NORMAN SHARPLESS

Summary

Affiliation: University of North Carolina
Country: USA

Publications

  1. ncbi request reprint The mighty mouse: genetically engineered mouse models in cancer drug development
    Norman E Sharpless
    Departments of Medicine and Genetics, The Lineberger Comprehensive Cancer Center, The University of North Carolina, Chapel Hill, North Carolina 27599 7295, USA
    Nat Rev Drug Discov 5:741-54. 2006
  2. pmc Multiple roles of cyclin-dependent kinase 4/6 inhibitors in cancer therapy
    Patrick J Roberts
    Department of Genetics, The University of North Carolina School of Medicine, Chapel Hill, NC, USA
    J Natl Cancer Inst 104:476-87. 2012
  3. pmc Telomeres, stem cells, senescence, and cancer
    Norman 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
  4. ncbi request reprint The differential impact of p16(INK4a) or p19(ARF) deficiency on cell growth and tumorigenesis
    Norman 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
  5. ncbi request reprint Ink4a/Arf links senescence and aging
    Norman E Sharpless
    Departments of Medicine and Genetics, The Lineberger Comprehensive Cancer Center, The University of North Carolina School of Medicine, Chapel Hill, NC 27599 7295, USA
    Exp Gerontol 39:1751-9. 2004
  6. ncbi request reprint INK4a/ARF: a multifunctional tumor suppressor locus
    Norman E Sharpless
    Department of Medicine, The Lineberger Comprehensive Cancer Center, The University of North Carolina School of Medicine, Chapel Hill, 27599 7295, USA
    Mutat Res 576:22-38. 2005
  7. ncbi request reprint How stem cells age and why this makes us grow old
    Norman E Sharpless
    Department of Medicine, The Lineberger Comprehensive Cancer Center, The University of North Carolina, Chapel Hill, North Carolina 27599 7295, USA
    Nat Rev Mol Cell Biol 8:703-13. 2007
  8. pmc HMGA2, microRNAs, and stem cell aging
    Scott M Hammond
    Department of Cell and Developmental Biology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
    Cell 135:1013-6. 2008
  9. pmc CHIP deficiency decreases longevity, with accelerated aging phenotypes accompanied by altered protein quality control
    Jin Na Min
    Carolina Cardiovascular Biology Center, University of North Carolina, Chapel Hill, North Carolina 27599 7126, USA
    Mol Cell Biol 28:4018-25. 2008
  10. ncbi request reprint Expression of p16Ink4a compensates for p18Ink4c loss in cyclin-dependent kinase 4/6-dependent tumors and tissues
    Matthew R Ramsey
    Department of Medicine, The Lineberger Comprehensive Cancer Center, The University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599 7295, USA
    Cancer Res 67:4732-41. 2007

Research Grants

  1. Melanoma in p16INK4a and p19ARF Deficient Mice
    NORMAN SHARPLESS; Fiscal Year: 2006
  2. The role of p16INK4a in mammalian aging
    NORMAN SHARPLESS; Fiscal Year: 2007
  3. The role of p16INK4a in mammalian aging
    Norman Edward Sharpless; Fiscal Year: 2010

