Evidence map›Paper›PMID 27863413›Full record

ArticleOncotarget2017

RICTOR amplification identifies a subgroup in small cell lung cancer and predicts response to drugs targeting mTOR.

Nneha Sakre, Gary Wildey, Mohadese Behtaj, Adam Kresak, Michael Yang, Pingfu Fu, Afshin Dowlati

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 2 pooled it
3.2field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 66 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  4. Review
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  6. Review
  7. Review
  8. Pathology oncology research : POR · 2024
    Article
  9. mTOR hyperactivity andPathology oncology research : POR · 2024
    Review
  10. Article
  11. Article
  12. SFPQ and Its Isoform as Potential Biomarker for Non-Small-Cell Lung Cancer.International journal of molecular sciences · 2023
    Article
  13. Article
  14. Review
  15. 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

7 authors at 2 institutions in 1 country.

Nneha SakreCase Comprehensive Cancer Center, Case Western Reserve University, Cleveland, Ohio, 44106 USA.
Gary WildeyCase Comprehensive Cancer Center, Case Western Reserve University, Cleveland, Ohio, 44106 USA.
Mohadese BehtajDepartment of Pathology, University Hospitals Cleveland Medical Center, Cleveland, Ohio, 44106 USA.
Adam KresakCase Comprehensive Cancer Center, Case Western Reserve University, Cleveland, Ohio, 44106 USA.
Michael YangDepartment of Pathology, University Hospitals Cleveland Medical Center, Cleveland, Ohio, 44106 USA.
Pingfu FuEpidemiology and Biostatistics, Case Western Reserve University, Cleveland, Ohio, 44106 USA.
Afshin DowlatiCase Comprehensive Cancer Center, Case Western Reserve University, Cleveland, Ohio, 44106 USA.
University Hospitals of Cleveland · USCase Western Reserve University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Small cell lung cancer (SCLC) is an aggressive cancer that represents ~15% of all lung cancers. Currently there are no targeted therapies to treat SCLC. Our genomic analysis of a metastatic SCLC cohort identified recurrent RICTOR amplification. Here, we examine the translational potential of this observation. RICTOR was the most frequently amplified gene observed (~14% patients), and co-amplified with FGF10 and IL7R on chromosome 5p13. RICTOR copy number variation correlated with RICTOR protein expression in SCLC cells. In parallel, cells with RICTOR copy number (CN) gain showed increased sensitivity to three mTOR inhibitors, AZD8055, AZD2014 and INK128 in cell growth assays, with AZD2014 demonstrating the best inhibition of downstream signaling. SCLC cells with RICTOR CN gain also migrated more rapidly in chemotaxis and scratch wound assays and were again more sensitive to mTOR inhibitors. The overall survival in SCLC patients with RICTOR amplification was significantly decreased (p = 0.021). Taken together, our results suggest that SCLC patients with RICTOR amplification may constitute a clinically important subgroup because of their potential response to mTORC1/2 inhibitors.

Indexed as

Gene AmplificationAdenineAdultAgedAged, 80 and overBenzamidesBenzoxazolesFemaleFibroblast Growth Factor 10HumansInterleukin-7 Receptor alpha SubunitLung NeoplasmsMaleMiddle AgedMolecular Targeted TherapyMorpholines(5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanolAdenineBenzamidesBenzoxazolesFGF10 protein, humanFibroblast Growth Factor 10IL7R protein, humanInterleukin-7 Receptor alpha SubunitMorpholinesProtein Kinase InhibitorsPyrimidinesRapamycin-Insensitive Companion of mTOR ProteinRICTOR protein, humansapanisertibvistusertibamplificationCNVmTORC1/2 inhibitorsRICTORsmall cell lung cancer

Identifiers

PMID27863413
PMCPMC5351607
OpenAlexW2556224846

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.