Evidence map›Paper›PMID 29730477›Full record

ReviewNeoplasia (New York, N.Y.)2018

eIF4E Phosphorylation in Prostate Cancer.

Leandro S D'Abronzo, Paramita M Ghosh

Open access · goldAbstract readReview
In one paragraph

Review in Neoplasia (New York, N.Y.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.8field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. The role of m5C, m1A and m7G modifications in tumors of urinary system.Frontiers in cell and developmental biology · 2025
    Review
  6. Article
  7. Review
  8. Regulations of mFrontiers of medicine · 2024
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Leandro S D'AbronzoVA Northern California Health Care System, Mather, CA; Department of Urological Surgery, University of California at Davis, Sacramento, CA.
Paramita M GhoshVA Northern California Health Care System, Mather, CA; Department of Urological Surgery, University of California at Davis, Sacramento, CA; Department of Biochemistry and Molecular Medicine, University of California at Davis, Sacramento, CA. Electronic address: paghosh@ucdavis.edu.
VA Northern California Health Care System · US

Funding

Rapamycin Regulation of the Androgen Receptor: Implications in Prostate CancerR01CA133209 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI GHOSH, PARAMITA M. · 2009 to 2013
$1.1M
(PQD-1) Selective pressure of antiandrogens on castration resistant prostate cancR01CA185509 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI GHOSH, PARAMITA M. · 2014 to 2017
$1.0M
Loss of Filamin A Nuclear Localization in Prostate Cancer ProgressionI01BX000400 · VA · VA NORTHERN CALIFORNIA HEALTH CARE SYS · PI GHOSH, PARAMITA M. · 2011 to 2019
–
BLRD VA I01 BX000400NCI NIH HHS R01 CA133209NCI NIH HHS R01 CA185509
6 · The paper itself

Abstract

Prostate cancer (PCa) progression involves a shift from endocrine to paracrine and eventually autocrine control resulting from alterations in molecular mechanisms in the cells. Deregulation of RNA translation is crucial for tumor cells to grow and proliferate; therefore, overactivation of the translation machinery is often observed in cancer. The two most important signal transduction pathways regulating PCa progression are PI3K/Akt/mTOR and Ras/MAPK. These two pathways converge on the eukaryotic translation initiation factor 4E (eIF4E) which binds to the protein scaffold eIF4G upon mechanistic target of rapamycin (mTOR) activation and is phosphorylated by the mitogen-activated protein kinase (MAPK) interacting protein kinases (Mnk1/2). This review describes the role of eIF4E in mRNA translation initiation mediated by its binding to the methylated 5' terminal structure (m7G-cap) of many mRNAs, and the ability of many tumor cells to bypass this mechanism. Hormonal therapy and chemotherapy are two of the most prevalent therapies used in patients with advanced PCa, and studies have implicated a role for eIF4E phosphorylation in promoting resistance to both these therapies. It appears that eIF4E phosphorylation enhances the rate of translation of oncogene mRNAs to increase tumorigenicity.

Indexed as

Eukaryotic Initiation Factor-4EHumansMaleMitogen-Activated Protein KinasesPhosphorylationProstatic NeoplasmsRNA, MessengerSignal TransductionEukaryotic Initiation Factor-4EMitogen-Activated Protein KinasesRNA, Messenger

Identifiers

PMID29730477
PMCPMC5994774
OpenAlexW2800947413

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.