M D Anderson Cancer Center, Houston, Texas 77030, USA
Genes Dev 19:2560-70. 2005.... - p16(Ink4a) in melanocyte senescence and differentiationElena V Sviderskaya
Department of Anatomy and Developmental Biology, St. George's Hospital Medical School, Cranmer Terrace, London SW17 0RE, U.K
J Natl Cancer Inst 94:446-54. 2002..Mutations of the INK4A-ARF locus may favor tumorigenesis from melanocytes by impairing senescence, cell differentiation, and (where ARF is disrupted) cell death... - Essential role of limiting telomeres in the pathogenesis of Werner syndromeSandy Chang
Department of Molecular Genetics, M D Anderson Cancer Center, Box 11, 1515 Holcombe Blvd, Houston, Texas 77030, USA
Nat Genet 36:877-82. 2004..These genetic data indicate that the delayed manifestation of the complex pleiotropic of Wrn deficiency relates to telomere shortening... - Genome-wide retroviral insertional tagging of genes involved in cancer in Cdkn2a-deficient miceAnders H Lund
Division of Molecular Genetics, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands
Nat Genet 32:160-5. 2002.... - Ink4a/arf deficiency promotes ultraviolet radiation-induced melanomagenesisJuan A Recio
Laboratory of Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892 4264, USA
Cancer Res 62:6724-30. 2002.... - Cancer biology: gone but not forgottenNorman E Sharpless
Nature 445:606-7. 2007 - Cellular transformation by the MSP58 oncogene is inhibited by its physical interaction with the PTEN tumor suppressorKoichi Okumura
Ludwig Institute for Cancer Research, San Diego Branch, University of California at San Diego, La Jolla, CA 92093-0660, USA
Proc Natl Acad Sci U S A 102:2703-6. 2005.... - Decreased cyclin-dependent kinase 5 (cdk5) activity is accompanied by redistribution of cdk5 and cytoskeletal proteins and increased cytoskeletal protein phosphorylation in p35 null miceJanice L Hallows
The Nathan Shock Center of Excellence in the Basic Biology of Aging and Department of Pathology, University of Washington, Seattle, Washington 98195, USA
J Neurosci 23:10633-44. 2003..Our studies illustrate that p35 regulates the subcellular distribution of cdk5 and cytoskeletal proteins in neurons and that cdk5 has a hierarchical role in regulating the phosphorylation and function of cytoskeletal proteins... - Cancer: crime and punishmentNorman E Sharpless
Nature 436:636-7. 2005 - Specific requirement of the chromatin modifier mSin3B in cell cycle exit and cellular differentiationGregory David
Department of Pharmacology and New York University Cancer Institute, New York University School of Medicine, New York, NY 10016, USA
Proc Natl Acad Sci U S A 105:4168-72. 2008.... - SLP-65 regulates immunoglobulin light chain gene recombination through the PI(3)K-PKB-Foxo pathwaySebastian Herzog
Max Planck Institute for Immunobiology, 79108 Freiburg, Germany
Nat Immunol 9:623-31. 2008..Together, these data illuminate a molecular function of SLP-65 and identify a key role for Foxo proteins in the regulation of light chain recombination, receptor editing and B cell selection... - Inhibitor of differentiation 4 drives brain tumor-initiating cell genesis through cyclin E and notch signalingHye Min Jeon
School of Life Sciences and Biotechnology, Korea University, Seoul 136 713, Republic of Korea
Genes Dev 22:2028-33. 2008..Thus, Id4 plays an integral role in the transformation of astrocytes via its combined actions on two-key cell cycle and differentiation regulatory molecules...
Research Grants
- TELOMERASE IN DEVELOPMENT, SENESCENCE AND NEOPLASIARonald DePinho; Fiscal Year: 2007....
- Genetics and Biology of Pancreatic Duct AdenocarcinomaRonald DePinho; Fiscal Year: 2007....
- Evolution of Primary and Resistant Solid TumorsRonald DePinho; Fiscal Year: 2007..Finally, nanosensors will be developed that are capable to detecting telomerase activity and quantifying telomere reserves. ..
- TELOMERASE IN DEVELOPMENT, SENESCENCE AND NEOPLASIARonald DePinho; Fiscal Year: 2009....
- Genetics and Biology of Malignant GliomaRonald DePinho; Fiscal Year: 2007..The goals of this P01 mirror precisely the priorities articulated by the recent NCI/NINDS Brain Tumor PRG. ..
- Conference on Mouse Models of CancerRonald DePinho; Fiscal Year: 2003..Such systems hold significant promise in accelerating and making more accurate the evaluation of these compounds prior to entry into the clinic. ..
- TELOMERASE IN DEVELOPMENT, SENESCENCE AND NEOPLASIARONALD ANTHONY DEPINHO; Fiscal Year: 2010..We will validate the principal of telomerase extinction as an anti-cancer therapy and define potential resistance mechanisms which should lead to new drugs that may synergize with anti-telomerase therapy. ..