Tenets of PTEN tumor suppression.

By L. Salmena, Arkaitz Carracedo, P. Pandolfi. Cell, 2008

1,069 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/17eadb8c34caee0a4d1b1d6aa80975a7050588d8

How researchers see this paper

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

In Immunology

1. K. Rajewsky
2. P. Pandolfi
3. R. DePinho
4. Arkaitz Carracedo
5. V. Schirrmacher

In Molecular Biology

1. P. Pandolfi
2. C. Lord
3. Arkaitz Carracedo
4. Alan Ashworth
5. T. Franke
6. L. Salmena
7. R. Brough
8. C. Abate-Shen

In Pathology and Forensic Medicine

1. Carlos L. Arteaga
2. D. Calado
3. Ingrid A. Mayer
4. P. Pandolfi

Citations in the corpus

• The GENCODE pseudogene resource (2012, background): “It has been suggested that this could be a general mechanism of regulation in cancer [27].”
• PI3 Kinase signals BCR dependent mature B cell survival (2009, positive): “Monoallelic loss of Pten also contributes to tumor growth in the context of other somatic mutations, with Pten protein levels correlating with disease severity (Salmena et al., 2008).”
• The PTEN–PI3K pathway: of feedbacks and cross-talks (2008, background): “The major function of PTEN is the buffering of PI3K signaling; yet recent studies point to additional novel, lipid phosphatase-independent functions that may contribute to its tumor-suppressive activity (Carracedo et al., 2008; Salmena et al., 2008).”
• Molecular genetics of prostate cancer: new prospects for old challenges. (2010, background): “PTEN was originally identified as a tumor suppressor that is frequently mutated or deleted in many cancers, including prostate (Salmena et al. 2008).”
• Synthetic lethal targeting of PTEN mutant cells with PARP inhibitors (2009, positive): “As PTEN loss of function mutations and loss of PTEN expression are common in a range of hereditary and sporadic cancers (Salmena et al, 2008), we reasoned that such data might significantly extend the utility of this class of drugs.”
• The PI3K/AKT Pathway as a Target for Cancer Treatment. (2016, background): “Convergent loss of PTEN leads to clinical resistance to a PI(3)Kalpha inhibitor.”
• Subtle variations in Pten dose determine cancer susceptibility (2010, background): “Pten is a TSG frequently lost in human cancer and mutated in inherited cancer-predisposition syndrome”
• PI3K/Akt: getting it right matters (2008, background): “Silencing of PTEN is frequently observed in primary tumors and cancer cell lines (for review, see Carnero et al., 2008; Maehama, 2007; Salmena et al., 2008).”
• PI3K pathway alterations in cancer: variations on a theme (2008, neutral): “Monoallelic loss of PTEN contributes to tumor growth in the context of other somatic mutations, and PTEN protein levels correlate with disease severity, suggesting that PTEN is functionally haploinsufficient (Salmena et al., 2008).”
• Epigenetic plasticity and the hallmarks of cancer (2017, background): “MLH1,MSH2, and PTENmethylation are also commonly observed without any obvious genetic trigger and are associated with poor prognosis (3, 4, 40, 88).”
• Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways (2017, neutral): “is frequently inactivated in cancer [231].”
• Targeting the phosphoinositide 3-kinase (PI3K) pathway in cancer (2009, background): “This action is essential to its function as a tumour suppressor (reviewed in Ref”