Oncogenes induce senescence with incomplete growth arrest and suppress the DNA damage response in immortalized cells
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M. Stampfer | M. Sherman | V. Gabai | L. Meng | J. Yaglom | Le Meng
[1] M. Jackson,et al. TGF-β signaling engages an ATM-CHK2-p53–independent RAS-induced senescence and prevents malignant transformation in human mammary epithelial cells , 2011, Proceedings of the National Academy of Sciences.
[2] J. Campisi. Cellular senescence: putting the paradoxes in perspective. , 2011, Current opinion in genetics & development.
[3] S. Turner,et al. Jailbreak: oncogene-induced senescence and its evasion. , 2011, Cellular signalling.
[4] M. Sherman,et al. HSP72 depletion suppresses γH2AX activation by genotoxic stresses via p53/p21 signaling , 2010, Oncogene.
[5] L. Donehower,et al. Defining the ATM-mediated barrier to tumorigenesis in somatic mammary cells following ErbB2 activation , 2010, Proceedings of the National Academy of Sciences.
[6] S. Devries,et al. Genetic and Phenotypic Characteristics of Pleomorphic Lobular Carcinoma In Situ of the Breast , 2009, The American journal of surgical pathology.
[7] Heidi S Feiler,et al. Molecular distinctions between stasis and telomere attrition senescence barriers shown by long-term culture of normal human mammary epithelial cells. , 2009, Cancer research.
[8] K. Miyagawa,et al. The ATR-Chk1 pathway plays a role in the generation of centrosome aberrations induced by Rad51C dysfunction , 2009, Nucleic acids research.
[9] C. Bassing,et al. ATR and H2AX Cooperate in Maintaining Genome Stability under Replication Stress* , 2009, Journal of Biological Chemistry.
[10] T. Waldman,et al. Heat Shock Protein Hsp72 Controls Oncogene-Induced Senescence Pathways in Cancer Cells , 2008, Molecular and Cellular Biology.
[11] F. Alt,et al. Complementary functions of ATM and H2AX in development and suppression of genomic instability , 2008, Proceedings of the National Academy of Sciences.
[12] M. Sherman,et al. Triggering senescence programs suppresses Chk1 kinase and sensitizes cells to genotoxic stresses. , 2008, Cancer research.
[13] Atsushi Miyawaki,et al. Visualizing Spatiotemporal Dynamics of Multicellular Cell-Cycle Progression , 2008, Cell.
[14] M. Malumbres,et al. Genetic cooperation between p21Cip1 and INK4 inhibitors in cellular senescence and tumor suppression , 2007, Oncogene.
[15] J. Campisi,et al. Cellular senescence: when bad things happen to good cells , 2007, Nature Reviews Molecular Cell Biology.
[16] Lewis A. Chodosh,et al. Dose-dependent oncogene-induced senescence in vivo and its evasion during mammary tumorigenesis , 2007, Nature Cell Biology.
[17] M. Sherman,et al. High levels of heat shock protein Hsp72 in cancer cells suppress default senescence pathways. , 2007, Cancer research.
[18] P. Yaswen,et al. Oncogene-Induced Senescence Pathways Weave an Intricate Tapestry , 2007, Cell.
[19] Frédérick A. Mallette,et al. The DNA damage signaling pathway is a critical mediator of oncogene-induced senescence. , 2007, Genes & development.
[20] Aaron Bensimon,et al. Oncogene-induced senescence is a DNA damage response triggered by DNA hyper-replication , 2006, Nature.
[21] Dimitris Kletsas,et al. Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints , 2006, Nature.
[22] P. Minoo,et al. Senescence and serration: a new twist to an old tale , 2006, The Journal of pathology.
[23] A. Weeraratna,et al. Interleukin-1 alpha mediates the growth proliferative effects of transforming growth factor-beta in p21 null MCF-10A human mammary epithelial cells , 2006, Oncogene.
[24] M. Barbacid,et al. Tumour biology: Senescence in premalignant tumours , 2005, Nature.
[25] J. Shay,et al. BRAFE600-associated senescence-like cell cycle arrest of human naevi , 2005, Nature.
[26] H. Stein,et al. Oncogene-induced senescence as an initial barrier in lymphoma development , 2005, Nature.
[27] Jason A. Koutcher,et al. Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis , 2005, Nature.
[28] J. Hayes,et al. Chromatin in need of a fix: phosphorylation of H2AX connects chromatin to DNA repair. , 2005, Molecular cell.
[29] T. Ørntoft,et al. DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis , 2005, Nature.
[30] Dimitris Kletsas,et al. Activation of the DNA damage checkpoint and genomic instability in human precancerous lesions , 2005, Nature.
[31] K. Helin,et al. Deregulated E2F Activity Induces Hyperplasia and Senescence-Like Features in the Mouse Pituitary Gland , 2005, Molecular and Cellular Biology.
[32] Jan G Hengstler,et al. Premature senescence is a primary fail-safe mechanism of ERBB2-driven tumorigenesis in breast carcinoma cells. , 2005, Cancer research.
[33] D. Mittelman,et al. DNA end joining becomes less efficient and more error-prone during cellular senescence. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[34] S. Lowe,et al. Executing Cell Senescence , 2004, Cell cycle.
[35] P. Yaswen,et al. Human epithelial cell immortalization as a step in carcinogenesis. , 2003, Cancer letters.
[36] P. Meltzer,et al. High frequency of BRAF mutations in nevi , 2003, Nature Genetics.
[37] Soyoung Lee,et al. A Senescence Program Controlled by p53 and p16INK4a Contributes to the Outcome of Cancer Therapy , 2002, Cell.
[38] P. Yaswen,et al. Raf-1-induced growth arrest in human mammary epithelial cells is p16-independent and is overcome in immortal cells during conversion , 2002, Oncogene.
[39] P. Yaswen,et al. Expression of the telomerase catalytic subunit, hTERT, induces resistance to transforming growth factor β growth inhibition in p16INK4A(−) human mammary epithelial cells , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[40] S. Lowe,et al. Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling. , 1998, Genes & development.
[41] D. Woods,et al. Senescence of human fibroblasts induced by oncogenic Raf. , 1998, Genes & development.
[42] A. Brenner,et al. Increased p16 expression with first senescence arrest in human mammary epithelial cells and extended growth capacity with p16 inactivation , 1998, Oncogene.
[43] C. Harley,et al. Extension of life-span by introduction of telomerase into normal human cells. , 1998, Science.
[44] S. Lowe,et al. Oncogenic ras Provokes Premature Cell Senescence Associated with Accumulation of p53 and p16INK4a , 1997, Cell.
[45] F. Ciardiello,et al. Invasive phenotype of MCF10A cells overexpressing c‐Ha‐ras and c‐erbB‐2 oncogenes , 1995, International journal of cancer.
[46] C. Harley,et al. Telomeres shorten during ageing of human fibroblasts , 1990, Nature.
[47] W Godolphin,et al. Studies of the HER-2/neu proto-oncogene in human breast and ovarian cancer. , 1989, Science.
[48] P. Leder,et al. Single-step induction of mammary adenocarcinoma in transgenic mice bearing the activated c-neu oncogene , 1988, Cell.
[49] M. Stampfer,et al. Induction of transformation and continuous cell lines from normal human mammary epithelial cells after exposure to benzo[a]pyrene. , 1985, Proceedings of the National Academy of Sciences of the United States of America.
[50] L. Hayflick,et al. The serial cultivation of human diploid cell strains. , 1961, Experimental cell research.