Dorothy C Bennett

Summary

Affiliation: St George's Hospital Medical School
Country: UK

Publications

  1. ncbi request reprint Molecular regulation of melanocyte senescence
    Dorothy C Bennett
    Department of Anatomy and Developmental Biology, St George s Hospital Medical School, London, UK
    Pigment Cell Res 15:242-50. 2002
  2. pmc Agouti protein, mahogunin, and attractin in pheomelanogenesis and melanoblast-like alteration of melanocytes: a cAMP-independent pathway
    Tokimasa Hida
    Division of Basic Medical Sciences, St George s, University of London, Cranmer Terrace, London, UK
    Pigment Cell Melanoma Res 22:623-34. 2009
  3. ncbi request reprint p16/cyclin-dependent kinase inhibitor 2A deficiency in human melanocyte senescence, apoptosis, and immortalization: possible implications for melanoma progression
    Elena V Sviderskaya
    Department of Basic Medical Sciences, St George s Hospital Medical School, London, UK
    J Natl Cancer Inst 95:723-32. 2003
  4. pmc Senescence evasion in melanoma progression: uncoupling of DNA-damage signaling from p53 activation and p21 expression
    Alastair D Mackenzie Ross
    Biomedical Sciences Research Centre Box J2A, St George s, University of London, Cranmer Terrace, London, SW17 0RE, UK
    Pigment Cell Melanoma Res 26:226-35. 2013
  5. pmc Functional neurons and melanocytes induced from immortal lines of postnatal neural crest-like stem cells
    Elena V Sviderskaya
    Centre for Molecular and Metabolic Signalling, Division of Basic Medical Sciences, St George s, University of London, London, UK
    FASEB J 23:3179-92. 2009
  6. ncbi request reprint Human melanocyte senescence and melanoma susceptibility genes
    Dorothy C Bennett
    Department of Basic Medical Sciences, St George s Hospital Medical School, London SW17 0RE, UK
    Oncogene 22:3063-9. 2003
  7. doi request reprint How to make a melanoma: what do we know of the primary clonal events?
    Dorothy C Bennett
    Division of Basic Medical Sciences, St George s, University of London, London, UK
    Pigment Cell Melanoma Res 21:27-38. 2008
  8. ncbi request reprint p16(Ink4a) in melanocyte senescence and differentiation
    Elena 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
  9. ncbi request reprint The color loci of mice--a genetic century
    Dorothy C Bennett
    Department of Basic Medical Sciences, St George s Hospital Medical School, London, UK
    Pigment Cell Res 16:333-44. 2003
  10. doi request reprint Receptor tyrosine kinases and their activation in melanoma
    David J Easty
    Department of Oncology, St James s Hospital, Dublin, Ireland Division of Biomedical Sciences, St George s, University of London, London, UK
    Pigment Cell Melanoma Res 24:446-61. 2011

