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Myc-Max-Mad: A transcription factor network controlling cell cycle progression, differentiation and death
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Amati B., Land H. Myc-Max-Mad: a transcription factor network controlling cell cycle progression, differentiation and death. Curr Opin Genet Dev. 4:1994;102-108.
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Amati, B.1
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0030481404
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Myc: A single gene controls both proliferation and apoptosis in mammalian cells
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Desbarats L., Schneider A., Muller D., Burgin A., Eilers M. Myc: a single gene controls both proliferation and apoptosis in mammalian cells. Experientia. 52:1996;1123-1129.
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Desbarats, L.1
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0033611644
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Control of cell proliferation by Myc family genes
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Eilers M. Control of cell proliferation by Myc family genes. Mol Cell. 9:1999;1-6.
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Mol Cell
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Eilers, M.1
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Integrated control of cell proliferation and cell death by the c-myc oncogene
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Evan G., Harrington E., Fanidi A., Land H., Amati B., Bennett M. Integrated control of cell proliferation and cell death by the c-myc oncogene. Philos Trans R Soc Lond B Biol Sci. 345:1994;269-275.
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0032575705
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A matter of life and cell death
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A very well written review discussing the propensity for growth-deregulating oncoproteins such as Myc, E1A and E2F, to induce apoptosis and propose the model that c-Myc acts to sensitise cells to a variety of apoptotic triggers rather than acting solely as a death effector. This potent mechanism to limit expansion of neoplastic cells and the cooperation between various oncoproteins are discussed.
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Evan G., Littlewood T. A matter of life and cell death. Science. 281:1998;1317-1322. A very well written review discussing the propensity for growth-deregulating oncoproteins such as Myc, E1A and E2F, to induce apoptosis and propose the model that c-Myc acts to sensitise cells to a variety of apoptotic triggers rather than acting solely as a death effector. This potent mechanism to limit expansion of neoplastic cells and the cooperation between various oncoproteins are discussed.
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Science
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Evan, G.1
Littlewood, T.2
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9
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0033551387
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Mechanisms of apoptosis by c-Myc
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A very well written review summarising molecular advances in apoptosis with specific attention made to the mechanisms of apoptosis induced by c-Myc.
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Prendergast G.C. Mechanisms of apoptosis by c-Myc. Oncogene. 18:1999;2967-2987. A very well written review summarising molecular advances in apoptosis with specific attention made to the mechanisms of apoptosis induced by c-Myc.
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Oncogene
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Prendergast, G.C.1
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The MYC protein activates transcription of the alpha-prothymosin gene
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0029002136
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A modified oestrogen receptor ligand-binding domain as an improved switch for the regulation of heterologous proteins
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Evan, G.I.5
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13
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0026642195
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Induction of apoptosis in fibroblasts by c-myc protein
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Evan G.I., Wyllie A.H., Gilbert C.S., Littlewood T.D., Land H., Brooks M., Waters C.M., Penn L.Z., Hancock D.C. Induction of apoptosis in fibroblasts by c-myc protein. Cell. 69:1992;119-128.
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Evan, G.I.1
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Littlewood, T.D.4
Land, H.5
Brooks, M.6
Waters, C.M.7
Penn, L.Z.8
Hancock, D.C.9
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14
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0033152390
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C-Myc-induced sensitization to apoptosis is mediated through cytochrome c release
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This elegant in vitro study shows that c-Myc promotes apoptosis of fibroblasts by causing the release of cytochrome c from mitochondria into the cytosol. Cytochrome c release, in itself, however, is not efficient at inducing apoptosis but can cooperate with other triggers of apoptosis such as CD95/Fas and p53. These data provide a mechanism for c-Myc-induced sensitisation to apoptosis.
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Juin P., Hueber A.O., Littlewood T., Evan G. c-Myc-induced sensitization to apoptosis is mediated through cytochrome c release. Genes Dev. 13:1999;1367-1381. This elegant in vitro study shows that c-Myc promotes apoptosis of fibroblasts by causing the release of cytochrome c from mitochondria into the cytosol. Cytochrome c release, in itself, however, is not efficient at inducing apoptosis but can cooperate with other triggers of apoptosis such as CD95/Fas and p53. These data provide a mechanism for c-Myc-induced sensitisation to apoptosis.
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Genes Dev
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Juin, P.1
Hueber, A.O.2
Littlewood, T.3
Evan, G.4
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15
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0028263811
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C-Myc-induced apoptosis in fibroblasts is inhibited by specific cytokines
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Harrington E.A., Bennett M.R., Fanidi A., Evan G.I. c-Myc-induced apoptosis in fibroblasts is inhibited by specific cytokines. EMBO J. 13:1994;3286-3295.
