Evidence map›Paper›PMID 22890559›Full record

ReviewTargeted oncology2012

Profiling mTOR pathway in neuroendocrine tumors.

S Cingarlini, M Bonomi, V Corbo, A Scarpa, G Tortora

Abstract readReview
PubMed Publisher
In one paragraph

Review in Targeted oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Effect of Hypoxia-Induced Micro-RNAs Expression on Oncogenesis.International journal of molecular sciences · 2022
    Article
  3. Review
  4. Review
  5. Transcriptomic Profiling ofFrontiers in oncology · 2021
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. MicroRNAs and the metabolic hallmarks of aging.Molecular and cellular endocrinology · 2017
    Review
  13. Review
  14. Article
  15. Review
  16. Medical treatment for gastro-entero-pancreatic neuroendocrine tumours.World journal of gastrointestinal oncology · 2016
    Review
  17. Article
  18. Review
  19. Article
  20. Review
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

5 authors at 1 institution in 1 country.

S CingarliniSection of Medical Oncology, Department of Medicine, Azienda Ospedaliera Universitaria Integrata (AOUI), Verona, Italy. sara.cingarlini@ospedaleuniverona.it
M Bonomi
V Corbo
A Scarpa
G Tortora
Azienda Ospedaliera Universitaria Integrata Verona · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The serine/threonine kinase mammalian target of rapamycin (mTOR) plays a central role in regulating critical cellular processes such as growth, proliferation, and protein synthesis. The study of cancer predisposing syndromes within which neuroendocrine tumors (NETs) may arise has furnished clues on the involvement of mTOR pathway in sporadic diseases so far. Recent comprehensive analyses have definitely shown activation of mTOR pathway in both experimental and human sporadic NETs. Upstream regulators of mTOR (PTEN and TSC2) have been found mutated in sporadic pNETs. Activation of mTOR pathways in NETs is already demonstrated by expression profiles analysis that revealed downregulation of TSC2 gene and alterations of TSC2 and PTEN protein expression in the vast majority of well-differentiated tumors. Moreover, a global microRNA expression analysis revealed the overexpression, in highly aggressive tumors, of a microRNA (miR-21) that targets PTEN reducing its expression and therefore leading to mTOR activation as well. Overall, these clues have furnished the rationale for the use of mTOR inhibitors the treatment of pNETs. With the recent approval of Everolimus (mTOR-targeted drug) for the treatment of advanced pNETs, this paradigm has been effectively translated into the clinical setting. In this review, we discuss mTOR pathway involvement in NETs, the clinical evidence supporting the use of mTOR inhibitors in cancer treatment, and the current clinical issues that remain to be elucidated to improve patient management.

Indexed as

Gene Expression Regulation, NeoplasticAntineoplastic AgentsCell DifferentiationCell ProliferationGenetic Predisposition to DiseaseHumansMicroRNAsModels, BiologicalNeovascularization, PathologicNeuroendocrine TumorsPhosphatidylinositol 3-KinasesPTEN PhosphohydrolaseTOR Serine-Threonine KinasesTuberous Sclerosis Complex 2 ProteinTumor Suppressor ProteinsAntineoplastic AgentsMicroRNAsMIRN21 microRNA, humanMTOR protein, humanPhosphatidylinositol 3-KinasesPTEN PhosphohydrolasePTEN protein, humanTOR Serine-Threonine KinasesTSC2 protein, humanTuberous Sclerosis Complex 2 ProteinTumor Suppressor Proteins

Identifiers

PMID22890559
OpenAlexW2119399167

What OpenQuestion holds

Textmetadata
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.