Collaborators

Detail Information

Publications36

  1. ncbi request reprint Molecular regulation of melanocyte senescence
    Dorothy C Bennett
    Department of Anatomy and Developmental Biology, St George s Hospital Medical School, London, UK
    Pigment Cell Res 15:242-50. 2002
    ..These findings are discussed in relation to the role of cell senescence in the development and molecular genetics of melanoma and its precursor lesions...
  2. pmc Agouti protein, mahogunin, and attractin in pheomelanogenesis and melanoblast-like alteration of melanocytes: a cAMP-independent pathway
    Tokimasa Hida
    Division of Basic Medical Sciences, St George s, University of London, Cranmer Terrace, London, UK
    Pigment Cell Melanoma Res 22:623-34. 2009
    ..Thus, ASIP-MC1R signaling includes a cAMP-independent pathway through attractin and mahogunin, while the known cAMP-dependent component requires neither attractin nor mahogunin...
  3. ncbi request reprint p16/cyclin-dependent kinase inhibitor 2A deficiency in human melanocyte senescence, apoptosis, and immortalization: possible implications for melanoma progression
    Elena V Sviderskaya
    Department of Basic Medical Sciences, St George s Hospital Medical School, London, UK
    J Natl Cancer Inst 95:723-32. 2003
    ..To investigate the role of p16 in melanocytes, we assessed aspects of growth, apoptosis, and immortalization in melanocytes cultured from two melanoma patients, both of whom had two inactive p16 alleles but functional ARF...
  4. pmc Senescence evasion in melanoma progression: uncoupling of DNA-damage signaling from p53 activation and p21 expression
    Alastair D Mackenzie Ross
    Biomedical Sciences Research Centre Box J2A, St George s, University of London, Cranmer Terrace, London, SW17 0RE, UK
    Pigment Cell Melanoma Res 26:226-35. 2013
    ..Two separate defects in p53 signaling appeared common: in nevi, lack of p53 phosphorylation by activated CHEK2, and in melanomas, defective p21 upregulation by p53 even when phosphorylated...
  5. pmc Functional neurons and melanocytes induced from immortal lines of postnatal neural crest-like stem cells
    Elena V Sviderskaya
    Centre for Molecular and Metabolic Signalling, Division of Basic Medical Sciences, St George s, University of London, London, UK
    FASEB J 23:3179-92. 2009
    ....
  6. ncbi request reprint Human melanocyte senescence and melanoma susceptibility genes
    Dorothy C Bennett
    Department of Basic Medical Sciences, St George s Hospital Medical School, London SW17 0RE, UK
    Oncogene 22:3063-9. 2003
    ..A speculative model is proposed, relating current concepts of early melanoma progression to the processes of cellular senescence and immortalization. This includes the suggestion that moles or nevi are senescent clones of melanocytes...
  7. doi request reprint How to make a melanoma: what do we know of the primary clonal events?
    Dorothy C Bennett
    Division of Basic Medical Sciences, St George s, University of London, London, UK
    Pigment Cell Melanoma Res 21:27-38. 2008
    ..The data support a model in which genesis of melanoma requires changes that (1) initiate clonal expansion, (2) overcome cell senescence, and (3) reduce apoptosis...
  8. ncbi request reprint p16(Ink4a) in melanocyte senescence and differentiation
    Elena 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
    ..Because senescence is believed to be an anticancer mechanism, we investigated the role of Ink4a-Arf and its individual components in melanocyte senescence...
  9. ncbi request reprint The color loci of mice--a genetic century
    Dorothy C Bennett
    Department of Basic Medical Sciences, St George s Hospital Medical School, London, UK
    Pigment Cell Res 16:333-44. 2003
    ..The mutant mice also provide valuable models for the study of human disease...
  10. doi request reprint Receptor tyrosine kinases and their activation in melanoma
    David J Easty
    Department of Oncology, St James s Hospital, Dublin, Ireland Division of Biomedical Sciences, St George s, University of London, London, UK
    Pigment Cell Melanoma Res 24:446-61. 2011
    ..Kinases are considered druggable targets, so characterization of global RTK activity in melanoma should assist the rational development of tyrosine kinase inhibitors for clinical use...
  11. doi request reprint Ultraviolet wavebands and melanoma initiation
    Dorothy C Bennett
    Division of Basic Medical Sciences, St George s, University of London, London, UK
    Pigment Cell Melanoma Res 21:520-4. 2008
    ..There is no experimental basis for a claim that UVA is safe, and recreational exposure to this known mutagen should be discouraged...
