A continuum model for tumour suppression (original) (raw)

• Nowell, P. C. & Hungerford, D. A. Chromosome studies on normal and leukemic human leukocytes. J. Natl Cancer Inst. 25, 85–109 (1960)
  CAS PubMed Google Scholar
• Rowley, J. D. A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining. Nature 243, 290–293 (1973)
  Article ADS CAS PubMed Google Scholar
• Rowley, J. D., Golomb, H. M. & Dougherty, C. 15/17 translocation, a consistent chromosomal change in acute promyelocytic leukaemia. Lancet 309, 549–550 (1977)
  Article Google Scholar
• Heisterkamp, N. et al. Localization of the c-abl oncogene adjacent to a translocation break point in chronic myelocytic leukaemia. Nature 306, 239–242 (1983)
  Article ADS CAS PubMed Google Scholar
• Pandolfi, P. P. et al. Structure and origin of the acute promyelocytic leukemia myl/RAR alpha cDNA and characterization of its retinoid-binding and transactivation properties. Oncogene 6, 1285–1292 (1991)
  CAS PubMed Google Scholar
• Stehelin, D., Varmus, H. E., Bishop, J. M. & Vogt, P. K. DNA related to the transforming gene(s) of avian sarcoma viruses is present in normal avian DNA. Nature 260, 170–173 (1976)
  Article ADS CAS PubMed Google Scholar
• Oppermann, H., Levinson, A. D., Varmus, H. E., Levintow, L. & Bishop, J. M. Uninfected vertebrate cells contain a protein that is closely related to the product of the avian sarcoma virus transforming gene (src). Proc. Natl Acad. Sci. USA 76, 1804–1808 (1979)
  Article ADS CAS PubMed PubMed Central Google Scholar
• Harris, H. The analysis of malignancy by cell fusion: the position in 1988. Cancer Res. 48, 3302–3306 (1988)
  CAS PubMed Google Scholar
• Knudson, A. G., Jr Mutation and cancer: statistical study of retinoblastoma. Proc. Natl Acad. Sci. USA 68, 820–823 (1971)The original statistical analysis of hereditary retinoblastoma that led to the two-hit hypothesis.
  Article ADS PubMed PubMed Central Google Scholar
• Lee, W. H. et al. Human retinoblastoma susceptibility gene: cloning, identification, and sequence. Science 235, 1394–1399 (1987)
  Article ADS CAS PubMed Google Scholar
• Fung, Y. K. et al. Structural evidence for the authenticity of the human retinoblastoma gene. Science 236, 1657–1661 (1987)
  Article ADS CAS PubMed Google Scholar
• Friend, S. H. et al. A human DNA segment with properties of the gene that predisposes to retinoblastoma and osteosarcoma. Nature 323, 643–646 (1986)Building on several years of work by many laboratories to localize the gene responsible for hereditary retinoblastoma, this study is the first to identify and clone the responsible gene, RB1 , and to show that it is altered in retinoblastoma tumours.
