Charles J Sherr

Summary

Affiliation: St. Jude Children's Research Hospital
Country: USA

Publications

  1. ncbi request reprint An Arf(GFP/GFP) reporter mouse reveals that the Arf tumor suppressor monitors latent oncogenic signals in vivo
    Charles J Sherr
    Howard Hughes Medical Institute, Department of Genetics and Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38117, USA
    Cell Cycle 3:239-40. 2004
  2. ncbi request reprint Principles of tumor suppression
    Charles J Sherr
    Howard Hughes Medical Institute, Department of Genetics and Tumor Cell Biology, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA
    Cell 116:235-46. 2004
  3. pmc Ink4-Arf locus in cancer and aging
    Charles J Sherr
    Howard Hughes Medical Institute, Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, TN, USA
    Wiley Interdiscip Rev Dev Biol 1:731-41. 2012
  4. ncbi request reprint Living with or without cyclins and cyclin-dependent kinases
    Charles J Sherr
    Howard Hughes Medical Institute and Department of Genetics and Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Genes Dev 18:2699-711. 2004
  5. ncbi request reprint Cancer cell cycles
    C J Sherr
    Howard Hughes Medical Institute, Department of Tumor Cell Biology, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA
    Science 274:1672-7. 1996
  6. ncbi request reprint Divorcing ARF and p53: an unsettled case
    Charles J Sherr
    Howard Hughes Medical Institute, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, Tennessee 38105, USA
    Nat Rev Cancer 6:663-73. 2006
  7. ncbi request reprint The RB and p53 pathways in cancer
    Charles J Sherr
    Howard Hughes Medical Institute, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Cancer Cell 2:103-12. 2002
  8. ncbi request reprint The Pezcoller lecture: cancer cell cycles revisited
    C J Sherr
    Howard Hughes Medical Institute and Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Cancer Res 60:3689-95. 2000
  9. ncbi request reprint The INK4a/ARF network in tumour suppression
    C J Sherr
    Department of Tumor Cell Biology, Howard Hughes Medical Institute, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, Tennessee 38105, USA
    Nat Rev Mol Cell Biol 2:731-7. 2001
  10. ncbi request reprint The ARF/p53 pathway
    C J Sherr
    Department of Tumor Cell Biology, Howard Hughes Medical Institute, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Curr Opin Genet Dev 10:94-9. 2000

Collaborators

Detail Information

Publications108 found, 100 shown here

  1. ncbi request reprint An Arf(GFP/GFP) reporter mouse reveals that the Arf tumor suppressor monitors latent oncogenic signals in vivo
    Charles J Sherr
    Howard Hughes Medical Institute, Department of Genetics and Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38117, USA
    Cell Cycle 3:239-40. 2004
    ..Studies of a knock-in mouse strain in which sequences encoding green fluorescent protein were substituted for those encoding p19Arf argue that the Arf gene responds to latent oncogenic signals in vivo to eliminate incipient cancer cells...
  2. ncbi request reprint Principles of tumor suppression
    Charles J Sherr
    Howard Hughes Medical Institute, Department of Genetics and Tumor Cell Biology, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA
    Cell 116:235-46. 2004
    ..Their study has become a centerpiece of contemporary cancer research...
  3. pmc Ink4-Arf locus in cancer and aging
    Charles J Sherr
    Howard Hughes Medical Institute, Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, TN, USA
    Wiley Interdiscip Rev Dev Biol 1:731-41. 2012
    ..Deletion of INK4-ARF contributes to the aberrant self-renewal capacity of tumor cells and occurs frequently in many forms of human cancer...
  4. ncbi request reprint Living with or without cyclins and cyclin-dependent kinases
    Charles J Sherr
    Howard Hughes Medical Institute and Department of Genetics and Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Genes Dev 18:2699-711. 2004
    ..Thus, none of these genes is strictly essential for cell cycle progression. To what extent is the prevailing dogma incorrect, and how can the recent findings be reconciled with past work?..
  5. ncbi request reprint Cancer cell cycles
    C J Sherr
    Howard Hughes Medical Institute, Department of Tumor Cell Biology, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA
    Science 274:1672-7. 1996
    ..Like the tumor suppressor protein p53, components of this "RB pathway," although not essential for the cell cycle per se, may participate in checkpoint functions that regulate homeostatic tissue renewal throughout life...
  6. ncbi request reprint Divorcing ARF and p53: an unsettled case
    Charles J Sherr
    Howard Hughes Medical Institute, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, Tennessee 38105, USA
    Nat Rev Cancer 6:663-73. 2006
    ..However, ARF has been reported to physically associate with proteins other than MDM2 and to have p53-independent activities, most of which remain controversial and poorly understood...
  7. ncbi request reprint The RB and p53 pathways in cancer
    Charles J Sherr
    Howard Hughes Medical Institute, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Cancer Cell 2:103-12. 2002
    ..Pinpointing the various ways by which the functions of RB and p53 are subverted in individual tumors should provide a rational basis for developing more refined tumor-specific therapies...
