The DOI matches its Crossref record; 220 of the 220 references it cites were found in a registry or an index.
Translational Control in Cancer Etiology
Open accessAbstract
The link between perturbations in translational control and cancer etiology is becoming a primary focus in cancer research. It has now been established that genetic alterations in several components of the translational apparatus underlie spontaneous cancers as well as an entire class of inherited syndromes known as "ribosomopathies" associated with increased cancer susceptibility. These discoveries have illuminated the importance of deregulations in translational control to very specific cellular processes that contribute to cancer etiology. In addition, a growing body of evidence supports the view that deregulation of translational control is a common mechanism by which diverse oncogenic pathways promote cellular transformation and tumor development. Indeed, activation of these key oncogenic pathways induces rapid and dramatic translational reprogramming both by increasing overall protein synthesis and by modulating specific mRNA networks. These translational changes promote cellular transformation, impacting almost every phase of tumor development. This paradigm represents a new frontier in the multihit model of cancer formation and offers significant promise for innovative cancer therapies. Current research, in conjunction with cutting edge technologies, will further enable us to explore novel mechanisms of translational control, functionally identify translationally controlled mRNA groups, and unravel their impact on cellular transformation and tumorigenesis.
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2 retracted
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RetractedRETRACTED: Elevated tRNAiMet Synthesis Can Drive Cell Proliferation and Oncogenic Transformation
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RetractedGene expression profiling predicts clinical outcome of breast cancer
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Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
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“OIS is characterized by cell-cycle arrest and induction of cellcycle inhibitors such as p15, p16, and p53, which restrain the proliferative potential of preneoplastic clones (Serrano et al. 1997; Gil and Peters 2006).”
BackgroundTumor Metastasis: Molecular Insights and Evolving Paradigms
Valastyan, S., & Weinberg, R. A. (2011) · Cell · doi:10.1016/j.cell.2011.09.024 · Cited by 4,011
mTOR: from growth signal integration to cancer, diabetes and ageing
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Genome-Wide Analysis in Vivo of Translation with Nucleotide Resolution Using Ribosome Profiling
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Regulation of Translation Initiation in Eukaryotes: Mechanisms and Biological Targets
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Molecular mechanisms of mTOR-mediated translational control
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FMRP Stalls Ribosomal Translocation on mRNAs Linked to Synaptic Function and Autism
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Cited by
Targeting the translation machinery in cancer
Bhat, M., Robichaud, N., Hulea, L., Sonenberg, N., Pelletier, J., & Topisirovic, I. (2015) · Nature Reviews Drug Discovery · doi:10.1038/nrd4505 · Cited by 799
Haematopoietic stem cells require a highly regulated protein synthesis rate
Signer, R. A. J., Magee, J. A., Salic, A., & Morrison, S. J. (2014) · Nature · doi:10.1038/nature13035 · Cited by 674
mTOR coordinates protein synthesis, mitochondrial activity and proliferation
Morita, M., Gravel, S.-P., Hulea, L., Larsson, O., Pollak, M., St-Pierre, J., & Topisirovic, I. (2015) · Cell Cycle · doi:10.4161/15384101.2014.991572 · Cited by 552
Tunable protein synthesis by transcript isoforms in human cells
Floor, S. N., & Doudna, J. A. (2016) · eLife · doi:10.7554/elife.10921 · Cited by 265
Jung, L. A., Gebhardt, A., Koelmel, W., Ade, C. P., Walz, S., Kuper, J., von Eyss, B., Letschert, S., Redel, C., d'Artista, L., et al. (2017) · Oncogene · doi:10.1038/onc.2016.354 · Cited by 101
Metadata
- Authors
- Ruggero, D.
- Venue
- Cold Spring Harbor Perspectives in Biology
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2012-07-05
- Volume
- 5
- Issue
- 2
- Pages
- a012336-a012336
- ISSN
- 1943-0264 (ISSN-L)
- OpenAlex
- W2165341580
- Cited by
- 367
- References
- 220
- Type
- posted content
- Language
- en
- Open access
- bronze
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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