Tumor Suppression at the Mouse INK4a Locus Mediated by the Alternative Reading Frame Product p19 ARF

[1]  F. Zindy,et al.  Expression of the p16INK4a tumor suppressor versus other INK4 family members during mouse development and aging , 1997, Oncogene.

[2]  S. Lowe,et al.  Oncogenic ras Provokes Premature Cell Senescence Associated with Accumulation of p53 and p16INK4a , 1997, Cell.

[3]  R. Weinberg.  The Cat and Mouse Games That Genes, Viruses, and Cells Play , 1997, Cell.

[4]  Y. Kubo,et al.  Mutations of the INK4a locus in squamous cell carcinomas of human skin. , 1997, Biochemical and biophysical research communications.

[5]  A. Lloyd,et al.  Cooperating oncogenes converge to regulate cyclin/cdk complexes. , 1997, Genes & development.

[6]  J. Herman,et al.  Frequent aberrant methylation of p16INK4a in primary rat lung tumors , 1997, Molecular and cellular biology.

[7]  M. Imamura,et al.  Multiple types of aberrations in the p16 (INK4a) and the p15(INK4b) genes in 30 esophageal squamous‐cell‐carcinoma cell lines , 1997, International journal of cancer.

[8]  A. Levine.  p53, the Cellular Gatekeeper for Growth and Division , 1997, Cell.

[9]  D. Quelle,et al.  Cancer-associated mutations at the INK4a locus cancel cell cycle arrest by p16INK4a but not by the alternative reading frame protein p19ARF. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[10]  Thierry Soussi,et al.  Database of p53 gene somatic mutations in human tumors and cell lines: updated compilation and future prospects , 1997, Nucleic Acids Res..

[11]  C. Sherr.  Cancer Cell Cycles , 1996, Science.

[12]  G. Hannon,et al.  Involvement of the cyclin-dependent kinase inhibitor p16 (INK4a) in replicative senescence of normal human fibroblasts. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[13]  Marshall W. Anderson,et al.  Homozygous codeletion and differential decreased expression of p15INK4b, p16INK4a-alpha and p16INK4a-beta in mouse lung tumor cells. , 1996, Oncogene.

[14]  R. Reddel,et al.  Association of extended in vitro proliferative potential with loss of p16INK4 expression. , 1996, Oncogene.

[15]  K. Isselbacher,et al.  Prevalence of germ-line mutations in p16, p19ARF, and CDK4 in familial melanoma: analysis of a clinic-based population. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[16]  G. Peters,et al.  Temperature-sensitive mutants of p16CDKN2 associated with familial melanoma , 1996, Molecular and cellular biology.

[17]  C. Reznikoff,et al.  Elevated p16 at senescence and loss of p16 at immortalization in human papillomavirus 16 E6, but not E7, transformed human uroepithelial cells. , 1996, Cancer research.

[18]  M. Oren,et al.  p53 in growth control and neoplasia. , 1996, Biochimica et biophysica acta.

[19]  C. Prives,et al.  p53: puzzle and paradigm. , 1996, Genes & development.

[20]  L. Chin,et al.  Role of the INK4a Locus in Tumor Suppression and Cell Mortality , 1996, Cell.

[21]  G. Woude,et al.  Abnormal Centrosome Amplification in the Absence of p53 , 1996, Science.

[22]  G. Peters,et al.  Regulation of p16CDKN2 expression and its implications for cell immortalization and senescence , 1996, Molecular and cellular biology.

[23]  P. Pollock,et al.  Compilation of somatic mutations of the CDKN2 gene in human cancers: Non‐random distribution of base substitutions , 1996, Genes, chromosomes & cancer.

[24]  G. Peters,et al.  Genetic alterations of cyclins, cyclin-dependent kinases, and Cdk inhibitors in human cancer. , 1996, Advances in cancer research.

[25]  C. D. Edwards,et al.  Multiple mechanisms of p16INK4A inactivation in non-small cell lung cancer cell lines. , 1995, Cancer research.

[26]  F. Zindy,et al.  Alternative reading frames of the INK4a tumor suppressor gene encode two unrelated proteins capable of inducing cell cycle arrest , 1995, Cell.

[27]  B. Peters,et al.  Analysis of the p16 gene, CDKN2, in 17 Australian melanoma kindreds. , 1995, Oncogene.

[28]  S. Wick,et al.  Biochemical and mutagenic analysis of the melanoma tumor suppressor gene product/p16. , 1995, Oncogene.

[29]  N. Hayward,et al.  Mutations of the CDKN2/p16INK4 gene in Australian melanoma kindreds. , 1995, Human molecular genetics.

[30]  A. Reymond,et al.  p16 proteins from melanoma-prone families are deficient in binding to Cdk4. , 1995, Oncogene.

[31]  R. Reddel,et al.  Alterations in p53 and p16INK4 expression and telomere length during spontaneous immortalization of Li-Fraumeni syndrome fibroblasts , 1995, Molecular and cellular biology.