  8. ncbi request reprint The Pezcoller lecture: cancer cell cycles revisited
    C J Sherr
    Howard Hughes Medical Institute and Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Cancer Res 60:3689-95. 2000
    ..Lesions in the p16--cyclin D-CDK4--Rb and ARF--Mdm2--p53 pathways occur so frequently in cancer, regardless of patient age or tumor type, that they appear to be part of the life history of most, if not all, cancer cells...
  9. ncbi request reprint The INK4a/ARF network in tumour suppression
    C J Sherr
    Department of Tumor Cell Biology, Howard Hughes Medical Institute, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, Tennessee 38105, USA
    Nat Rev Mol Cell Biol 2:731-7. 2001
    ..A complex signalling network that interconnects the activities of RB and p53 monitors oncogenic stimuli to provide a cell-autonomous mode of tumour surveillance...
  10. ncbi request reprint The ARF/p53 pathway
    C J Sherr
    Department of Tumor Cell Biology, Howard Hughes Medical Institute, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Curr Opin Genet Dev 10:94-9. 2000
    ..Nucleolar relocalization of Mdm2 by ARF connotes a novel mechanism for preventing p53 turnover and provides a framework for understanding how stress signals cooperate to regulate p53 function...
  11. ncbi request reprint Arf-induced turnover of the nucleolar nucleophosmin-associated SUMO-2/3 protease Senp3
    Mei Ling Kuo
    Howard Hughes Medical Institute, Department of Genetics and Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Cell Cycle 7:3378-87. 2008
    ....
  12. pmc Differential post-transcriptional regulation of two Ink4 proteins, p18 Ink4c and p19 Ink4d
    Antoine Forget
    Department of Tumor Cell Biology and Genetics, St Jude Children s Research Hospital, Memphis, Tennessee, USA
    Cell Cycle 7:3737-46. 2008
    ..Although it has been generally assumed that p18(Ink4c) and p19(Ink4d) are biochemically similar Cdk inhibitors, the major differences in their stability and turnover are likely key to understanding their distinct biological functions...
  13. ncbi request reprint Genetic alterations in mouse medulloblastomas and generation of tumors de novo from primary cerebellar granule neuron precursors
    Frederique Zindy
    Department of Genetics, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Cancer Res 67:2676-84. 2007
    ..These results underscore the functional interplay between a network of specific genes that recurrently contribute to medulloblastoma formation...
  14. pmc Cytokine-dependent imatinib resistance in mouse BCR-ABL+, Arf-null lymphoblastic leukemia
    Richard T Williams
    Department of Oncology, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Genes Dev 21:2283-7. 2007
    ..Hence, salutary cytokines in the hematopoietic microenvironment can facilitate leukemic proliferation and confer resistance to targeted therapy...
  15. pmc Atoh1 inhibits neuronal differentiation and collaborates with Gli1 to generate medulloblastoma-initiating cells
    Olivier Ayrault
    Department of Genetics and Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee, USA
    Cancer Res 70:5618-27. 2010
    ..Therefore, by targeting multiple genes regulating the differentiation state of GNPs, Atoh1 collaborates with the pro-proliferative Gli1-dependent transcriptional program to influence medulloblastoma development...
  16. pmc Two tumor suppressors, p27Kip1 and patched-1, collaborate to prevent medulloblastoma
    Olivier Ayrault
    Department of Genetics and Tumor Cell Biology, Mail Stop no 350, 262 Danny Thomas Place, Memphis, TN 38105 3678, USA
    Mol Cancer Res 7:33-40. 2009
    ..In this respect, this mouse medulloblastoma model recapitulates the vast majority of human medulloblastomas that do not sustain TP53 mutations and are not aneuploid...
  17. pmc Sumoylation induced by the Arf tumor suppressor: a p53-independent function
    Kenji Tago
    Howard Hughes Medical Institute, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Proc Natl Acad Sci U S A 102:7689-94. 2005
    ..Reduction of Ubc9 levels with short hairpin RNAs rendered similar results. We suggest that Arf's p53-independent effects on gene expression and tumor suppression might depend on Arf-induced sumoylation...
  18. pmc N-terminal polyubiquitination and degradation of the Arf tumor suppressor
    Mei Ling Kuo
    Department of Genetics and Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Genes Dev 18:1862-74. 2004
    ..Re-engineering of the p19Arf N terminus to provide consensus sequences for N-acetylation limited Arf ubiquitination and decelerated its turnover...
  19. ncbi request reprint Myc-mediated proliferation and lymphomagenesis, but not apoptosis, are compromised by E2f1 loss
    Troy A Baudino
    Department of Biochemistry, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Mol Cell 11:905-14. 2003
    ..Therefore, Myc does not require E2f1 to induce Arf, p53, or apoptosis in B cells, but depends upon E2f1 to accelerate cell cycle progression and downregulate p27(Kip1)...
  20. pmc N-Myc and the cyclin-dependent kinase inhibitors p18Ink4c and p27Kip1 coordinately regulate cerebellar development
    Frederique Zindy
    Department of Genetics and Tumor Cell Biology, Howard Hughes Medical Institute, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Proc Natl Acad Sci U S A 103:11579-83. 2006
    ..These results provide definitive genetic evidence that expression of N-Myc and concomitant down-regulation of Ink4c and Kip1 contribute to the proper development of the cerebellum...
