ArticleExpert review of anticancer therapy2013
Rational cotargeting of Pim-1 and Akt in prostate cancer.
Article in Expert review of anticancer therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Co-targeting PIM and PI3K/mTOR using multikinase inhibitor AUM302 and a combination of AZD-1208 and BEZ235 in prostate cancer.Scientific reports · 2020Article
- PIM kinase inhibition: co-targeted therapeutic approaches in prostate cancer.Signal transduction and targeted therapy · 2020Review
- PIM Kinases and Their Relevance to the PI3K/AKT/mTOR Pathway in the Regulation of Ovarian Cancer.Biomolecules · 2018Review
Corrections and comments
- Comment on
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Evaluation of: Cen B, Mahajan S, Wang W, Kraft AS. Elevation of receptor tyrosine kinases by small molecule AKT inhibitors in prostate cancer is mediated by Pim-1. Cancer Res. 73(11), 3402-3411 (2013). The PI3K/Akt pathway is a key pathway in many advanced and aggressive cancers. Targeted inhibition of this pathway is currently an actively pursued therapeutic strategy. However, blockade of this pathway with inhibitors has been challenging, with up-regulation of reciprocal feedback pathways contributing to treatment failures. The article evaluated presents mechanistic data on how Pim is a critical mediator of the receptor tyrosine elevation induced by Akt inhibition. Pim-1 kinases are overexpressed in resistant and aggressive cancers. Following Akt inhibition, Pim- regulates receptor tyrosine kinases up-regulation, at least in part, through a cap-independent translation. This research leads the way for further evaluation of co-targeting strategies using Pim-1 inhibitors in combination with PI3K/Akt pathway inhibitors.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.