Detail Information

Publications56

  1. ncbi request reprint The mighty mouse: genetically engineered mouse models in cancer drug development
    Norman E Sharpless
    Departments of Medicine and Genetics, The Lineberger Comprehensive Cancer Center, The University of North Carolina, Chapel Hill, North Carolina 27599 7295, USA
    Nat Rev Drug Discov 5:741-54. 2006
    ....
  2. pmc Multiple roles of cyclin-dependent kinase 4/6 inhibitors in cancer therapy
    Patrick J Roberts
    Department of Genetics, The University of North Carolina School of Medicine, Chapel Hill, NC, USA
    J Natl Cancer Inst 104:476-87. 2012
    ....
  3. pmc Telomeres, stem cells, senescence, and cancer
    Norman 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...
  4. ncbi request reprint The differential impact of p16(INK4a) or p19(ARF) deficiency on cell growth and tumorigenesis
    Norman 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
    ....
  5. ncbi request reprint Ink4a/Arf links senescence and aging
    Norman E Sharpless
    Departments of Medicine and Genetics, The Lineberger Comprehensive Cancer Center, The University of North Carolina School of Medicine, Chapel Hill, NC 27599 7295, USA
    Exp Gerontol 39:1751-9. 2004
    ..Expression of the INK4a/ARF locus, therefore, appears not only to be a major suppressor of cancer, but also an effector of mammalian aging...
  6. ncbi request reprint INK4a/ARF: a multifunctional tumor suppressor locus
    Norman E Sharpless
    Department of Medicine, The Lineberger Comprehensive Cancer Center, The University of North Carolina School of Medicine, Chapel Hill, 27599 7295, USA
    Mutat Res 576:22-38. 2005
    ....
  7. ncbi request reprint How stem cells age and why this makes us grow old
    Norman E Sharpless
    Department of Medicine, The Lineberger Comprehensive Cancer Center, The University of North Carolina, Chapel Hill, North Carolina 27599 7295, USA
    Nat Rev Mol Cell Biol 8:703-13. 2007
    ....
  8. pmc HMGA2, microRNAs, and stem cell aging
    Scott M Hammond
    Department of Cell and Developmental Biology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
    Cell 135:1013-6. 2008
    ..2008; Nishino et al., 2008; Sanna et al., 2008; Weedon et al., 2008) link a chromatin-associated protein, HMGA2, to development, height, and mouse stem cell aging during late fetal development and young adulthood...
  9. pmc CHIP deficiency decreases longevity, with accelerated aging phenotypes accompanied by altered protein quality control
    Jin Na Min
    Carolina Cardiovascular Biology Center, University of North Carolina, Chapel Hill, North Carolina 27599 7126, USA
    Mol Cell Biol 28:4018-25. 2008
    ..Taken together, these data reveal that impaired protein quality control contributes to cellular senescence and implicates CHIP-dependent quality control mechanisms in the regulation of mammalian longevity in vivo...
  10. ncbi request reprint Expression of p16Ink4a compensates for p18Ink4c loss in cyclin-dependent kinase 4/6-dependent tumors and tissues
    Matthew R Ramsey
    Department of Medicine, The Lineberger Comprehensive Cancer Center, The University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599 7295, USA
    Cancer Res 67:4732-41. 2007
    ..These data suggest that p16(Ink4a) and p18(Ink4c) coordinately regulate the in vivo catalytic activity of cdk4/6 in specific compartments of adult mice...
  11. pmc Defective cell cycle checkpoint functions in melanoma are associated with altered patterns of gene expression
    William K Kaufmann
    Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
    J Invest Dermatol 128:175-87. 2008
    ..The results suggest that defects in DNA damage checkpoints may be recognized in melanomas through analysis of gene expression...
  12. pmc HIF2alpha cooperates with RAS to promote lung tumorigenesis in mice
    William Y Kim
    Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina 27599, USA
    J Clin Invest 119:2160-70. 2009
    ..They further suggest a possible causal relationship between HIF2alpha and prognosis in patients with NSCLC...
  13. pmc Overexpression of the cell cycle inhibitor p16INK4a promotes a prothrombotic phenotype following vascular injury in mice
    Jessica C Cardenas
    Department of Pathology and Laboratory Medicine, University of North Carolina Chapel Hill, NC 27599 7035, USA
    Arterioscler Thromb Vasc Biol 31:827-33. 2011
    ..p16(INK4a) is a cell cycle inhibitor that promotes senescence and is upregulated during normal aging. In this study, we examine the contribution of p16(INK4a) overexpression to venous thrombosis...
  14. ncbi request reprint The persistence of senescence
    Norman E Sharpless
    Department of Medicine, Lineberger Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA
    Sci Aging Knowledge Environ 2003:PE24. 2003
    ..In this Perspective, I discuss two recent publications (1, 2) that deal with the durability of senescence. These findings are of interest not only to those who study aging, but to those who study cancer as well...