  21. ncbi request reprint Nucleolar Arf tumor suppressor inhibits ribosomal RNA processing
    Masataka Sugimoto
    Howard Hughes Medical Institute, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA
    Mol Cell 11:415-24. 2003
    ..Evolution may have linked a primordial nucleolar Arf function to Mdm2 and p53, creating a more efficient checkpoint-signaling pathway for coordinating ribosomal biogenesis and cell cycle progression...
  22. ncbi request reprint The ARF tumor suppressor in acute leukemias: insights from mouse models of Bcr-Abl-induced acute lymphoblastic leukemia
    Richard T Williams
    Department of Oncology, St Jude Children s Research Hospital, USA
    Adv Exp Med Biol 604:107-14. 2007
    ..Hence, IL-7 can reduce the sensitivity of Bcr-Abl+ pre-B cells to imatinib. Selective inhibitors of both Bcr-Abl and the IL-7 transducing JAK kinases may therefore prove beneficial in treating Ph+ ALL...
  23. pmc Arf tumor suppressor promoter monitors latent oncogenic signals in vivo
    Frederique Zindy
    Departments of Genetics and Tumor Cell Biology, St Jude Children s Research Hospital, 332 North Lauderdale Street, Memphis, TN 38105, USA
    Proc Natl Acad Sci U S A 100:15930-5. 2003
    ..Inactivation of Arf in this manner led to the outgrowth of tumor cells expressing GFP, thereby providing direct evidence that the Arf promoter monitors latent oncogenic signals in vivo...
  24. pmc Transient expression of the Arf tumor suppressor during male germ cell and eye development in Arf-Cre reporter mice
    Adam Gromley
    Howard Hughes Medical Institute and Department of Genetics and Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Proc Natl Acad Sci U S A 106:6285-90. 2009
    ..Crossing the Arf(Cre/FL) alleles onto a Pdgfrbeta(FL/FL) background normalized all histopathology and restored vision fully...
  25. ncbi request reprint Ubiquitination of, and sumoylation by, the Arf tumor suppressor
    Willem den Besten
    Department of Genetics and Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Isr Med Assoc J 8:249-51. 2006
    ..Thus, ubiquitination and sumoylation can each influence Arf tumor suppressor activity...
  26. ncbi request reprint Regulation of the Arf tumor suppressor in Emicro-Myc transgenic mice: longitudinal study of Myc-induced lymphomagenesis
    David Bertwistle
    Department of Genetics and Tumor Cell Biology, Howard Hughes Medical Institute, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Blood 109:792-4. 2007
    ..We infer that very low levels of Arf are tumor suppressive, and that further induction provides the selective pressure for the emergence of tumors that have inactivated the gene...
  27. ncbi request reprint Myeloid leukemia-associated nucleophosmin mutants perturb p53-dependent and independent activities of the Arf tumor suppressor protein
    Willem den Besten
    Department of Genetics and Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Cell Cycle 4:1593-8. 2005
    ..We favor the idea that NPMc also contributes to AML by dominantly perturbing other functions of the wild type NPM protein...
  28. ncbi request reprint The CDK inhibitor p18Ink4c is a tumor suppressor in medulloblastoma
    Tamar Uziel
    Department of Genetics and Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Cell Cycle 5:363-5. 2006
    ..Methylation of the INK4C (CDKN2C) promoter and complete loss of p18(INK4C) protein expression were detected in a significant fraction of human MBs again pointing toward a role for INK4C in suppression of MB formation...
  29. pmc Expression of arf tumor suppressor in spermatogonia facilitates meiotic progression in male germ cells
    Michelle L Churchman
    Howard Hughes Medical Institute, St Jude Children s Research Hospital, Memphis, Tennessee, United States of America
    PLoS Genet 7:e1002157. 2011
    ....
  30. pmc Epigenetic regulation of the Ink4a-Arf (Cdkn2a) tumor suppressor locus in the initiation and progression of Notch1-driven T cell acute lymphoblastic leukemia
    Emmanuel J Volanakis
    Division of Pediatric Hematology Oncology, Vanderbilt University, Nashville, TN, USA
    Exp Hematol 41:377-86. 2013
    ..Epigenetic remodeling during tumor progression licenses Arf as a tumor suppressor and in turn provides the selective pressure for Ink4a-Arf deletion in clonal T-ALLs that emerge...
  31. ncbi request reprint Arf induces p53-dependent and -independent antiproliferative genes
    Mei Ling Kuo
    Department of Genetics and Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Cancer Res 63:1046-53. 2003
    ..Together, the results indicate that p19(Arf) induces a broad spectrum of proteins that likely act in concert to arrest cell proliferation...
  32. pmc Failure of CDKN2A/B (INK4A/B-ARF)-mediated tumor suppression and resistance to targeted therapy in acute lymphoblastic leukemia induced by BCR-ABL
    Charles G Mullighan
    Department of Pathology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Genes Dev 22:1411-5. 2008
    ..Why is this the case, and how do these genetic lesions contribute to an aggressive disease that fails to durably respond to targeted kinase inhibitors?..
