The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Role of Transforming Growth Factor-beta Signaling in Cancer
Abstract
Signaling from transforming growth factor-beta (TGF-beta) through its unique transmembrane receptor serine-threonine kinases plays a complex role in carcinogenesis, having both tumor suppressor and oncogenic activities. Tumor cells often escape from the antiproliferative effects of TGF-beta by mutational inactivation or dysregulated expression of components in its signaling pathway. Decreased receptor function and altered ratios of the TGF-beta type I and type II receptors found in many tumor cells compromise the tumor suppressor activities of TGF-beta and enable its oncogenic functions. Recent identification of a family of intracellular mediators, the Smads, has provided new paradigms for understanding mechanisms of subversion of TGF-beta signaling by tumor cells. In addition, several proteins recently have been identified that can modulate the Smad-signaling pathway and may also be targets for mutation in cancer. Other pathways such as various mitogen-activated protein kinase cascades also contribute substantially to TGF-beta signaling. Understanding the interplay between these signaling cascades as well as the complex patterns of cross-talk with other signaling pathways is an important area of investigation that will ultimately contribute to understanding of the bifunctional tumor suppressor/oncogene role of TGF-beta in carcinogenesis.
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Cites
Lessons from hereditary colorectal cancer
Kinzler, K. W., & Vogelstein, B. (1996) · Cell · doi:10.1016/s0092-8674(00)81333-1 · Cited by 4,919
DPC4 , A Candidate Tumor Suppressor Gene at Human Chromosome 18q21.1
Hahn, S. A., Schutte, M., Shamsul Hoque, A. T. M., Moskaluk, C. A., da Costa, L. T., Rozenblum, E., Weinstein, C. L., Fischer, A., Yeo, C. J., Hruban, R. H., et al. (1996) · Science · doi:10.1126/science.271.5247.350 · Cited by 2,337
pl5INK4B is a potentia| effector of TGF-β-induced cell cycle arrest
Hannon, G. J., & Beach, D. (1994) · Nature · doi:10.1038/371257a0 · Cited by 1,950
Smad3 and Smad4 cooperate with c-Jun/c-Fos to mediate TGF-β-induced transcription
Zhang, Y., Feng, X.-H., & Derynck, R. (1998) · Nature · doi:10.1038/29814 · Cited by 809
Cited by
Gressner, A. M., & Weiskirchen, R. (2006) · Journal of Cellular and Molecular Medicine · doi:10.1111/j.1582-4934.2006.tb00292.x · Cited by 718
The transforming growth factor-β superfamily of receptors
de Caestecker, M. (2004) · Cytokine & Growth Factor Reviews · doi:10.1016/j.cytogfr.2003.10.004 · Cited by 464
Yang, Y.-A., Dukhanina, O., Tang, B., Mamura, M., Letterio, J. J., MacGregor, J., Patel, S. C., Khozin, S., Liu, Z.-Y., Green, J., et al. (2002) · Journal of Clinical Investigation · doi:10.1172/jci200215333 · Cited by 404
Hayashida, T., de Caestecker, M., & Schnaper, H. W. (2003) · The FASEB Journal · doi:10.1096/fj.03-0037fje · Cited by 361
Self-citationHalder, S. K., Beauchamp, R. D., & Datta, P. K. (2005) · Neoplasia · doi:10.1593/neo.04640 · Cited by 288
Metadata
- Authors
- de Caestecker, M. P.
- Venue
- Journal of the National Cancer Institute
- Publisher
- Oxford University Press (OUP)
- Published
- 2000-09-06
- Volume
- 92
- Issue
- 17
- Pages
- 1388-1402
- ISSN
- 0027-8874 (ISSN-L)
- 1460-2105
- OpenAlex
- W2262976102
- Cited by
- 522
- References
- 4
- FWCI
- 14.87
- Type
- journal article
- Language
- en
- Open access
- closed
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