  15. pmc Hot topics in stem cells and self-renewal: 2010
    Norman E Sharpless
    Department of Medicine and Genetics, The University of North Carolina School of Medicine, Chapel Hill, NC 27599 7295, USA
    Aging Cell 9:457-61. 2010
    ..This period has also been marked by the recent award of the Nobel Prize in Physiology or Medicine for elucidation of telomeres and telomerase, a topic of critical importance to stem cell aging...
  16. ncbi request reprint Lack of extracellular signal-regulated kinase mitogen-activated protein kinase signaling shows a new type of melanoma
    Janiel M Shields
    Department of Biochemistry and Biophysics, The Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA
    Cancer Res 67:1502-12. 2007
    ..These results show a molecularly distinct melanoma subtype that does not require ERK activation or epithelial-mesenchymal transformation for progression...
  17. ncbi request reprint p53: good cop/bad cop
    Norman 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...
  18. doi request reprint LKB1 and lung cancer: more than the usual suspects
    Usman Shah
    Departments of Medicine and Genetics, The Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina, USA
    Cancer Res 68:3562-5. 2008
    ..One is reminded of an Agatha Christie murder mystery where nearly every character in the book has reason to be suspected of committing the crime-there are too many suspects for how LKB1 might repress lung cancer...
  19. ncbi request reprint Stem cells and the rate of living
    Janakiraman Krishnamurthy
    Departments of Medicine and Genetics, The Lineberger Comprehensive Cancer Center, The University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA
    Cell Stem Cell 1:9-11. 2007
    ..While this theory as originally conceived has been debunked, new work (Ruzankina et al. [2007], in this issue of Cell Stem Cell) suggests that mammals in fact do have a finite number of stem cell replications per life...
  20. ncbi request reprint The regulation of INK4/ARF in cancer and aging
    William Y Kim
    Department of Medicine, The University of North Carolina School of Medicine, Chapel Hill, 27599, USA
    Cell 127:265-75. 2006
    ..Here, we discuss the regulation and role of p16(INK4a), ARF, and p15(INK4b) in cancer and aging...
  21. pmc p16(Ink4a) inhibits histologic progression and angiogenic signaling in min colon tumors
    Steven L Gibson
    Department of Medicine, Cell and Molecular Biology Graduate Group, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104 6140, USA
    Cancer Biol Ther 4:1389-94. 2005
    ..01). Exogenous p16 expression in human colon tumor cells in vitro inhibited VEGF production. These results suggest that p16 constrains colon tumor progression, in part through inhibiting angiogenic signaling...
  22. ncbi request reprint p16INK4a induces an age-dependent decline in islet regenerative potential
    Janakiraman Krishnamurthy
    Department of Medicine, The Lineberger Comprehensive Cancer Center, The University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599, USA
    Nature 443:453-7. 2006
    ..These genetic data support the view that an age-induced increase of p16INK4a expression limits the regenerative capacity of beta-cells with ageing...
  23. pmc Tumor suppressor mechanisms in immune aging
    Yan Liu
    Department of Genetics and Medicine, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA
    Curr Opin Immunol 21:431-9. 2009
    ..Here we will argue on the basis of recent advances in our understanding of tumor suppressor mechanisms in immune cells; however, that aspects of these same beneficial pathways have the potential to induce intrinsic immune aging...
  24. ncbi request reprint RNA expression analysis of formalin-fixed paraffin-embedded tumors
    Shannon K Penland
    Department of Medicine, The University of North Carolina School of Medicine, Chapel Hill, NC 27599 7295, USA
    Lab Invest 87:383-91. 2007
    ..Although only a minority of FFPE blocks could be analyzed, we show that informative RNA expression analysis can be derived from selected FFPE samples...
  25. pmc CD200 is induced by ERK and is a potential therapeutic target in melanoma
    Kimberly B Petermann
    Department of Genetics, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599 7295, USA
    J Clin Invest 117:3922-9. 2007
    ....
  26. pmc Mitigation of hematologic radiation toxicity in mice through pharmacological quiescence induced by CDK4/6 inhibition
    Søren M Johnson
    Department of Genetics, The Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599, USA
    J Clin Invest 120:2528-36. 2010
    ..These results demonstrate an effective method to mitigate the hematopoietic toxicity of IR in mammals, which may be potentially useful after radiological disaster or as an adjuvant to anticancer therapy...
  27. pmc What's so special about RB?
    Christin E Burd