  33. pmc Arf tumor suppressor and miR-205 regulate cell adhesion and formation of extraembryonic endoderm from pluripotent stem cells
    Chunliang Li
    Howard Hughes Medical Institute, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Proc Natl Acad Sci U S A 110:E1112-21. 2013
    ..The noncanonical and canonical roles of Arf in ExEn development and tumor suppression, respectively, may be conceptually linked through mechanisms that govern cell attachment and migration...
  34. pmc Chemotherapeutic agents circumvent emergence of dasatinib-resistant BCR-ABL kinase mutations in a precise mouse model of Philadelphia chromosome-positive acute lymphoblastic leukemia
    Nidal Boulos
    Department of Oncology, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Blood 117:3585-95. 2011
    ....
  35. pmc The tumor suppressors Ink4c and p53 collaborate independently with Patched to suppress medulloblastoma formation
    Tamar Uziel
    Department of Tumor Cell Biology and Genetics, Memphis, Tennessee 38105, USA
    Genes Dev 19:2656-67. 2005
    ..Methylation of INK4C (CDKN2C) was observed in four of 23 human MBs, and p18(INK4C) protein expression was extinguished in 14 of 73 cases. Hence, p18(INK4C) loss may contribute to MB formation in children...
  36. pmc Physical and functional interactions of the Arf tumor suppressor protein with nucleophosmin/B23
    David Bertwistle
    Howard Hughes Medical Institute and Department of Genetics and Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Mol Cell Biol 24:985-96. 2004
    ..An NPM mutant lacking its carboxyl-terminal nucleic acid-binding domain oligomerizes with endogenous NPM, inhibits p19(Arf) from entering into 2- to 5-MDa particles, and overrides the ability of p19(Arf) to retard rRNA processing...
  37. pmc Stage-specific Arf tumor suppression in Notch1-induced T-cell acute lymphoblastic leukemia
    Emmanuel J Volanakis
    Department of Oncology, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Blood 114:4451-9. 2009
    ..Arf activation by ICN1 in T cells thereby provides stage-specific tumor suppression but also a strong selective pressure for deletion of the locus in T-ALL...
  38. pmc Arf gene loss enhances oncogenicity and limits imatinib response in mouse models of Bcr-Abl-induced acute lymphoblastic leukemia
    Richard T Williams
    Department of Hematology Oncology, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA
    Proc Natl Acad Sci U S A 103:6688-93. 2006
    ....
  39. ncbi request reprint Antagonism of Myc functions by Arf
    John L Cleveland
    Department of Biochemistry, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Cancer Cell 6:309-11. 2004
    ..A recent study reveals a novel level of feedback control, whereby induced p19(Arf) binds to Myc and blocks cell proliferation by selectively impairing its transactivation functions...
  40. ncbi request reprint Hemangiosarcomas, medulloblastomas, and other tumors in Ink4c/p53-null mice
    Frederique Zindy
    Department of Genetics and Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Cancer Res 63:5420-7. 2003
    ....
  41. pmc Functional interactions between Lmo2, the Arf tumor suppressor, and Notch1 in murine T-cell malignancies
    Louise M Treanor
    Division of Experimental Hematology, Department of Hematology, St Jude Children s Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA
    Blood 117:5453-62. 2011
    ..Notch mutation and Arf inactivation appear to independently cooperate in no requisite order with Lmo2 overexpression in inducing T-ALL, and all 3 events remained insufficient to guarantee immediate tumor development...
  42. pmc Hzf, a p53-responsive gene, regulates maintenance of the G2 phase checkpoint induced by DNA damage
    Masataka Sugimoto
    Howard Hughes Medical Institute, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, Tennessee 38105, USA
    Mol Cell Biol 26:502-12. 2006
    ..Thus, two p53-inducible gene products, Hzf and p21Cip1, act concomitantly to enforce the G(2) checkpoint...
  43. ncbi request reprint Monoclonal antibodies to the mouse p19(Arf) tumor suppressor protein
    David Bertwistle
    Department of Genetics and Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Hybrid Hybridomics 23:293-300. 2004
    ..This indicates that these antibodies should be useful in detecting the endogenous p(19Arf) protein at specific stages of mouse development and during early stages of tumorigenesis...
  44. pmc p53-independent functions of the p19(ARF) tumor suppressor
    J D Weber
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Genes Dev 14:2358-65. 2000
    ..Inhibition of the retinoblastoma protein had no effect on the ability of ARF to arrest TKO MEFs. Thus, in the absence of Mdm2, p19(ARF) interacts with other targets to inhibit cell proliferation...
  45. pmc Regulation of cyclin D-dependent kinase 4 (cdk4) by cdk4-activating kinase
    J Y Kato
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105
    Mol Cell Biol 14:2713-21. 1994
    ....
  46. pmc Cancer-associated mutations at the INK4a locus cancel cell cycle arrest by p16INK4a but not by the alternative reading frame protein p19ARF
    D E Quelle
    Howard Hughes Medical Institute, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Proc Natl Acad Sci U S A 94:669-73. 1997
    ..Therefore, cancer-associated mutations within exon 2 of the INK4a gene specifically target p16INK4a, and not p19ARF, for inactivation...