  12. doi request reprint Isolation and culture of melanoma and naevus cells and cell lines
    Julia K Soo
    Division of Basic Medical Sciences, Molecular and Metabolic Signalling Centre, St George s, University of London, London, UK
    Methods Mol Biol 731:141-50. 2011
    ..The conditions involve the use of growth-inactivated keratinocytes initially, and a combination of mitogens similar to those routinely used for normal human melanocytes: stem cell factor, endothelin 1, TPA, and cholera toxin...
  13. pmc BLOC-1 is required for cargo-specific sorting from vacuolar early endosomes toward lysosome-related organelles
    Subba Rao Gangi Setty
    Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
    Mol Biol Cell 18:768-80. 2007
    ....
  14. pmc Slc7a11 gene controls production of pheomelanin pigment and proliferation of cultured cells
    Sreenivasulu Chintala
    Department of Molecular and Cellular Biology, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA
    Proc Natl Acad Sci U S A 102:10964-9. 2005
    ..Thus, we have found that the Slc7a11 gene controls the production of pheomelanin pigment directly. Cells from sut mice provide a model for oxidative stress-related diseases and their therapies...
  15. 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...
  16. ncbi request reprint UV-induced expression of key component of the tanning process, the POMC and MC1R genes, is dependent on the p-38-activated upstream stimulating factor-1 (USF-1)
    Sébastien Corre
    CNRS UMR 6061 Laboratoire de Génétique et Développement, Faculte de Medecine, Universite de Rennes 1, 2 Avenue du Pr Leon Bernard, 35043 Rennes, France
    J Biol Chem 279:51226-33. 2004
    ..The results define USF-1 as a critical UV-responsive activator of genes implicated in protection from solar radiation...
  17. ncbi request reprint Reduced pigmentation (rp), a mouse model of Hermansky-Pudlak syndrome, encodes a novel component of the BLOC-1 complex
    Babette Gwynn
    The Jackson Laboratory, 600 Main St, Bar Harbor, ME 04609, USA
    Blood 104:3181-9. 2004
    ..Defects in all the 5 known components of BLOC-1, including RP, cause severe HPS in mice, suggesting that the subunits are nonredundant and that BLOC-1 plays a key role in organelle biogenesis...
  18. doi request reprint Comment on "Absence of senescence-associated beta-galactosidase activity in human melanocytic nevi in vivo"
    Vanessa C Gray-Schopfer
    J Invest Dermatol 128:1581; author reply 1583-4. 2008
  19. pmc A genomewide screen for generalized vitiligo: confirmation of AIS1 on chromosome 1p31 and evidence for additional susceptibility loci
    Pamela R Fain
    Human Medical Genetics Program and Department of Medicine, University of Colorado Health Sciences Center, Denver, CO 80262, USA
    Am J Hum Genet 72:1560-4. 2003
    ..An additional seven signals, on chromosomes 1, 7, 8, 11, 19, and 22, met genomewide criteria for "suggestive linkage," and will thus be of particular importance for follow-up studies...
  20. pmc Cell-specific ATP7A transport sustains copper-dependent tyrosinase activity in melanosomes
    Subba Rao Gangi Setty
    Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    Nature 454:1142-6. 2008
    ....
  21. pmc The ocular albinism type 1 protein, an intracellular G protein-coupled receptor, regulates melanosome transport in pigment cells
    Ilaria Palmisano
    San Raffaele Scientific Institute, DIBIT, Milan, Italy
    Hum Mol Genet 17:3487-501. 2008
    ....
  22. pmc Novel vitiligo susceptibility loci on chromosomes 7 (AIS2) and 8 (AIS3), confirmation of SLEV1 on chromosome 17, and their roles in an autoimmune diathesis
    Richard A Spritz
    Am J Hum Genet 74:188-91. 2004
  23. ncbi request reprint Regulation of breast cancer cell chemotaxis by the phosphoinositide 3-kinase p110delta
    Carol Sawyer
    Cell Signalling Group, The Ludwig Institute for Cancer Research, University College and Royal Free Medical School Branch, London, W1W 7BS
    Cancer Res 63:1667-75. 2003
    ..The potential clinical implications of p110delta expression in non-WBC-derived tumors are discussed...
  24. ncbi request reprint Mapping of an autoimmunity susceptibility locus (AIS1) to chromosome 1p31.3-p32.2
    Asem Alkhateeb
    Human Medical Genetics Program, Department of Medicine, University of Colorado Health Sciences Center, 4200 East Ninth Ave, B161, Denver, CO 80262, USA
    Hum Mol Genet 11:661-7. 2002
    ....
  25. ncbi request reprint PTPN22 is genetically associated with risk of generalized vitiligo, but CTLA4 is not
    Greggory S Laberge
    Human Medical Genetics Program, University of Colorado Denver, Anschutz Medical Campus, Aurora, Colorado 80045, USA
