TGF-β signaling in tumor suppression and cancer progression

By R. Derynck, R. Akhurst, Allan Balmain. Nature Genetics, 2001

1,524 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/1527864ee5946ab1959987d782c5b40e92d921c5

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. J. Massagué
2. J. Seoane
3. R. Derynck
4. D. Wotton
5. Jiri Zavadil
6. Varda Rotter
7. Moshe Oren
8. Erwin P. Bottinger

In Oncology

1. J. Massagué
2. J. Seoane
3. R. Derynck
4. D. Wotton
5. M. Mareel
6. O. De Wever
7. Varda Rotter
8. Moshe Oren

Citations in the corpus

• TGF‐β activates Erk MAP kinase signalling through direct phosphorylation of ShcA (2007, background): “The low level interaction of ShcAwith TbRI in the absence of exogenous TGF-b likely reflects autocrine TGF-b signalling, which is common in cultured cells (Derynck et al, 2001).”
• A Mutant-p53/Smad complex opposes p63 to empower TGFbeta-induced metastasis. (2009, neutral): “, 2005), that is, tumor types characterized by a clear promalignant-switch in TGFb responses (Derynck et al., 2001).”
• A cytokine-mediated link between innate immunity, inflammation, and cancer. (2007, neutral): “TGF-β signals mainly through activation of SMAD transcription factors, but it also leads to MAPK activation (Figure 2) (116, 117).”
• Mutant p53 gain-of-function in cancer. (2010, background): “…stages of the process, it serves as a tumor suppressor, strongly inhibiting the proliferation of epithelial cells; however, at advanced stages of the disease, it can turn into a potent driver of tumor spread and metastasis, severely worsening patient prognosis (Derynck et al. 2001; Massague 2008).”
• TGF-β and epithelial-to-mesenchymal transitions (2005, background): “Thus, a cooperation of TGF-b, Ras and NF-kB is critical for epithelial plasticity manifested by EMT and the finding is consistent with the observation that NF-kB positively regulates expression of Snail and is itself inhibited by upstream GSK3, the main mediator of E-cadherin levels and of epithelia”
• Modern pathogenetic concepts of liver fibrosis suggest stellate cells and TGF-β as major players and therapeutic targets (2006, background): “in which heterozygous or homozygous TGF-β1-nulls show an increased incidence of chemically or spontaneously induced tumours, respectively [91–93].”