Evidence map›Paper›PMID 22767671›Full record

ReviewCold Spring Harbor perspectives in biology2013

Translational control in cancer etiology.

Davide Ruggero

Erratum issued Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. It is linked to trial NCT02730923 (A Multicentric, Randomized, Non Comparative, Open-label Phase I/II Evaluating AZD2014), which is not on this map. Cited by 196 papers.

0numbers the graph read from it
0cells of the map it votes in
196citing papers in PubMed
–field-weighted citation impact
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.

NCT02730923 phase1 / phase2unknown statusnot on this mapstarted 2016, after this paper: background citation

A Multicentric, Randomized, Non Comparative, Open-label Phase I/II Evaluating AZD2014 (Dual Mammalian Target of Rapamycin Complex 1/2 (mTORC1/mTORC2) Inhibitor) in Combination With Anastrozole Versus Anastrozole Alone in the Treatment of Metastatic Hormone Receptor-positive Endometrial Adenocarcinoma

TypeinterventionalSponsorCentre Leon BerardRan2016 to 2024Enrolled72ConditionsEndometrial Carcinoma, Metastatic Carcinoma, Hormone Receptor Positive TumorArmsAZD2014, Anastrozole
3 · Its place in the literature

Who cites it

196 citing papers in PubMed, 356 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Article
  6. Journal of ginseng research · 2026
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Ribosome specialization by cancer-associated ribosomal protein mutations: progress made and open questions.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  18. Article
  19. Article
  20. Article

136 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Davide RuggeroHelen Diller Cancer Center, School of Medicine, University of California, San Francisco, CA 94158, USA. davide.ruggero@ucsf.edu
UCSF Helen Diller Family Comprehensive Cancer Center · US

Funding

The role of deregulated protein synthesis control in Myc-induced tumorigenesisR01CA140456 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RUGGERO, DAVIDE · 2009 to 2019
$3.3M
Pharmcogenomic dissection of mTOR translational targets in prostate cancerR01CA154916 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RUGGERO, DAVIDE · 2011 to 2018
$2.8M
Role of rRNA Modifications in Dyskeratosis Congenita and Translation ControlR01HL085572 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RUGGERO, DAVIDE · 2006 to 2009
$1.8M
Role of ribosome impairments in X-linked Dyskeratosis Congenita pathogenesisR01DK098057 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RUGGERO, DAVIDE · 2012 to 2015
$1.2M
NCI NIH HHS R01 CA140456NCI NIH HHS R01 CA154916NHLBI NIH HHS R01 HL085572NIDDK NIH HHS R01 DK098057
6 · The paper itself

Abstract

The link between perturbations in translational control and cancer etiology is becoming a primary focus in cancer research. It has now been established that genetic alterations in several components of the translational apparatus underlie spontaneous cancers as well as an entire class of inherited syndromes known as "ribosomopathies" associated with increased cancer susceptibility. These discoveries have illuminated the importance of deregulations in translational control to very specific cellular processes that contribute to cancer etiology. In addition, a growing body of evidence supports the view that deregulation of translational control is a common mechanism by which diverse oncogenic pathways promote cellular transformation and tumor development. Indeed, activation of these key oncogenic pathways induces rapid and dramatic translational reprogramming both by increasing overall protein synthesis and by modulating specific mRNA networks. These translational changes promote cellular transformation, impacting almost every phase of tumor development. This paradigm represents a new frontier in the multihit model of cancer formation and offers significant promise for innovative cancer therapies. Current research, in conjunction with cutting edge technologies, will further enable us to explore novel mechanisms of translational control, functionally identify translationally controlled mRNA groups, and unravel their impact on cellular transformation and tumorigenesis.

Indexed as

Cell Transformation, NeoplasticGenetic Predisposition to DiseaseHumansModels, GeneticMutationNeoplasm MetastasisNeoplasmsPeptide Initiation FactorsProtein BiosynthesisRibosomesPeptide Initiation Factors

Identifiers

PMID22767671
PMCPMC3552512
OpenAlexW2165341580

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.