    J Invest Dermatol 128:1757-62. 2008
    ..These results implicate PTPN22 in mediating susceptibility to generalized vitiligo and associated autoimmune diseases, but do not support a role for CTLA4...
  26. ncbi request reprint Vitiligo-associated multiple autoimmune disease is not associated with genetic variation in AIRE
    Ying Jin
    Pigment Cell Res 20:402-4. 2007
  27. ncbi request reprint Human melanoblasts in culture: expression of BRN2 and synergistic regulation by fibroblast growth factor-2, stem cell factor, and endothelin-3
    Anthony L Cook
    The Institute for Molecular Bioscience, Center for Functional and Applied Genomics, The University of Queensland, Brisbane, Australia
    J Invest Dermatol 121:1150-9. 2003
    ..These finding implicate BRN2 as an early marker of melanoblasts that may contribute to the hierarchy of melanocytic gene control...
  28. ncbi request reprint FAPalpha, a surface peptidase expressed during wound healing, is a tumor suppressor
    Teresa Ramirez-Montagut
    Swim Across America Laboratory, Memorial Sloan Kettering Cancer Center and Weill Graduate School of Medical Sciences of Cornell University, 1275 York Avenue, New York, NY 10021, USA
    Oncogene 23:5435-46. 2004
    ..These results show that expression of FAP is a tumor suppressor that abrogates tumorigenicity through regulation of cell growth and survival...
  29. ncbi request reprint Early disease onset and increased risk of other autoimmune diseases in familial generalized vitiligo
    Greggory Laberge
    Human Medical Genetics Program, University of Colorado Health Sciences Center, Denver, CO, USA
    Pigment Cell Res 18:300-5. 2005
    ..These findings have important implications for autoimmune disease surveillance in families in which multiple members are affected with vitiligo...
  30. pmc Functions of adaptor protein (AP)-3 and AP-1 in tyrosinase sorting from endosomes to melanosomes
    Alexander C Theos
    Cambridge Institute for Medical Research, University of Cambridge, Wellcome Trust, Cambridge CB2 2XY, United Kingdom
    Mol Biol Cell 16:5356-72. 2005
    ....
  31. ncbi request reprint EMX homeobox genes regulate microphthalmia and alter melanocyte biology
    Walter Bordogna
    Wolfson Institute for Biomedical Research, London WC1E 6BT, UK
    Exp Cell Res 311:27-38. 2005
    ....
  32. ncbi request reprint Epidemiology of vitiligo and associated autoimmune diseases in Caucasian probands and their families
    Asem Alkhateeb
    Human Medical Genetics Program, University of Colorado Health Sciences Center, Denver, CO, USA
    Pigment Cell Res 16:208-14. 2003
    ..These results suggest that genomic analysis of families with generalized vitiligo and this specific constellation of associated autoimmune disorders will be important to identify the mechanisms of genetic susceptibility to autoimmunity...
  33. pmc Dual loss of ER export and endocytic signals with altered melanosome morphology in the silver mutation of Pmel17
    Alexander C Theos
    Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
    Mol Biol Cell 17:3598-612. 2006
    ..These data reveal a dual sorting defect in a natural mutant of Pmel17 and support a requirement of endocytic trafficking in Pmel17 fibril formation...
  34. pmc Rab38 and Rab32 control post-Golgi trafficking of melanogenic enzymes
    Christina Wasmeier
    Molecular and Cellular Medicine, Division of Biomedical Sciences, Imperial College London, London SW7 2AZ, England, UK
    J Cell Biol 175:271-81. 2006
    ..This work identifies a key role for the Rab38/Rab32 subfamily of Rab proteins in the biogenesis of melanosomes and potentially other lysosome-related organelles...
  35. ncbi request reprint NALP1 in vitiligo-associated multiple autoimmune disease
    Ying Jin
    Human Medical Genetics Program, University of Colorado at Denver and Health Sciences Center, Aurora, CO 80045, USA
    N Engl J Med 356:1216-25. 2007
    ..The group includes various combinations of generalized vitiligo, autoimmune thyroid disease, latent autoimmune diabetes in adults, rheumatoid arthritis, psoriasis, pernicious anemia, systemic lupus erythematosus, and Addison's disease...
  36. ncbi request reprint HLA class II haplotype DRB1*04-DQB1*0301 contributes to risk of familial generalized vitiligo and early disease onset
    Pamela R Fain
    Human Medical Genetics Program, University of Colorado at Denver and Health Sciences Center, Aurora, USA
    Pigment Cell Res 19:51-7. 2006
    ..Overall, our results indicate that specific MHC-linked genetic variation contributes to risk of familial vitiligo, although HLA does not completely explain familial clustering of vitiligo-associated autoimmune/autoinflammatory diseases...