  47. pmc Functional and physical interactions of the ARF tumor suppressor with p53 and Mdm2
    T Kamijo
    Howard Hughes Medical Institute, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA
    Proc Natl Acad Sci U S A 95:8292-7. 1998
    ..In this setting, reintroduction of p19(ARF) restores p53's ability to induce p21(Cip1) and mdm2, implying that, in addition to stabilizing p53, ARF modulates p53-dependent function through an additional mechanism...
  48. ncbi request reprint N-Terminal polyubiquitination of the ARF tumor suppressor, a natural lysine-less protein
    Mei Ling Kuo
    Howard Hughes Medical Institute, Department of Genetics and Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Cell Cycle 3:1367-9. 2004
    ....
  49. ncbi request reprint Tumor spectrum in ARF-deficient mice
    T Kamijo
    Howard Hughes Medical Institute, and Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Cancer Res 59:2217-22. 1999
    ..The longer latency of tumor formation in ARF-null versus p53-null mice, therefore, appears to enable a broader spectrum of tumors to emerge...
  50. pmc Control of spermatogenesis in mice by the cyclin D-dependent kinase inhibitors p18(Ink4c) and p19(Ink4d)
    F Zindy
    Departments of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Mol Cell Biol 21:3244-55. 2001
    ..Our data indicate that p18(Ink4c) and p19(Ink4d) are essential for male fertility. These two Cdk inhibitors collaborate in regulating spermatogenesis, helping to ensure mitotic exit and the normal meiotic maturation of spermatocytes...
  51. ncbi request reprint Overexpression of mouse D-type cyclins accelerates G1 phase in rodent fibroblasts
    D E Quelle
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105
    Genes Dev 7:1559-71. 1993
    ..Thus, cyclin D1, and most likely D2, are rate limiting for G1 progression...
  52. ncbi request reprint Cloning and chromosomal localization of the gene encoding human cyclin D-binding Myb-like protein (hDMP1)
    S M Bodner
    Department of Pathology and Laboratory Medicine, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Gene 229:223-8. 1999
    ..Further study will be needed to determine whether gene-specific mutations implicate hDMP1 as a tumor suppressor in acute leukemias with deletions of the long arm of chromosome 7 or in other types of human malignancy...
  53. ncbi request reprint Loss of the ARF tumor suppressor reverses premature replicative arrest but not radiation hypersensitivity arising from disabled atm function
    T Kamijo
    Howard Hughes Medical Institute, and Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Cancer Res 59:2464-9. 1999
    ..Therefore, whereas ARF and Atm signal to p53 through distinct pathways, the loss of ARF can modify p53-dependent features of the Atm-null phenotype...
  54. ncbi request reprint Identification and properties of an atypical catalytic subunit (p34PSK-J3/cdk4) for mammalian D type G1 cyclins
    H Matsushime
    Howard Hughes Medical Institute, St Jude Children s Research Hospital, Memphis, Tennessee 38105
    Cell 71:323-34. 1992
    ..Thus, p34PSK-J3 is a cyclin D-regulated catalytic subunit that acts as an Rb (but not H1) kinase...
  55. ncbi request reprint Coamplification of the CDK4 gene with MDM2 and GLI in human sarcomas
    Z A Khatib
    Department of Experimental Oncology and Hematology Oncology, St Jude Children s Research Hospital, Memphis, Tennessee 38105
    Cancer Res 53:5535-41. 1993
    ....
  56. pmc Disruption of the ARF-Mdm2-p53 tumor suppressor pathway in Myc-induced lymphomagenesis
    C M Eischen
    Department of Biochemistry, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Genes Dev 13:2658-69. 1999
    ..Therefore, Myc activation strongly selects for spontaneous inactivation of the ARF-Mdm2-p53 pathway in vivo, cancelling its protective checkpoint function and accelerating progression to malignancy...
  57. ncbi request reprint Alternative reading frames of the INK4a tumor suppressor gene encode two unrelated proteins capable of inducing cell cycle arrest
    D E Quelle
    Howard Hughes Medical Institute, St Jude Children s Research Hospital, Memphis, Tennessee 38101, USA
    Cell 83:993-1000. 1995
    ..Economical reutilization of coding sequences in this manner is practically without precedent in mammalian genomes, and the unitary inheritance of p16INK4a and p19ARF may underlie their dual requirement in cell cycle control...
  58. ncbi request reprint Direct binding of cyclin D to the retinoblastoma gene product (pRb) and pRb phosphorylation by the cyclin D-dependent kinase CDK4
    J Kato
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105
    Genes Dev 7:331-42. 1993
    ..The D-type cyclins may play dual roles as cdk4 regulatory subunits and as adaptor proteins that physically target active enzyme complexes to particular substrates...
  59. pmc Novel INK4 proteins, p19 and p18, are specific inhibitors of the cyclin D-dependent kinases CDK4 and CDK6
    H Hirai
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Mol Cell Biol 15:2672-81. 1995
    ..However, introduction of a vector encoding p19 into mouse NIH 3T3 cells leads to constitutive p19 synthesis, inhibits cyclin D1-CDK4 activity in vivo, and induces G1 phase arrest...
  60. pmc Interaction of D-type cyclins with a novel myb-like transcription factor, DMP1
    H Hirai
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Mol Cell Biol 16:6457-67. 1996
    ..These results raise the possibility that cyclin D-dependent kinases regulate gene expression in an RB independent manner, thereby serving to link other genetic programs to the cell cycle clock...
