ArticleSmall GTPases2010
Cooperative interactions of PTEN deficiency and RAS activation in melanoma metastasis.
Article in Small GTPases, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed.
- Refining mutanome-based individualised immunotherapy of melanoma using artificial intelligence.European journal of medical research · 2024Review
- Article
- Aetiology and Pathogenesis of Cutaneous Melanoma: Current Concepts and Advances.International journal of molecular sciences · 2021Review
- Born to be alive: a role for the BCL-2 family in melanoma tumor cell survival, apoptosis, and treatment.Frontiers in oncology · 2011Article
Corrections and comments
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Authors and funding
1 author.
Funding
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Abstract
Melanoma displays frequent activation of RAS/RAF/MAPK and PI3K/AKT signaling pathways as well as inactivation of CDKN2A (INK4a/ARF) and PTEN tumor suppressors via genetic and epigenetic alterations. Pathogenetic roles of these melanoma-prone mutations and their genetic interactions have been established in genetically engineered mouse models. Here, we catalog frequent genetic alterations observed in human melanomas and describe mouse models of melanoma initiation and progression, including our recent study that investigated the genetic interactions of RAS activation and PTEN loss in a CDKN2A (INK4a/ARF) null melanoma prone genetic background. We showed that loss of PTEN cooperates with HRAS activation, leading to increased development of melanoma and emergence of metastasis. Moreover, we observed that RNA i-mediated PTEN inactivation in RAS-driven melanomas enhanced migration and invasion with concomitant downregulation of E-cadherin, the major regulator of epithelial and mesenchymal transition, and enhanced AKT2 phosphorylation, which has been previously linked to invasion and metastasis of several cancer types, including breast and ovary. These data show that activated RAS cooperates with PTEN loss in melanoma genesis and progression.
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Registered trials
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