The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Ras in Cancer and Developmental Diseases
Open accessAbstract
Somatic, gain-of-function mutations in ras genes were the first specific genetic alterations identified in human cancer about 3 decades ago. Studies during the last quarter century have characterized the Ras proteins as essential components of signaling networks controlling cellular proliferation, differentiation, or survival. The oncogenic mutations of the H-ras, N-ras, or K-ras genes frequently found in human tumors are known to throw off balance the normal outcome of those signaling pathways, thus leading to tumor development. Oncogenic mutations in a number of other upstream or downstream components of Ras signaling pathways (including membrane RTKs or cytosolic kinases) have been detected more recently in association with a variety of cancers. Interestingly, the oncogenic Ras mutations and the mutations in other components of Ras/MAPK signaling pathways appear to be mutually exclusive events in most tumors, indicating that deregulation of Ras-dependent signaling is the essential requirement for tumorigenesis. In contrast to sporadic tumors, separate studies have identified germline mutations in Ras and various other components of Ras signaling pathways that occur in specific association with a number of different familial, developmental syndromes frequently sharing common phenotypic cardiofaciocutaneous features. Finally, even without being a causative force, defective Ras signaling has been cited as a contributing factor to many other human illnesses, including diabetes and immunological and inflammatory disorders. We aim this review at summarizing and updating current knowledge on the contribution of Ras mutations and altered Ras signaling to development of various tumoral and nontumoral pathologies.
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Mutations of the BRAF gene in human cancer
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Wild-Type KRAS Is Required for Panitumumab Efficacy in Patients With Metastatic Colorectal Cancer
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Hyperactive Ras in developmental disorders and cancer
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Germline KRAS mutations cause Noonan syndrome
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Germline gain-of-function mutations in SOS1 cause Noonan syndrome
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Genomic and Biological Characterization of Exon 4 KRAS Mutations in Human Cancer
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Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways
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Behjati, S., Tarpey, P. S., Presneau, N., Scheipl, S., Pillay, N., Van Loo, P., Wedge, D. C., Cooke, S. L., Gundem, G., Davies, H., et al. (2013) · Nature Genetics · doi:10.1038/ng.2814 · Cited by 854
The PI3K-AKT-mTOR Pathway and Prostate Cancer: At the Crossroads of AR, MAPK, and WNT Signaling
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RAF-MEK-ERK pathway in cancer evolution and treatment
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Metadata
- Authors
- Fernandez-Medarde, A., & Santos, E.
- Venue
- Genes & Cancer
- Publisher
- SAGE Publications
- Published
- 2011-03-01
- Volume
- 2
- Issue
- 3
- Pages
- 344-358
- ISSN
- 1947-6019 (ISSN-L)
- 1947-6027
- OpenAlex
- W2143881980
- Cited by
- 897
- References
- 12
- FWCI
- 15.87
- Type
- journal article
- Language
- en
- Open access
- bronze
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