The DOI matches its Crossref record; 28 of the 28 references it cites were found in a registry or an index.
Modelling Myc inhibition as a cancer therapy
Open accessAbstract
Myc is a pleiotropic basic helix–loop–helix leucine zipper transcription factor that coordinates expression of the diverse intracellular and extracellular programs that together are necessary for growth and expansion of somatic cells. In principle, this makes inhibition of Myc an attractive pharmacological approach for treating diverse types of cancer. However, enthusiasm has been muted by lack of direct evidence that Myc inhibition would be therapeutically efficacious, concerns that it would induce serious side effects by inhibiting proliferation of normal tissues, and practical difficulties in designing Myc inhibitory drugs. We have modelled genetically both the therapeutic impact and the side effects of systemic Myc inhibition in a preclinical mouse model of Ras-induced lung adenocarcinoma by reversible, systemic expression of a dominant-interfering Myc mutant. We show that Myc inhibition triggers rapid regression of incipient and established lung tumours, defining an unexpected role for endogenous Myc function in the maintenance of Ras-dependent tumours in vivo. Systemic Myc inhibition also exerts profound effects on normal regenerating tissues. However, these effects are well tolerated over extended periods and rapidly and completely reversible. Our data demonstrate the feasibility of targeting Myc, a common downstream conduit for many oncogenic signals, as an effective, efficient and tumour-specific cancer therapy.
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Cites
‘Green mice’ as a source of ubiquitous green cells
Okabe, M., Ikawa, M., Kominami, K., Nakanishi, T., & Nishimune, Y. (1997) · FEBS Letters · doi:10.1016/s0014-5793(97)00313-x · Cited by 2,581
Analysis of lung tumor initiation and progression using conditional expression of oncogenic K-ras
Jackson, E. L., Willis, N., Mercer, K., Bronson, R. T., Crowley, D., Montoya, R., Jacks, T., & Tuveson, D. A. (2001) · Genes & Development · doi:10.1101/gad.943001 · Cited by 1,898
Depletion of epithelial stem-cell compartments in the small intestine of mice lacking Tcf-4
Korinek, V., Barker, N., Moerer, P., van Donselaar, E., Huls, G., Peters, P. J., & Clevers, H. (1998) · Nature Genetics · doi:10.1038/1270 · Cited by 1,581
Reversible Tumorigenesis by MYC in Hematopoietic Lineages
Felsher, D. W., & Bishop, J. M. (1999) · Molecular Cell · doi:10.1016/s1097-2765(00)80367-6 · Cited by 881
Recognition by Max of its cognate DNA through a dimeric b/HLH/Z domain
Ferré-D'Amaré, A. R., Prendergast, G. C., Ziff, E. B., & Burley, S. K. (1993) · Nature · doi:10.1038/363038a0 · Cited by 724
Sustained Loss of a Neoplastic Phenotype by Brief Inactivation of MYC
Jain, M., Arvanitis, C., Chu, K., Dewey, W., Leonhardt, E., Trinh, M., Sundberg, C. D., Bishop, J. M., & Felsher, D. W. (2002) · Science · doi:10.1126/science.1071489 · Cited by 644
Pelengaris, S., Khan, M., & Evan, G. I. (2002) · Cell · doi:10.1016/s0092-8674(02)00738-9 · Cited by 626
Self-citationOncogenic activity of the c-Myc protein requires dimerization with Max
Amati, B., Brooks, M. W., Levy, N., Littlewood, T. D., Evan, G. I., & Land, H. (1993) · Cell · doi:10.1016/0092-8674(93)90663-b · Cited by 560
Self-citationThe Differential Effects of Mutant p53 Alleles on Advanced Murine Lung Cancer
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Reversible Activation of c-Myc in Skin
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Cited by
Dang, C. V. (2012) · Cell · doi:10.1016/j.cell.2012.03.003 · Cited by 3,390
A view on drug resistance in cancer
Vasan, N., Baselga, J., & Hyman, D. M. (2019) · Nature · doi:10.1038/s41586-019-1730-1 · Cited by 2,770
The transcription factor Myc controls metabolic reprogramming upon T lymphocyte activation
Wang, R., Dillon, C. P., Shi, L. Z., Milasta, S., Carter, R., Finkelstein, D., McCormick, L. L., Fitzgerald, P., Chi, H., Munger, J., et al. (2011) · Immunity · doi:10.1016/j.immuni.2011.09.021 · Cited by 2,140
“We observed that acute depletion of Myc, in vivo, did not compromise the health of the animals over a period of 1 week, consistent with a recent report (Soucek et al., 2008).”
ResultOncogenic Kras maintains pancreatic tumors through regulation of anabolic glucose metabolism
Ying, H., Kimmelman, A. C., Lyssiotis, C. A., Hua, S., Chu, G. C., Fletcher-Sananikone, E., Locasale, J. W., Son, J., Zhang, H., Coloff, J. L., et al. (2012) · Cell · doi:10.1016/j.cell.2012.01.058 · Cited by 2,043
RNAi screen identifies Brd4 as a therapeutic target in acute myeloid leukaemia
Zuber, J., Shi, J., Wang, E., Rappaport, A. R., Herrmann, H., Sison, E. A., Magoon, D., Qi, J., Blatt, K., Wunderlich, M., et al. (2011) · Nature · doi:10.1038/nature10334 · Cited by 1,870
Metadata
- Authors
- Soucek, L., Whitfield, J., Martins, C. P., Finch, A. J., Murphy, D. J., Sodir, N. M., Karnezis, A. N., Swigart, L. B., Nasi, S., & Evan, G. I.
- Venue
- Nature
- Published
- 2008-08-17
- Volume
- 455
- Issue
- 7213
- Pages
- 679-683
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W1990320777
- Cited by
- 817
- References
- 28
- FWCI
- 20.94
- Type
- journal article
- Language
- en
- Open access
- green
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- Soucek, L., Whitfield, J., Martins, C. P., Finch, A. J., Murphy, D. J., Sodir, N. M., Karnezis, A. N., Swigart, L. B., Nasi, S., & Evan, G. I. (2008). Modelling Myc inhibition as a cancer therapy. Nature. https://doi.org/10.1038/nature07260
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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