  61. pmc Cooperative signals governing ARF-mdm2 interaction and nucleolar localization of the complex
    J D Weber
    Howard Hughes Medical Institute, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Mol Cell Biol 20:2517-28. 2000
    ..Hence, the ARF-Mdm2 interaction can be viewed as bidirectional, with each protein being capable of regulating the subnuclear localization of the other...
  62. ncbi request reprint Oncogenic potential of the c-FMS proto-oncogene (CSF-1 receptor)
    Martine F Roussel
    Dept of Genetics and Tumor Cell Biology, Howard Hughes Medical Institute, St Jude Children s Research Hospital, 332 N Lauderdale, Memphis, TN 38105, USA
    Cell Cycle 2:5-6. 2003
  63. ncbi request reprint Expression arrays illuminate a way forward for mantle cell lymphoma
    William E Evans
    Department of Pharmaceutical Science, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Cancer Cell 3:100-2. 2003
  64. ncbi request reprint The RING domain of Mdm2 can inhibit cell proliferation
    Jinjun Dang
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Cancer Res 62:1222-30. 2002
    ..However, such interactions do not inhibit Mdm2 E3 ubiquitin ligase activity in vitro using p53 as a substrate. Expression of growth-inhibitory Mdm2 isoforms in tumors remains an enigma...
  65. pmc Activation of cyclin-dependent kinase 4 (cdk4) by mouse MO15-associated kinase
    M Matsuoka
    Howard Hughes Medical Institute, St Jude Children s Research Hospital, Memphis, Tennessee 38105
    Mol Cell Biol 14:7265-75. 1994
    ....
  66. ncbi request reprint Molecular cloning, expression pattern, and chromosomal localization of human CDKN2D/INK4d, an inhibitor of cyclin D-dependent kinases
    T Okuda
    Department of Pathology, Howard Hughes Medical Institute, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Genomics 29:623-30. 1995
    ....
  67. ncbi request reprint Cloning and characterization of murine p16INK4a and p15INK4b genes
    D E Quelle
    Howard Hughes Medical Institute, Memphis, Tennessee, USA
    Oncogene 11:635-45. 1995
    ..Expression vectors encoding human or mouse p16INK4a caused G1 phase arrest in NIH3T3 fibroblasts, and cyclin D1- and cdk4-dependent pRb kinase activities were inhibited in the p16INK4a-arrested cells...
  68. pmc Induction of ARF tumor suppressor gene expression and cell cycle arrest by transcription factor DMP1
    K Inoue
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Proc Natl Acad Sci U S A 96:3993-8. 1999
    ..Therefore, apart from its recently recognized role in protecting cells from potentially oncogenic signals, ARF can be induced in response to antiproliferative stimuli that do not obligatorily lead to apoptosis...
  69. ncbi request reprint Expression of INK4 inhibitors of cyclin D-dependent kinases during mouse brain development
    F Zindy
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Cell Growth Differ 8:1139-50. 1997
    ..Therefore, p19INK4d may contribute to maintaining the quiescent state, acting as a buffer to prevent reactivation of cyclin D-dependent kinases in terminally differentiated cells...
  70. ncbi request reprint Tumor suppression at the mouse INK4a locus mediated by the alternative reading frame product p19ARF
    T Kamijo
    Howard Hughes Medical Institute, Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Cell 91:649-59. 1997
    ..Therefore, INK4a encodes growth inhibitory proteins that act upstream of the retinoblastoma protein and p53. Mutations and deletions targeting this locus in cancer cells are unlikely to be functionally equivalent...
  71. ncbi request reprint Colony-stimulating factor 1 regulates novel cyclins during the G1 phase of the cell cycle
    H Matsushime
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105
    Cell 65:701-13. 1991
    ..The timing of p36CYL expression, its rapid turnover in the absence of CSF-1, and its phosphorylation and transient binding to a cdc2-related polypeptide suggest that CYL genes may function during S phase commitment...
  72. pmc The p21(Cip1) and p27(Kip1) CDK 'inhibitors' are essential activators of cyclin D-dependent kinases in murine fibroblasts
    M Cheng
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, 332 N Lauderdale, Memphis, TN 38105, USA
    EMBO J 18:1571-83. 1999
    ..In the absence of both CKIs, the severe reduction in cyclin D-dependent kinase activity was well tolerated and had no overt effects on the cell cycle...
  73. ncbi request reprint Autophagy by ARF: a short story
    Charles J Sherr
    Howard Hughes Medical Institute, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Mol Cell 22:436-7. 2006
    ..Could this account for the Mdm2- and p53-independent tumor suppressive effects of ARF?..
  74. pmc Postnatal neuronal proliferation in mice lacking Ink4d and Kip1 inhibitors of cyclin-dependent kinases
    F Zindy
    Department of Tumor Cell Biology, Memphis TN 38105, USA
    Proc Natl Acad Sci U S A 96:13462-7. 1999
    ..Therefore, p19(Ink4d) and p27(Kip1) cooperate to maintain differentiated neurons in a quiescent state that is potentially reversible...
