The multiple roles of PTEN in tumor suppression.

By A. D. Cristofano, P. Pandolfi. Cell, 2000

1,253 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/2b2c8d797367439073ea7ab6f33e890446774668

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. T. Balla
2. J. Testa
3. C. Heinlein
4. Chawnshang Chang
5. Scott W. Lowe
6. M. Clarke
7. P. Pandolfi
8. G. Semenza

In Molecular Biology

1. Nahum Sonenberg
2. D. Altomare
3. J. Testa
4. T. Balla
5. A. Gingras
6. B. Raught
7. G. Semenza
8. B. Burgering

Citations in the corpus

• Cancer stem cells: models and concepts. (2007, background): “A second molecule that is likely to play a key role in the molecular machinery of both HSC and LSC self-renewal is the protein phosphatase and tensin homologue (PTEN), a known tumor suppressor (36).”
• MicroRNA control of signal transduction (2010, background): “Negative regulators are in place to prevent this risk; these include phosphatase and tensin homologue (PTEN; which reverses PI3K-mediated phosphorylation of PtdIns(3,4,5)P 3 (Ref”
• Androgen receptor in prostate cancer. (2004, background): “In contrast to Rb, BRCA1, and BRCA2, the tumor suppressor PTEN inhibits AR function by promoting the degradation of AR (H. K. Lin, and C. Chang, unpublished observations).”
• FIH-1: a novel protein that interacts with HIF-1alpha and VHL to mediate repression of HIF-1 transcriptional activity. (2001, background): “A common finding in brain tumors is loss-of-function mutations in the gene encoding PTEN, a phosphatase that negatively regulates PI3K signaling (for review, see Di Cristofano and Pandolfi 2000).”
• miR-19 is a key oncogenic component of mir-17-92. (2009, background): “…of which are dependent on the intact miR-19 -binding sites within the Pten mRNA. miR-19 activates the Akt–mTOR pathway both in vitro and in vivo PTEN is a tumor suppressor that is mutated or deleted in multiple tumor types with high frequency (Di Cristofano and Pandolfi 2000; Knobbe et al. 2008).”
• Tumor-derived exosomal miR-934 induces macrophage M2 polarization to promote liver metastasis of colorectal cancer (2020, background): “[22], and PI3K/AKT signaling is one of the most important pathways targeted by PTEN through its phosphatase activity [23].”
• Perturbations of the AKT signaling pathway in human cancer (2005, background): “PTEN is a major lipid phosphatase that dephosphorylates phosphatidylinositol (3,4,5) triphosphate (PIP3) and phosphatidylinositol (3,4) diphosphate to inhibit AKT activation and thereby suppresses tumor formation by restraining PI3K/AKT signaling (reviewed in Di Cristofano and Pandolfi, 2000).”
• Prostate-specific deletion of the murine Pten tumor suppressor gene leads to metastatic prostate cancer. (2003, background): “…209 glycogen synthase kinase-3 (GSK3), BAD, Caspase 9, and I B, Results leading to increased cell metabolism, cell growth, and cell sur- Cre-mediated Pten homozygous deletionvival (Di Cristofano and Pandolfi, 2000; Hanahan and Weinberg, and upregulated AKT activity2000; Vivanco and Sawyers, 2002).”
• Regulation of B‐cell activation and differentiation by the phosphatidylinositol 3‐kinase and phospholipase Cγ pathways (2000, background): “The PTEN phosphatase gene is altered in a small subset of B-cell lines and lymphomas (200), suggesting that deregulated PI3K activity can lead to malignant growth of B cells.”
• Lipid signalling in disease (2008, neutral): “Here, we provide a simplified overview of the intracellular and extracellular lipid-derived signals that function in tumour growth, and provide some insight into current attempts to modulate deviations in lipid synthesis in cancer (we will not cover other lipid-independent signal transduction pathwa”