  Article ADS CAS PubMed Google Scholar
• Sparkes, R. S. et al. Gene for hereditary retinoblastoma assigned to human chromosome 13 by linkage to esterase D. Science 219, 971–973 (1983)
  Article ADS CAS PubMed Google Scholar
• Benedict, W. F. et al. Patient with 13 chromosome deletion: evidence that the retinoblastoma gene is a recessive cancer gene. Science 219, 973–975 (1983)
  Article ADS CAS PubMed Google Scholar
• Dryja, T. P. et al. Homozygosity of chromosome 13 in retinoblastoma. N. Engl. J. Med. 310, 550–553 (1984)
  Article CAS PubMed Google Scholar
• Cavenee, W. K. et al. Genetic origin of mutations predisposing to retinoblastoma. Science 228, 501–503 (1985)
  Article ADS CAS PubMed Google Scholar
• Cavenee, W. K. et al. Expression of recessive alleles by chromosomal mechanisms in retinoblastoma. Nature 305, 779–784 (1983)
  Article ADS CAS PubMed Google Scholar
• Baker, S. J. et al. Chromosome 17 deletions and p53 gene mutations in colorectal carcinomas. Science 244, 217–221 (1989)
  Article ADS CAS PubMed Google Scholar
• Levy, D. B. et al. Inactivation of both APC alleles in human and mouse tumors. Cancer Res. 54, 5953–5958 (1994)
  CAS PubMed Google Scholar
• Smith, S. A., Easton, D. F., Evans, D. G. & Ponder, B. A. Allele losses in the region 17q12–21 in familial breast and ovarian cancer involve the wild-type chromosome. Nature Genet. 2, 128–131 (1992)
  Article CAS PubMed Google Scholar
• Gudmundsson, J. et al. Different tumor types from BRCA2 carriers show wild-type chromosome deletions on 13q12–q13. Cancer Res. 55, 4830–4832 (1995)
  CAS PubMed Google Scholar
• Volinia, S. et al. Genome wide identification of recessive cancer genes by combinatorial mutation analysis. PLoS ONE 3, e3380 (2008)
  Article ADS PubMed PubMed Central Google Scholar
• Bignell, G. R. et al. Signatures of mutation and selection in the cancer genome. Nature 463, 893–898 (2010)
  Article ADS CAS PubMed PubMed Central Google Scholar
• Vogelstein, B. & Kinzler, K. W. Cancer genes and the pathways they control. Nature Med. 10, 789–799 (2004)
  Article CAS PubMed Google Scholar
• Vogelstein, B. & Kinzler, K. W. The multistep nature of cancer. Trends Genet. 9, 138–141 (1993)
  Article CAS PubMed Google Scholar
• Hagstrom, S. A. & Dryja, T. P. Mitotic recombination map of 13cen-13q14 derived from an investigation of loss of heterozygosity in retinoblastomas. Proc. Natl Acad. Sci. USA 96, 2952–2957 (1999)
  Article ADS CAS PubMed PubMed Central Google Scholar
• Fisher, E. & Scambler, P. Human haploinsufficiency – one for sorrow, two for joy. Nature Genet. 7, 5–7 (1994)
  Article CAS PubMed Google Scholar
• Croce, C. M. Oncogenes and cancer. N. Engl. J. Med. 358, 502–511 (2008)
  Article CAS PubMed Google Scholar
• Venkatachalam, S. et al. Retention of wild-type p53 in tumors from p53 heterozygous mice: reduction of p53 dosage can promote cancer formation. EMBO J. 17, 4657–4667 (1998)
  Article CAS PubMed PubMed Central Google Scholar
• Varley, J. M., Evans, D. G. & Birch, J. M. Li-Fraumeni syndrome – a molecular and clinical review. Br. J. Cancer 76, 1–14 (1997)
  Article CAS PubMed PubMed Central Google Scholar
• Clarke, A. R. et al. Thymocyte apoptosis induced by p53-dependent and independent pathways. Nature 362, 849–852 (1993)
  Article ADS CAS PubMed Google Scholar
• Lynch, C. J. & Milner, J. Loss of one p53 allele results in four-fold reduction of p53 mRNA and protein: a basis for p53 haplo-insufficiency. Oncogene 25, 3463–3470 (2006)
  Article CAS PubMed Google Scholar
• Bellacosa, A. et al. Altered gene expression in morphologically normal epithelial cells from heterozygous carriers of BRCA1 or BRCA2 mutations. Cancer Prev. Res. 3, 48–61 (2010)
  Article CAS Google Scholar
• Burga, L. N. et al. Altered proliferation and differentiation properties of primary mammary epithelial cells from BRCA1 mutation carriers. Cancer Res. 69, 1273–1278 (2009)
  Article CAS PubMed PubMed Central Google Scholar
• Proia, T. A. et al. Genetic predisposition directs breast cancer phenotype by dictating progenitor cell fate. Cell Stem Cell 8, 149–163 (2011)
  Article CAS PubMed PubMed Central Google Scholar
• Mullighan, C. G. et al. Genome-wide analysis of genetic alterations in acute lymphoblastic leukaemia. Nature 446, 758–764 (2007)
  Article ADS CAS PubMed Google Scholar
• Sancho, R. et al. F-box and WD repeat domain-containing 7 regulates intestinal cell lineage commitment and is a haploinsufficient tumor suppressor. Gastroenterology 139, 929–941 (2010)
  Article CAS PubMed Google Scholar
• Chen, Z. et al. Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis. Nature 436, 725–730 (2005)This paper defined the paradigm of obligate haploinsufficiency of the PTEN gene by demonstrating that homozygous loss of PTEN is less tumorigenic than heterozygous loss of PTEN owing to the induction of a p53-dependent senescence response.