  75. ncbi request reprint The colony-stimulating factor 1 (CSF-1) receptor (c-fms proto-oncogene product) and its ligand
    C W Rettenmier
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105
    J Cell Sci Suppl 9:27-44. 1988
    ..The study of CSF-1 and its receptor should provide information concerning the role of tyrosine kinases in regulating the normal growth and differentiation of haematopoietic cells and in contributing to their malignant transformation...
  76. ncbi request reprint The role of the CSF-1 receptor gene (C-fms) in cell transformation
    C J Sherr
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105
    Leukemia 2:132S-142S. 1988
    ..Thus, constitutive activation of the CSF-1 receptor gene, either by mutation or gene rearrangement, might be expected to contribute to leukemia...
  77. pmc INK4d-deficient mice are fertile despite testicular atrophy
    F Zindy
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Mol Cell Biol 20:372-8. 2000
    ..The absence of tumors in INK4d-deficient animals demonstrates that, unlike INK4a, INK4d is not a tumor suppressor but is instead involved in spermatogenesis...
  78. pmc Colony-stimulating factor 1-mediated regulation of a chimeric c-fms/v-fms receptor containing the v-fms-encoded tyrosine kinase domain
    M F Roussel
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, TN 38101
    Proc Natl Acad Sci U S A 85:5903-7. 1988
    ..The results confirm that C-terminal truncation of the c-fms gene is insufficient to activate its transforming potential and suggest that an additional mutation in its distal extracellular domain is required for oncogenic activation...
  79. ncbi request reprint Mitogenic response to colony-stimulating factor 1
    C J Sherr
    Howard Hughes Medical Institute, Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, TN 38105
    Trends Genet 7:398-402. 1991
    ..Targets of the delayed-early response include novel cyclin genes that may play a role in S phase commitment...
  80. ncbi request reprint A rate limiting function of cdc25A for S phase entry inversely correlates with tyrosine dephosphorylation of Cdk2
    V Sexl
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Oncogene 18:573-82. 1999
    ..At face value, these results are inconsistent with the hypothesis that cdc25A acts directly on cdk2 to activate its S phase promoting function...
  81. ncbi request reprint Genomic organization, chromosomal localization, and independent expression of human cyclin D genes
    T Inaba
    Department of Hematology Oncology, St Jude Children s Research Hospital, Memphis, Tennessee 38105
    Genomics 13:565-74. 1992
    ..The complex patterns of expression of individual cyclin D genes and their evolutionary conservation across species suggest that each family member may play a distinct role in cell cycle progression...
  82. pmc Glycogen synthase kinase-3beta regulates cyclin D1 proteolysis and subcellular localization
    J A Diehl
    Howard Hughes Medical Institute, St Jude Children s Research Hospital, Memphis, Tennessee 38105 USA
    Genes Dev 12:3499-511. 1998
    ..Therefore, phosphorylation and proteolytic turnover of cyclin D1 and its subcellular localization during the cell division cycle are linked through the action of GSK-3beta...
  83. pmc Early pre-B-cell transformation induced by the v-fms oncogene in long-term mouse bone marrow cultures
    G V Borzillo
    Howard Hughes Medical Institute, Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105
    Mol Cell Biol 9:3973-81. 1989
    ..The ability of v-fms to induce transformation of early pre-B cells in vitro underscores the capacity of oncogenic mutants of the colony-stimulating factor-1 receptor to function outside the mononuclear phagocyte lineage...
  84. ncbi request reprint Multilineage hematopoietic disorders induced by transplantation of bone marrow cells expressing the v-fms oncogene
    J M Heard
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38101
    Cell 51:663-73. 1987
    ..Although expression of the c-fms product (CSF-1 receptor) is normally restricted to cells of the mononuclear phagocyte series, the v-fms-coded glycoprotein can contribute to proliferative abnormalities of multiple hematopoietic lineages...
  85. pmc Differential effects of p19(Arf) and p16(Ink4a) loss on senescence of murine bone marrow-derived preB cells and macrophages
    D H Randle
    Department of Tumor Cell Biology and Howard Hughes Medical Institute, St. Jude Children's Research Hospital, Memphis, TN 38105, USA
    Proc Natl Acad Sci U S A 98:9654-9. 2001
    ..Therefore, whereas Arf loss alone appears to be the major determinant of establishment of murine fibroblast and preB cell lines in culture, p16(Ink4a) provides an effective barrier to immortalization of bone marrow-derived macrophages...
  86. ncbi request reprint Cloning and expression of murine interleukin-1 receptor antagonist in macrophages stimulated by colony-stimulating factor 1
    H Matsushime
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, TN 38105
    Blood 78:616-23. 1991
    ....
  87. ncbi request reprint Expression of the p16INK4a tumor suppressor versus other INK4 family members during mouse development and aging
    F Zindy
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Oncogene 15:203-11. 1997
    ..Whereas p18INK4c and p19INK4d may regulate pre- and postnatal development, p16INK4a more likely plays a checkpoint function during cell senescence that underscores its selective role as a tumor suppressor...
  88. pmc Disruption of the ARF transcriptional activator DMP1 facilitates cell immortalization, Ras transformation, and tumorigenesis
    K Inoue
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Genes Dev 14:1797-809. 2000
    ..Together, these data suggest that ARF function is compromised, but not eliminated, in animals lacking functional DMP1...