    Department of Genetics, The Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599 7295, USA
    Cancer Cell 17:313-4. 2010
    ..However, only RB is frequently mutated in cancer. In this issue of Cancer Cell, Chicas et al. shed new light on this conundrum, defining a "special," nonredundant role for RB in promoting cellular senescence...
  28. pmc Ink4a/Arf expression is a biomarker of aging
    Janakiraman Krishnamurthy
    Department of Medicine, The Lineberger Comprehensive Cancer Center, The University of North Carolina School of Medicine, Chapel Hill, North Carolina, 27599 7295, USA
    J Clin Invest 114:1299-307. 2004
    ..These data suggest that expression of the Ink4a/Arf tumor suppressor locus is a robust biomarker, and possible effector, of mammalian aging...
  29. pmc A quantitative model for age-dependent expression of the p16INK4a tumor suppressor
    Denis Tsygankov
    Departments of Pharmacology, Medicine, and Genetics, and the Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA
    Proc Natl Acad Sci U S A 106:16562-7. 2009
    ..This analysis is most consistent with the model that p16(INK4a) expression monotonically increases with age, and higher expression is associated with increased subject attrition...
  30. pmc Expression of p16(INK4a) in peripheral blood T-cells is a biomarker of human aging
    Yan Liu
    Department of Genetics, The University of North Carolina School of Medicine, Chapel Hill, USA
    Aging Cell 8:439-48. 2009
    ..These data suggest that p16(INK4a) expression in PBTL is an easily measured, peripheral blood biomarker of molecular age...
  31. pmc INK4/ARF transcript expression is associated with chromosome 9p21 variants linked to atherosclerosis
    Yan Liu
    Department of Genetics, The Lineberger Comprehensive Cancer Center, The University of North Carolina School of Medicine, Chapel Hill, NC, USA
    PLoS ONE 4:e5027. 2009
    ..To explore the mechanism of this association, we investigated whether expression of proximate transcripts (p16(INK4a), p15(INK4b), ARF, ANRIL and MTAP) correlate with genotype of representative 9p21 SNPs...
  32. ncbi request reprint RAS unplugged: negative feedback and oncogene-induced senescence
    Nabeel Bardeesy
    Department of Medicine, Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, Massachusetts 02114, USA
    Cancer Cell 10:451-3. 2006
    ....
  33. pmc Engineering and selection of shuffled AAV genomes: a new strategy for producing targeted biological nanoparticles
    Wuping Li
    Gene Therapy Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 7352, USA
    Mol Ther 16:1252-60. 2008
    ..Application of this technology to alternative cell/tissue types using AAV or other viral capsid sequences is likely to yield a new class of biological nanoparticles as vectors for human gene transfer...
  34. doi request reprint VHL inactivation: a new road to senescence
    William Y Kim
    Department of Medicine, Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599 7295, USA
    Cancer Cell 13:295-7. 2008
    ....
  35. ncbi request reprint LKB1 modulates lung cancer differentiation and metastasis
    Hongbin Ji
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Nature 448:807-10. 2007
    ..These studies establish LKB1 as a critical barrier to pulmonary tumorigenesis, controlling initiation, differentiation and metastasis...
  36. pmc Components of the Rb pathway are critical targets of UV mutagenesis in a murine melanoma model
    Karuppiah Kannan
    Department of Medical Oncology, Dana Farber Cancer Institute, Brigham and Women s Hospital, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 100:1221-5. 2003
    ..Together, these molecular and genetic data identify components of the Rb pathway as critical biological targets of UV-induced mutagenesis in the development of murine melanoma in vivo...
  37. ncbi request reprint p16(INK4a) and p53 deficiency cooperate in tumorigenesis
    Norman E Sharpless
    Department of Adult Oncology, Dana Farber Cancer Institute and Harvard Medical School, 44 Binney Street M413, Boston, MA 02115, USA
    Cancer Res 62:2761-5. 2002
    ..This cooperation between p16(INK4a) and p53 loss in tumorigenesis is consistent with the view that these genes function in distinct anticancer pathways...
  38. pmc Constitutive telomerase expression promotes mammary carcinomas in aging mice
    Steven 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...
  39. ncbi request reprint Loss of the Lkb1 tumour suppressor provokes intestinal polyposis but resistance to transformation
    Nabeel 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...
  40. pmc A mouse model of human oral-esophageal cancer
    Oliver G Opitz
    Division of Gastroenterology, Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    J Clin Invest 110:761-9. 2002
    ..These data demonstrate that L2D1(+)/p53(+/-) mice provide a well-defined, novel, and faithful model of oral-esophageal cancer, which allows for the testing of novel chemopreventive, diagnostic, and therapeutic approaches...