  Article ADS CAS PubMed PubMed Central Google Scholar
• Yilmaz, O. H. et al. Pten dependence distinguishes haematopoietic stem cells from leukaemia-initiating cells. Nature 441, 475–482 (2006)
  Article ADS CAS PubMed Google Scholar
• Lee, J. Y. et al. mTOR activation induces tumor suppressors that inhibit leukemogenesis and deplete hematopoietic stem cells after Pten deletion. Cell Stem Cell 7, 593–605 (2010)In this work, an analysis of the contextual dependencies of leukaemia induced by loss of PTEN shows that loss of PTEN cooperates with p53 mutation in the haematopoietic compartment.
  Article CAS PubMed PubMed Central Google Scholar
• Kumar, M. S. et al. Dicer1 functions as a haploinsufficient tumor suppressor. Genes Dev. 23, 2700–2704 (2009)
  Article CAS PubMed PubMed Central Google Scholar
• Lambertz, I. et al. Monoallelic but not biallelic loss of Dicer1 promotes tumorigenesis in vivo . Cell Death Differ. 17, 633–641 (2010)
  Article CAS PubMed Google Scholar
• Bric, A. et al. Functional identification of tumor-suppressor genes through an in vivo RNA interference screen in a mouse lymphoma model. Cancer Cell 16, 324–335 (2009)
  Article CAS PubMed PubMed Central Google Scholar
• Sportoletti, P. et al. Npm1 is a haploinsufficient suppressor of myeloid and lymphoid malignancies in the mouse. Blood 111, 3859–3862 (2008)
  Article CAS PubMed PubMed Central Google Scholar
• Grisendi, S. et al. Role of nucleophosmin in embryonic development and tumorigenesis. Nature 437, 147–153 (2005)
  Article ADS CAS PubMed Google Scholar
• Su, X. et al. TAp63 suppresses metastasis through coordinate regulation of Dicer and miRNAs. Nature 467, 986–990 (2010)
  Article ADS CAS PubMed PubMed Central Google Scholar
• Zhou, X. Z. et al. The telomerase inhibitor PinX1 is a major haploinsufficient tumor suppressor essential for chromosome stability in mice. J. Clin. Invest. 121, 1266–1282 (2011)
  Article CAS PubMed PubMed Central Google Scholar
• Deutschbauer, A. M. et al. Mechanisms of haploinsufficiency revealed by genome-wide profiling in yeast. Genetics 169, 1915–1925 (2005)
  Article CAS PubMed PubMed Central Google Scholar
• Fodde, R. & Smits, R. Cancer biology. A matter of dosage. Science 298, 761–763 (2002)
  Article CAS PubMed Google Scholar
• Payne, S. R. & Kemp, C. J. Tumor suppressor genetics. Carcinogenesis 26, 2031–2045 (2005)
  Article CAS PubMed Google Scholar
• Trotman, L. C. et al. Pten dose dictates cancer progression in the prostate. PLoS Biol. 1, E59 (2003)
  Article PubMed PubMed Central Google Scholar
• Alimonti, A. et al. Subtle variations in Pten dose determine cancer susceptibility. Nature Genet. 42, 454–458 (2010)A subtle reduction in Pten expression is shown to induce cancer in mice in a tissue-specific manner, demonstrating that very small changes in expression can promote cancer, and thereby defining the phenomenon of quasi-insufficiency.
  Article CAS PubMed 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)An example of the complex dosage effects of oncogenes, this paper demonstrates that aberrantly high expression of an oncogene can promote senescence, rather than proliferation.
