Defects in a cell cycle checkpoint may be responsible for the genomic instability of cancer cells
暂无分享,去创建一个
[1] Y. Nakamura,et al. Allelotype of colorectal carcinomas. , 1989, Science.
[2] L. Hartwell,et al. The RAD9 gene controls the cell cycle response to DNA damage in Saccharomyces cerevisiae. , 1988, Science.
[3] P. Gorman,et al. Distinctive chromosomal structures are formed very early in the amplification of CAD genes in Syrian hamster cells , 1990, Cell.
[4] A. Fornace,et al. Induction by ionizing radiation of the gadd45 gene in cultured human cells: lack of mediation by protein kinase C. , 1991, Molecular and cellular biology.
[5] G Buttin,et al. Co‐amplified markers alternate in megabase long chromosomal inverted repeats and cluster independently in interphase nuclei at early steps of mammalian gene amplification. , 1992, The EMBO journal.
[6] B. Vogelstein,et al. Participation of p53 protein in the cellular response to DNA damage. , 1991, Cancer research.
[7] R. W. Jones,et al. The action of caffeine on X-irradiated HeLa cells. III. Enhancement of X-ray-induced killing during G2 arrest. , 1978, Radiation research.
[8] B. Mcclintock,et al. The significance of responses of the genome to challenge. , 1984, Science.
[9] B. Trask,et al. Early dihydrofolate reductase gene amplification events in CHO cells usually occur on the same chromosome arm as the original locus. , 1989, Genes & development.
[10] W. Bigbee,et al. Evidence for an elevated frequency of in vivo somatic cell mutations in ataxia telangiectasia. , 1989, American journal of human genetics.
[11] F. Toledo,et al. The evolution of the amplified adenylate deaminase 2 domains in Chinese hamster cells suggests the sequential operation of different mechanisms of DNA amplification. , 1992, Mutation research.
[12] T. Tlsty,et al. Suppression of gene amplification in human cell hybrids. , 1992, Science.
[13] T. Pandita,et al. Initial chromosome damage but not DNA damage is greater in ataxia telangiectasia cells. , 1992, Radiation research.
[14] Bert Vogelstein,et al. p53 function and dysfunction , 1992, Cell.
[15] Thea D. Tlsty,et al. Altered cell cycle arrest and gene amplification potential accompany loss of wild-type p53 , 1992, Cell.
[16] G. Wahl,et al. Wild-type p53 restores cell cycle control and inhibits gene amplification in cells with mutant p53 alleles , 1992, Cell.
[17] B. Vogelstein,et al. A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia , 1992, Cell.
[18] R T Schimke,et al. Gene amplification in cultured cells. , 1988, The Journal of biological chemistry.
[19] R. Rowley,et al. Checkpoint controls in Schizosaccharomyces pombe: rad1. , 1992, The EMBO journal.
[20] L. Donehower,et al. Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours , 1992, Nature.
[21] P. Nowell. The clonal evolution of tumor cell populations. , 1976, Science.
[22] J. D. Funkhouser,et al. Cancer susceptibility in ataxia-telangiectasia. , 1992, Leukemia.
[23] Brian J. Reid,et al. Flow-cytometric and histological progression to malignancy in Barrett's esophagus: Prospective endoscopic surveillance of a cohort , 1992 .
[24] G. Wahl,et al. A central role for chromosome breakage in gene amplification, deletion formation, and amplicon integration. , 1991, Genes & development.
[25] L. Hartwell,et al. Checkpoints: controls that ensure the order of cell cycle events. , 1989, Science.
[26] J. Bedford,et al. On the nature of a defect in cells from individuals with ataxia-telangiectasia. , 1985, Science.