  89. ncbi request reprint Signal-response coupling mediated by the transduced colony-stimulating factor-1 receptor and its oncogenic fms variants in naive cells
    C J Sherr
    Howard Hughes Medical Institute, Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105
    Ciba Found Symp 148:96-104; discussion 104-9. 1990
    ..Therefore, critical mutations in the c-fms gene or overexpression of CSF-1R in immature myeloid precursors might each contribute to leukaemia...
  90. pmc Dmp1 is haplo-insufficient for tumor suppression and modifies the frequencies of Arf and p53 mutations in Myc-induced lymphomas
    K Inoue
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Genes Dev 15:2934-9. 2001
    ..Although p53 mutations or Arf deletion normally occur in approximately 50% of E(mu)-Myc-induced lymphomas, Dmp1 loss obviates selection for such mutations, indicating that Dmp1 is a potent genetic modifier of the Arf-p53 pathway in vivo...
  91. ncbi request reprint Colony-stimulating factor-1 receptor (c-fms)
    C J Sherr
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38101
    J Cell Biochem 38:179-87. 1988
    ..The genetic alterations in the c-fms gene that unmask its latent transforming potential abrogate its lineage-specific activity and enable v-fms to transform a variety of cells that do not normally express CSF-1 receptors...
  92. pmc Phospholipase C-gamma, a substrate for PDGF receptor kinase, is not phosphorylated on tyrosine during the mitogenic response to CSF-1
    J R Downing
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, TN 38105
    EMBO J 8:3345-50. 1989
    ..Thus, although the PDGF and CSF-1 receptors are structurally related and appear to be derived from a single ancestor gene, only PDGF-induced mitogenesis in fibroblasts correlated with tyrosine phosphorylation of PLC-gamma...
  93. ncbi request reprint Fibroblast and hematopoietic cell transformation by the fms oncogene (CSF-1 receptor)
    C J Sherr
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38101
    J Cell Physiol Suppl . 1987
    ..The ability of v-fms to transform hematopoietic target cells suggests that critical alterations in the c-fms proto-oncogene might similarly contribute to leukemia...
  94. ncbi request reprint A dominant suppressive mutation in a cellular gene restores the nontransformed phenotype to v-fms-transformed mink cells
    J Kato
    Howard Hughes Medical Institute, Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105
    Oncogene 6:687-93. 1991
    ....
  95. pmc Ligand-induced tyrosine kinase activity of the colony-stimulating factor 1 receptor in a murine macrophage cell line
    J R Downing
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105
    Mol Cell Biol 8:1795-9. 1988
    ..By contrast, the mature cell surface glycoprotein encoded by the v-fms oncogene was phosphorylated on tyrosine in the absence of CSF-1, suggesting that it functions as a ligand-independent kinase...
  96. ncbi request reprint Regulation of the CD13/aminopeptidase N gene by DMP1, a transcription factor antagonized by D-type cyclins
    K Inoue
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    J Biol Chem 273:29188-94. 1998
    ..These data indicate that two different Myb family proteins collaborate in regulating APN gene expression and point to a role for DMP1 in normal myeloid cell development...
  97. ncbi request reprint Inhibition of colony-stimulating factor-1 activity by monoclonal antibodies to the human CSF-1 receptor
    C J Sherr
    Howard Hughes Medical Institute, St Jude Children s Research Hospital, Memphis, TN 38105
    Blood 73:1786-93. 1989
    ..These antibodies should prove useful not only for identifying and quantitating CSF-1R on receptor-bearing cells but for abrogating specific receptor signals that govern the proliferation and survival of human mononuclear phagocytes...
  98. ncbi request reprint p53-Dependent and -independent functions of the Arf tumor suppressor
    C J Sherr
    Howard Hughes Medical Institute, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Cold Spring Harb Symp Quant Biol 70:129-37. 2005
    ..We speculate that transcriptional down-regulation in response to Arf-induced sumoylation may account for Arf's p53-independent functions...
  99. ncbi request reprint Tandem linkage of human CSF-1 receptor (c-fms) and PDGF receptor genes
    W M Roberts
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Howard Hughes Medical Institute, Memphis, Tennessee
    Cell 55:655-61. 1988
    ..The as yet unidentified c-fms promoter/enhancer sequences may be confined to the nucleotides separating the two genes or could potentially lie within the PDGF receptor gene itself...
  100. ncbi request reprint Requirements for transformation by the fms oncogene product (CSF-1 receptor)
    C W Rettenmier
    Department of Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105
    Princess Takamatsu Symp 17:211-8. 1986
    ..Thus, complete oncogenic activation of the c-fms gene appears to require two events: one which alters a putative negative regulatory site of tyrosine phosphorylation, and a second which phenocopies a ligand-induced conformational change...
  101. ncbi request reprint Tumor suppression by Ink4a-Arf: progress and puzzles
    Scott W Lowe
    Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA
    Curr Opin Genet Dev 13:77-83. 2003
    ..Recent evidence emerging from mouse tumor models distinguishes the activities of p16(Ink4a) and p19(Arf) in regulating tumor onset and identifies differences in their responsiveness to drugs...