Genetic instability and darwinian selection in tumours.

[1]  Frank McCormick,et al.  Signalling networks that cause cancer. , 1999, Trends in cell biology.

[2]  P. Duesberg,et al.  How aneuploidy affects metabolic control and causes cancer. , 1999, The Biochemical journal.

[3]  S. Tavaré,et al.  Colorectal adenoma and cancer divergence. Evidence of multilineage progression. , 1999, The American journal of pathology.

[4]  D. Felsher,et al.  Transient excess of MYC activity can elicit genomic instability and tumorigenesis. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[5]  R. Lenski,et al.  Diminishing returns from mutation supply rate in asexual populations. , 1999, Science.

[6]  K. Kinzler,et al.  Genetic instabilities in human cancers , 1998, Nature.

[7]  K. Kinzler,et al.  Requirement for p53 and p21 to sustain G2 arrest after DNA damage. , 1998, Science.

[8]  P. Duesberg,et al.  Genetic instability of cancer cells is proportional to their degree of aneuploidy. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[9]  A. Jackson,et al.  The mutation rate and cancer. , 1998, Genetics.

[10]  Bert Vogelstein,et al.  Mutations of mitotic checkpoint genes in human cancers , 1998, Nature.

[11]  Bert Vogelstein,et al.  Mutational Analysis of the APC/β-Catenin/Tcf Pathway in Colorectal Cancer , 1998 .

[12]  F. Taddei,et al.  Role of mutator alleles in adaptive evolution , 1997, Nature.

[13]  R. Lenski,et al.  Evolution of high mutation rates in experimental populations of E. coli , 1997, Nature.

[14]  K. Kinzler,et al.  Genetic instability in colorectal cancers , 1997, Nature.

[15]  Hans Clevers,et al.  Activation of β-Catenin-Tcf Signaling in Colon Cancer by Mutations in β-Catenin or APC , 1997, Science.

[16]  J. Miller,et al.  Proliferation of mutators in A cell population , 1997, Journal of bacteriology.

[17]  K. Kinzler,et al.  Lessons from Hereditary Colorectal Cancer , 1996, Cell.

[18]  N. Ellis,et al.  Molecular genetics of Bloom's syndrome. , 1996, Human molecular genetics.

[19]  K. Kinzler,et al.  APC mutations in colorectal tumors with mismatch repair deficiency. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[20]  B. Vogelstein,et al.  Increased mutation rate at the hprt locus accompanies microsatellite instability in colon cancer. , 1995, Oncogene.

[21]  K. Kinzler,et al.  Inactivation of both APC alleles in human and mouse tumors. , 1994, Cancer research.

[22]  Sajeev P. Cherian,et al.  Human chromosome 3 corrects mismatch repair deficiency and microsatellite instability and reduces N-methyl-N'-nitro-N-nitrosoguanidine tolerance in colon tumor cells with homozygous hMLH1 mutation. , 1994, Cancer research.

[23]  M. Meuth,et al.  Mutator phenotypes in human colorectal carcinoma cell lines. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[24]  A. Giaccia,et al.  The human Ha-ras oncogene induces genomic instability in murine fibroblasts within one cell cycle. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[25]  Bert Vogelstein,et al.  Hypermutability and mismatch repair deficiency in RER+ tumor cells , 1993, Cell.

[26]  M. Lynch,et al.  The mutational meltdown in asexual populations. , 1993, The Journal of heredity.

[27]  Darryl Shibata,et al.  Ubiquitous somatic mutations in simple repeated sequences reveal a new mechanism for colonic carcinogenesis , 1993, Nature.

[28]  K. Kinzler,et al.  Clues to the pathogenesis of familial colorectal cancer. , 1993, Science.

[29]  S N Thibodeau,et al.  Microsatellite instability in cancer of the proximal colon. , 1993, Science.

[30]  S. Shirasawa,et al.  Altered growth of human colon cancer cell lines disrupted at activated Ki-ras. , 1993, Science.

[31]  Leland Hartwell,et al.  Defects in a cell cycle checkpoint may be responsible for the genomic instability of cancer cells , 1992, Cell.

[32]  Thea D. Tlsty,et al.  Altered cell cycle arrest and gene amplification potential accompany loss of wild-type p53 , 1992, Cell.

[33]  Y. Nakamura,et al.  Inactivation of both APC alleles in an early stage of colon adenomas in a patient with familial adenomatous polyposis (FAP). , 1992, Human molecular genetics.

[34]  K. Kinzler,et al.  Progression of colorectal cancer is associated with multiple tumor suppressor gene defects but inhibition of tumorigenicity is accomplished by correction of any single defect via chromosome transfer , 1992, Molecular and cellular biology.

[35]  B. Roberts,et al.  S. cerevisiae genes required for cell cycle arrest in response to loss of microtubule function , 1991, Cell.

[36]  Andrew W. Murray,et al.  Feedback control of mitosis in budding yeast , 1991, Cell.

[37]  K. Kinzler,et al.  Mutations of chromosome 5q21 genes in FAP and colorectal cancer patients. , 1991, Science.

[38]  L. Loeb,et al.  Mutator phenotype may be required for multistage carcinogenesis. , 1991, Cancer research.

[39]  B. Vogelstein,et al.  Suppression of human colorectal carcinoma cell growth by wild-type p53. , 1990, Science.

[40]  P. Nowell.  The clonal evolution of tumor cell populations. , 1976, Science.

[41]  L. Loeb,et al.  Errors in DNA replication as a basis of malignant changes. , 1974, Cancer research.

[42]  John Calvin Reed.  Mechanisms of apoptosis avoidance in cancer. , 1999, Current opinion in oncology.

[43]  A. de la Chapelle,et al.  Mutations predisposing to hereditary nonpolyposis colorectal cancer. , 1997, Advances in cancer research.

[44]  J. Miller.  The relevance of bacterial mutators to understanding human cancer. , 1996, Cancer surveys.

[45]  Theodor Boveri.  Zur Frage der Entstehung maligner Tumoren , 1914 .