Oncogene-induced senescence as an initial barrier in lymphoma development (original) (raw)

• Campisi, J. Cellular senescence as a tumour-suppressor mechanism. Trends Cell Biol. 11, S27–S31 (2001)
  Article CAS Google Scholar
• Schmitt, C. A. Senescence, apoptosis and therapy—cutting the lifelines of cancer. Nature Rev. Cancer 3, 286–295 (2003)
  Article CAS Google Scholar
• Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D. & Lowe, S. W. Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a. Cell 88, 593–602 (1997)
  Article CAS Google Scholar
• Trimarchi, J. M. & Lees, J. A. Sibling rivalry in the E2F family. Nature Rev. Mol. Cell Biol. 3, 11–20 (2002)
  Article CAS Google Scholar
• Narita, M. et al. Rb-mediated heterochromatin formation and silencing of E2F target genes during cellular senescence. Cell 113, 703–716 (2003)
  Article CAS Google Scholar
• Rea, S. et al. Regulation of chromatin structure by site-specific histone H3 methyltransferases. Nature 406, 593–599 (2000)
  Article ADS CAS Google Scholar
• Nielsen, S. J. et al. Rb targets histone H3 methylation and HP1 to promoters. Nature 412, 561–565 (2001)
  Article ADS CAS Google Scholar
• Bannister, A. J. et al. Selective recognition of methylated lysine 9 on histone H3 by the HP1 chromo domain. Nature 410, 120–124 (2001)
  Article ADS CAS Google Scholar
• Lachner, M., O'Carroll, D., Rea, S., Mechtler, K. & Jenuwein, T. Methylation of histone H3 lysine 9 creates a binding site for HP1 proteins. Nature 410, 116–120 (2001)
  Article ADS CAS Google Scholar
• Ait-Si-Ali, S. et al. A Suv39h-dependent mechanism for silencing S-phase genes in differentiating but not in cycling cells. EMBO J. 23, 605–615 (2004)
  Article CAS Google Scholar
• Haupt, Y., Harris, A. W. & Adams, J. M. Retroviral infection accelerates T lymphomagenesis in E mu-N-ras transgenic mice by activating c-myc or N-myc. Oncogene 7, 981–986 (1992)
  CAS PubMed Google Scholar
• Peters, A. H. et al. Loss of the Suv39h histone methyltransferases impairs mammalian heterochromatin and genome stability. Cell 107, 323–337 (2001)
  Article CAS Google Scholar
• Kemp, C. J., Donehower, L. A., Bradley, A. & Balmain, A. Reduction of p53 gene dosage does not increase initiation or promotion but enhances malignant progression of chemically induced skin tumors. Cell 74, 813–822 (1993)
  Article CAS Google Scholar
• Lin, A. W. et al. Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signalling. Genes Dev. 12, 3008–3019 (1998)
  Article CAS Google Scholar
• Lyon, M. F. Gene action in the X-chromosome of the mouse (Mus musculus L.). Nature 190, 372–373 (1961)
  Article ADS CAS Google Scholar
• Ohtani, N. et al. Opposing effects of Ets and Id proteins on p16_INK4a_ expression during cellular senescence. Nature 409, 1067–1070 (2001)
  Article ADS CAS Google Scholar
• Chang, B. D. et al. A senescence-like phenotype distinguishes tumour cells that undergo terminal proliferation arrest after exposure to anticancer agents. Cancer Res. 59, 3761–3767 (1999)
  CAS PubMed Google Scholar
• Schmitt, C. A. et al. A senescence program controlled by p53 and p16INK4a contributes to the outcome of cancer therapy. Cell 109, 335–346 (2002)
  Article CAS Google Scholar
• Dimri, G. P. et al. A biomarker that identifies senescent human cells in culture and in aging skin in vivo. Proc. Natl Acad. Sci. USA 92, 9363–9367 (1995)
  Article ADS CAS Google Scholar
• Nguyen, C. T. et al. Histone H3-lysine 9 methylation is associated with aberrant gene silencing in cancer cells and is rapidly reversed by 5-aza-2′-deoxycytidine. Cancer Res. 62, 6456–6461 (2002)
  CAS Google Scholar
• Fuks, F., Hurd, P. J., Deplus, R. & Kouzarides, T. The DNA methyltransferases associate with HP1 and the SUV39H1 histone methyltransferase. Nucleic Acids Res. 31, 2305–2312 (2003)
  Article CAS Google Scholar
• Leone, G., Voso, M. T., Teofili, L. & Lubbert, M. Inhibitors of DNA methylation in the treatment of hematological malignancies and MDS. Clin. Immunol. 109, 89–102 (2003)
  Article CAS Google Scholar
• Rane, S. G., Cosenza, S. C., Mettus, R. V. & Reddy, E. P. Germ line transmission of the Cdk4(R24C) mutation facilitates tumorigenesis and escape from cellular senescence. Mol. Cell. Biol. 22, 644–656 (2002)
  Article CAS Google Scholar
• Guerra, C. et al. Tumor induction by an endogenous K-ras oncogene is highly dependent on cellular context. Cancer Cell 4, 111–120 (2003)
  Article MathSciNet CAS Google Scholar
• Tuveson, D. A. et al. Endogenous oncogenic K-ras(G12D) stimulates proliferation and widespread neoplastic and developmental defects. Cancer Cell 5, 375–387 (2004)
  Article CAS Google Scholar
• Kim, K. C., Geng, L. & Huang, S. Inactivation of a histone methyltransferase by mutations in human cancers. Cancer Res. 63, 7619–7623 (2003)
  CAS PubMed Google Scholar
• Steele-Perkins, G. et al. Tumor formation and inactivation of RIZ1, an Rb-binding member of a nuclear protein-methyltransferase superfamily. Genes Dev. 15, 2250–2262 (2001)
  Article CAS Google Scholar
• Schmitt, C. A., McCurrach, M. E., de Stanchina, E., Wallace-Brodeur, R. R. & Lowe, S. W. INK4a/ARF mutations accelerate lymphomagenesis and promote chemoresistance by disabling p53. Genes Dev. 13, 2670–2677 (1999)
  Article CAS Google Scholar
• Schmitt, C. A. et al. Dissecting p53 tumour suppressor functions in vivo. Cancer Cell 1, 289–298 (2002)
  Article CAS Google Scholar
• Frank, O. et al. Tumor cells escape suicide gene therapy by genetic and epigenetic instability. Blood 104, 3543–3549 (2004)
  Article CAS Google Scholar
• Hamrouni, A., Aublin, A., Guillaume, P. & Maryanski, J. L. T cell receptor gene rearrangement lineage analysis reveals clues for the origin of highly restricted antigen-specific repertoires. J. Exp. Med. 197, 601–614 (2003)
  Article CAS Google Scholar