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Harrington, E.A.1
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Fanidi, A.3
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Control of c-myc regulation in normal and neoplastic cells
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0028373224
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Use of transgenic mice to study myc family gene function in normal mammalian development and in cancer
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Myc-induced cyclin D2 genomic instability in murine B cell neoplasms
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[Discussion 190-192]
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Mushinski J.F., Hanley-Hyde J., Rainey G.J., Kuschak T.I., Taylor C., Fluri M., Stevens L.M., Henderson D.W., Mai S. Myc-induced cyclin D2 genomic instability in murine B cell neoplasms. Curr Top Microbiol Immunol. 246:1999;183-189. [Discussion 190-192].
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Mushinski, J.F.1
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Taylor, C.5
Fluri, M.6
Stevens, L.M.7
Henderson, D.W.8
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Transient excess of MYC activity can elicit genomic instability and tumorigenesis
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Felsher D.W., Bishop J.M. Transient excess of MYC activity can elicit genomic instability and tumorigenesis. Proc Natl Acad Sci USA. 96:1999;3940-3944.
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0033171062
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Chromosomal and extrachromosomal instability of the cyclin D2 gene in induced by Myc overexpression
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Mai S., Hanley-Hyde J., Rainey G.J., Kuschak T.I., Paul J.T., Littlewood T.D., Mischak H., Stevens L.M., Henderson D.W., Mushinski J.K. Chromosomal and extrachromosomal instability of the cyclin D2 gene in induced by Myc overexpression. Neoplasia. 1:1999;241-252.
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Stevens, L.M.8
Henderson, D.W.9
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0029739901
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Progenitor tumours from Emu-bcl-2-myc transgenic mice have lymphomyeloid differentiation potential and reveal developmental differences in cell survival
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Novel primitive lymphoid tumours induced in transgenic mice by cooperation between myc and bcl-2
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0034628513
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Sensitivity to myc-induced apoptosis is retained in spontaneous and transplanted lymphomas of CD2-mycER™ mice
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in press
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Blyth K., Stewart M., Bell M., James C., Evan G., Neil J.C., Cameron E.R. Sensitivity to myc-induced apoptosis is retained in spontaneous and transplanted lymphomas of CD2-mycER™ mice. Oncogene. 2000;. in press.
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Blyth, K.1
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Cameron, E.R.7
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26
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0033180211
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Reversible tumorigenesis by MYC in hematopoietic lineages
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This paper describes the use of the tetracycline regulatory system to conditionally express myc in haematopoietic cells of transgenic mice. Although sustained myc expression during development leads to malignant T cell lymphomas and acute myeloid leukaemias, inactivation of the transgene causes regression of the majority of established tumours. These results show for the first time that, despite the multistep nature of tumourigenesis in haematopoietic lineages, inactivation of a single genetic lesion, myc, is sufficient to reverse malignancy.
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Felsher D.W., Bishop J.M. Reversible tumorigenesis by MYC in hematopoietic lineages. Mol Cell. 4:1999;199-207. This paper describes the use of the tetracycline regulatory system to conditionally express myc in haematopoietic cells of transgenic mice. Although sustained myc expression during development leads to malignant T cell lymphomas and acute myeloid leukaemias, inactivation of the transgene causes regression of the majority of established tumours. These results show for the first time that, despite the multistep nature of tumourigenesis in haematopoietic lineages, inactivation of a single genetic lesion, myc, is sufficient to reverse malignancy.
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Mol Cell
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Felsher, D.W.1
Bishop, J.M.2
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0033001621
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Reversible activation of c-Myc in skin: Induction of a complex neoplastic phenotype by a single oncogenic lesion
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™, was targeted to suprabasal keratinocytes of murine epidermis and activation of the chimaeric protein achieved with administration of tamoxifen. The authors describe the phenotype observed following immediate and short-term activation of c-Myc in the epidermis and, perhaps surprisingly, shows that c-Myc alone is sufficient to induce pre-malignant skin lesions (papillomatosis) with profound angiogenesis.
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™, was targeted to suprabasal keratinocytes of murine epidermis and activation of the chimaeric protein achieved with administration of tamoxifen. The authors describe the phenotype observed following immediate and short-term activation of c-Myc in the epidermis and, perhaps surprisingly, shows that c-Myc alone is sufficient to induce pre-malignant skin lesions (papillomatosis) with profound angiogenesis.
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Mol Cell
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0027340203
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The bacterial and mouse mammary tumor virus superantigens; Two different families of proteins with the same functions
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Adams J.M., Harris A.W., Pinkert C.A., Corcoran L.M., Alexander W.S., Cory S., Palmiter R.D., Brinster R.L. The c-myc oncogene driven by immunoglobulin enhancers induces lymphoid malignancy in transgenic mice. Nature. 318:1985;533-538.
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