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Cited by 989

The DOI matches its Crossref record; 151 of the 151 references it cites were found in a registry or an index.

Signal Transduction in Cancer

Open access
Sever, R., Brugge, J. S.·2015·Cold Spring Harbor Perspectives in Medicine

Abstract

Cancer is driven by genetic and epigenetic alterations that allow cells to overproliferate and escape mechanisms that normally control their survival and migration. Many of these alterations map to signaling pathways that control cell growth and division, cell death, cell fate, and cell motility, and can be placed in the context of distortions of wider signaling networks that fuel cancer progression, such as changes in the tumor microenvironment, angiogenesis, and inflammation. Mutations that convert cellular proto-oncogenes to oncogenes can cause hyperactivation of these signaling pathways, whereas inactivation of tumor suppressors eliminates critical negative regulators of signaling. An examination of the PI3K-Akt and Ras-ERK pathways illustrates how such alterations dysregulate signaling in cancer and produce many of the characteristic features of tumor cells.

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Crossref · 10.1101/cshperspect.a006098

Cites

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Citations

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Metadata

Authors
Sever, R., & Brugge, J. S.
Venue
Cold Spring Harbor Perspectives in Medicine
Published
2015-04-01
Volume
5
Issue
4
Pages
a006098-a006098
ISSN
2157-1422 (ISSN-L)
OpenAlex
W2108215899
Cited by
989
References
151
Type
posted content
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Signal Transduction in Cancer. https://app.cochat.ai/papers/10.1101/cshperspect.a006098
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Sever, R., & Brugge, J. S. (2015). Signal Transduction in Cancer. Cold Spring Harbor Perspectives in Medicine. https://doi.org/10.1101/cshperspect.a006098

Data sources

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).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.