[32]  Stephen J. Elledge,et al.  Mice Lacking p21 CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control , 1995, Cell.

[33]  G. Hannon,et al.  Cloning and characterization of murine p16INK4a and p15INK4b genes. , 1995, Oncogene.

[34]  H. Koeffler,et al.  Role of the cyclin-dependent kinase inhibitors in the development of cancer. , 1995, Blood.

[35]  M. Fornerod,et al.  Cre-mediated site-specific translocation between nonhomologous mouse chromosomes. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[36]  C. D. Edwards,et al.  A novel p16INK4A transcript. , 1995, Cancer research.

[37]  S. Tavtigian,et al.  Complex structure and regulation of the P16 (MTS1) locus. , 1995, Cancer research.

[38]  R. Berger,et al.  A new type of p16INK4/MTS1 gene transcript expressed in B-cell malignancies. , 1995, Oncogene.

[39]  J. Herman,et al.  5′ CpG island methylation is associated with transcriptional silencing of the tumour suppressor p16/CDKN2/MTS1 in human cancers , 1995, Nature Medicine.

[40]  L. Sandkuijl,et al.  Homozygotes for CDKN2 (p16) germline mutation in Dutch familial melanoma kindreds , 1995, Nature Genetics.

[41]  H P Koeffler,et al.  Mutational effects on the p16INK4a tumor suppressor protein. , 1995, Cancer research.

[42]  B. Dynlacht,et al.  Tumour-derived p16 alleles encoding proteins defective in cell-cycle inhibition , 1995, Nature.

[43]  J. Bartek,et al.  Retinoblastoma-protein-dependent cell-cycle inhibition by the tumour suppressor p16 , 1995, Nature.

[44]  R. Weinberg,et al.  The retinoblastoma protein and cell cycle control , 1995, Cell.

[45]  H. Varmus,et al.  Mutations associated with familial melanoma impair p16INK4 function , 1995, Nature Genetics.

[46]  T. Hunter,et al.  Cyclins and cancer II: Cyclin D and CDK inhibitors come of age , 1994, Cell.

[47]  R Montesano,et al.  Database of p53 gene somatic mutations in human tumors and cell lines. , 1994, Nucleic acids research.

[48]  A. Balmain,et al.  p53-deficient mice are extremely susceptible to radiation-induced tumorigenesis , 1994, Nature Genetics.

[49]  D. Carson,et al.  Deletions of the cyclin-dependent kinase-4 inhibitor gene in multiple human cancers , 1994, Nature.

[50]  M. Skolnick,et al.  A cell cycle regulator potentially involved in genesis of many tumor types. , 1994, Science.

[51]  J. R. Smith,et al.  Cloning of senescent cell-derived inhibitors of DNA synthesis using an expression screen. , 1994, Experimental cell research.

[52]  R. Weinberg,et al.  Tumor spectrum analysis in p53-mutant mice , 1994, Current Biology.

[53]  G. Hannon,et al.  A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4 , 1993, Nature.

[54]  J. Trent,et al.  WAF1, a potential mediator of p53 tumor suppression , 1993, Cell.

[55]  L. Donehower,et al.  In vitro growth characteristics of embryo fibroblasts isolated from p53-deficient mice. , 1993, Oncogene.

[56]  M. Kastan,et al.  Wild-type p53 is a cell cycle checkpoint determinant following irradiation. , 1992, Proceedings of the National Academy of Sciences of the United States of America.

[57]  D. Denhardt,et al.  p53 mutations in spontaneously immortalized 3T12 but not 3T3 mouse embryo cells. , 1992, Oncogene.

[58]  L. Donehower,et al.  Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours , 1992, Nature.

[59]  A. Levine,et al.  p53 alteration is a common event in the spontaneous immortalization of primary BALB/c murine embryo fibroblasts. , 1991, Genes & development.

[60]  B. Vogelstein,et al.  Participation of p53 protein in the cellular response to DNA damage. , 1991, Cancer research.

[61]  D. Lane,et al.  Activating mutations in p53 produce a common conformational effect. A monoclonal antibody specific for the mutant form. , 1990, The EMBO journal.

[62]  J. DiGiovanni,et al.  Genetic background and development of skin tumors. , 1989, Carcinogenesis; a comprehensive survey.

[63]  J. Yewdell,et al.  Monoclonal antibody analysis of p53 expression in normal and transformed cells , 1986, Journal of virology.

[64]  S. Nesnow,et al.  Murine susceptibility to two-stage skin carcinogenesis is influenced by the agent used for promotion. , 1984, Carcinogenesis.

[65]  D. Stadler.  Temperature-sensitive mutants , 1981 .

[66]  H. Green,et al.  QUANTITATIVE STUDIES OF THE GROWTH OF MOUSE EMBRYO CELLS IN CULTURE AND THEIR DEVELOPMENT INTO ESTABLISHED LINES , 1963, The Journal of cell biology.