  41. pmc p16(Ink4a) interferes with Abelson virus transformation by enhancing apoptosis
    Zohar 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...
  42. ncbi request reprint Impaired processing of DNA photoproducts and ultraviolet hypermutability with loss of p16INK4a or p19ARF
    Papri 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...
  43. ncbi request reprint How disruption of cell cycle regulating genes might predispose to sun-induced skin cancer
    Thomas 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...
  44. ncbi request reprint Cancer: crime and punishment
    Norman E Sharpless
    Nature 436:636-7. 2005
  45. pmc ARF functions as a melanoma tumor suppressor by inducing p53-independent senescence
    Linan Ha
    Laboratory of Cancer Biology and Genetics, National Cancer Institute, Bethesda, MD 20892 4264, USA
    Proc Natl Acad Sci U S A 104:10968-73. 2007
    ..Thus, therapeutics designed to restore wild-type p53 function may be insufficient to counter melanoma and other malignancies in which ARF holds p53-independent tumor suppressor activity...
  46. ncbi request reprint Stem-cell ageing modified by the cyclin-dependent kinase inhibitor p16INK4a
    Viktor 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...
  47. pmc Increasing p16INK4a expression decreases forebrain progenitors and neurogenesis during ageing
    Anna V Molofsky
    Howard Hughes Medical Institute, Department of Internal Medicine, and Center for Stem Cell Biology, University of Michigan, Ann Arbor, Michigan 48109 2216, USA
    Nature 443:448-52. 2006
    ..Declining subventricular zone progenitor function and olfactory bulb neurogenesis during ageing are thus caused partly by increasing p16INK4a expression...
  48. ncbi request reprint Telomeres, p21 and the cancer-aging hypothesis
    Jessica F Bell
    Nat Genet 39:11-2. 2007
  49. ncbi request reprint ROS as a tumour suppressor?
    Matthew R Ramsey
    Nat Cell Biol 8:1213-5. 2006
  50. pmc Targeting of C-terminal binding protein (CtBP) by ARF results in p53-independent apoptosis
    Seema Paliwal
    Department of Cancer Biology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA
    Mol Cell Biol 26:2360-72. 2006
    ..CtBP proteins represent putative targets for p53-independent tumor suppression by ARF...
  51. ncbi request reprint Cancer biology: gone but not forgotten
    Norman E Sharpless
    Nature 445:606-7. 2007
  52. ncbi request reprint Epidermal growth factor receptor and Ink4a/Arf: convergent mechanisms governing terminal differentiation and transformation along the neural stem cell to astrocyte axis
    Robert 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...
  53. ncbi request reprint A phase II study of troglitazone, an activator of the PPARgamma receptor, in patients with chemotherapy-resistant metastatic colorectal cancer
    Matthew H Kulke
    Department of Adult Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer J 8:395-9. 2002
    ..We therefore assessed the efficacy of troglitazone in the treatment of metastatic colon cancer in humans...
  54. ncbi request reprint Array comparative genome hybridization for tumor classification and gene discovery in mouse models of malignant melanoma
    Rónán C O'Hagan
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Res 63:5352-6. 2003
    ..Kannan, et al., Proc. Natl. Acad. Sci. USA, 21: 2003). These results are the first to establish the utility of array-CGH as a means of etiology-based tumor classification in genetically defined cancer-prone models...
  55. ncbi request reprint EGFR targeted therapy: view from biological standpoint
    Hongbin Ji
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cell Cycle 5:2072-6. 2006
    ....
  56. ncbi request reprint The impact of human EGFR kinase domain mutations on lung tumorigenesis and in vivo sensitivity to EGFR-targeted therapies
    Hongbin Ji
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Cell 9:485-95. 2006
    ..These data suggest that persistent EGFR signaling is required for tumor maintenance in human lung adenocarcinomas expressing EGFR mutants...

Research Grants8

  1. Melanoma in p16INK4a and p19ARF Deficient Mice
    NORMAN SHARPLESS; Fiscal Year: 2006
    ..Such a model could then serve as a foundation for future studies of melanoma progression and therapy, and the results of this work will have implications for the treatment of human MM. ..
  2. The role of p16INK4a in mammalian aging
    NORMAN SHARPLESS; Fiscal Year: 2007
    ..Through these approaches, we will examine the in vivo tissue and age-specific effects of p16INK4a expression, and delineate its contribution to a variety of mammalian aging phenotypes. ..
  3. The role of p16INK4a in mammalian aging
    Norman Edward Sharpless; Fiscal Year: 2010
    ..In this work, we use experimental systems in humans and mice to investigate the role of anti-cancer mechanisms in aging. ..