  Article CAS PubMed Google Scholar
• Evan, G. I. et al. Induction of apoptosis in fibroblasts by c-myc protein. Cell 69, 119–128 (1992)
  Article CAS PubMed Google Scholar
• Takano, T. et al. Epidermal growth factor receptor gene mutations and increased copy numbers predict gefitinib sensitivity in patients with recurrent non-small-cell lung cancer. J. Clin. Oncol. 23, 6829–6837 (2005)
  Article CAS PubMed Google Scholar
• Ding, L. et al. Somatic mutations affect key pathways in lung adenocarcinoma. Nature 455, 1069–1075 (2008)
  Article ADS CAS PubMed PubMed Central Google Scholar
• Bartel, D. P. MicroRNAs: target recognition and regulatory functions. Cell 136, 215–233 (2009)
  Article CAS PubMed PubMed Central Google Scholar
• Huse, J. T. et al. The PTEN-regulating microRNA miR-26a is amplified in high-grade glioma and facilitates gliomagenesis in vivo . Genes Dev. 23, 1327–1337 (2009)
  Article CAS PubMed PubMed Central Google Scholar
• Poliseno, L. et al. Identification of the miR-106b∼25 microRNA cluster as a proto-oncogenic _PTEN_-targeting intron that cooperates with its host gene MCM7 in transformation. Sci. Signal. 3, ra29 (2010)
  Article PubMed PubMed Central Google Scholar
• Poliseno, L. et al. A coding-independent function of gene and pseudogene mRNAs regulates tumour biology. Nature 465, 1033–1038 (2010)Identification of a coding-independent function of mRNAs whereby they act as ceRNAs that ‘sponge’ miRNAs to regulate distinct mRNAs in trans.
  Article ADS CAS PubMed PubMed Central Google Scholar
• Salmena, L., Poliseno, L., Tay, Y., Kats, L. & Pandolfi, P. P. A ceRNA hypothesis: the Rosetta stone of a hidden RNA language? Cell //10.1016/j.cell.2011.07.014 (2011)
• Teresi, R. E., Planchon, S. M., Waite, K. A. & Eng, C. Regulation of the PTEN promoter by statins and SREBP. Hum. Mol. Genet. 17, 919–928 (2008)
  Article CAS PubMed Google Scholar
• Lin, H. K. et al. Skp2 targeting suppresses tumorigenesis by _Arf-p53_-independent cellular senescence. Nature 464, 374–379 (2008)
  Article ADS Google Scholar
• Jemal, A., Siegel, R., Xu, J. & Ward, E. Cancer statistics, 2010. CA Cancer J. Clin. 60, 277–300 (2010)
  Article PubMed Google Scholar
• Di Cristofano, A. et al. Impaired Fas response and autoimmunity in Pten+/− mice. Science 285, 2122–2125 (1999)
  Article CAS PubMed Google Scholar
• Suzuki, A. et al. High cancer susceptibility and embryonic lethality associated with mutation of the PTEN tumor suppressor gene in mice. Curr. Biol. 8, 1169–1178 (1998)
  Article CAS PubMed Google Scholar
• Podsypanina, K. et al. Mutation of Pten/Mmac1 in mice causes neoplasia in multiple organ systems. Proc. Natl Acad. Sci. USA 96, 1563–1568 (1999)
  Article ADS CAS PubMed PubMed Central Google Scholar
• Di Cristofano, A., Pesce, B., Cordon-Cardo, C. & Pandolfi, P. P. Pten is essential for embryonic development and tumour suppression. Nature Genet. 19, 348–355 (1998)
  Article CAS PubMed Google Scholar
• Alimonti, A. et al. A novel type of cellular senescence that can be enhanced in mouse models and human tumor xenografts to suppress prostate tumorigenesis. J. Clin. Invest. 120, 681–693 (2010)
  Article CAS PubMed PubMed Central Google Scholar
• Daikoku, T. et al. Conditional loss of uterine Pten unfailingly and rapidly induces endometrial cancer in mice. Cancer Res. 68, 5619–5627 (2008)
  Article CAS PubMed PubMed Central Google Scholar
• Li, G. et al. Conditional loss of PTEN leads to precocious development and neoplasia in the mammary gland. Development 129, 4159–4170 (2002)
  CAS PubMed Google Scholar