Evidence map›Paper›PMID 25450580›Full record

ReviewBiochimica et biophysica acta2014

mTOR signaling in tumorigenesis.

Kai Xu, Pengda Liu, Wenyi Wei

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
9.3field-weighted citation impact, top 1% 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

92 citing papers in PubMed, 165 citations in OpenAlex.

  1. Article
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  14. Autophagy Regulators in Cancer.International journal of molecular sciences · 2023
    Review
  15. Article
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32 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 2 countries.

Kai XuDepartment of Otolaryngology-Head and Neck Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, People's Republic of China; Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Pengda LiuDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA. Electronic address: pliu1@bidmc.harvard.edu.
Wenyi WeiDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA. Electronic address: wwei2@bidmc.harvard.edu.
Beth Israel Deaconess Medical Center · USTongji Hospital · CN

Funding

Training Program in Angiogenesis &InflammationT32HL007893 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI DVORAK, HAROLD FISHER · 1998 to 2017
$5.5M
Novel regulation of PI3K/Akt to direct targeted breast cancer therapiesR01CA177910 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEI, WENYI · 2013 to 2023
$3.9M
Functional analysis of beta-TRCP in cell cycle control and DNA damage responseR01GM094777 · NIGMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEI, WENYI · 2012 to 2015
$1.3M
Elucidating a Novel Akt Activation Mechanism for Targeted Prostate Cancer TherapyR00CA181342 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LIU, PENGDA · 2016 to 2018
$653k
Elucidating a Novel Akt Activation Mechanism for Targeted Prostate Cancer TherapyK99CA181342 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LIU, PENGDA · 2014 to 2015
$339k
NCI NIH HHS 1K99CA181342NCI NIH HHS CA177910NCI NIH HHS K99 CA181342NCI NIH HHS R00 CA181342NCI NIH HHS R01 CA177910NHLBI NIH HHS T32 HL007893NIGMS NIH HHS GM094777NIGMS NIH HHS R01 GM094777
6 · The paper itself

Abstract

mTOR (the mechanistic target of rapamycin) is an atypical serine/threonine kinase involved in regulating major cellular functions including growth and proliferation. Deregulation of the mTOR signaling pathway is one of the most commonly observed pathological alterations in human cancers. To this end, oncogenic activation of the mTOR signaling pathway contributes to cancer cell growth, proliferation and survival, highlighting the potential for targeting the oncogenic mTOR pathway members as an effective anti-cancer strategy. In order to do so, a thorough understanding of the physiological roles of key mTOR signaling pathway components and upstream regulators would guide future targeted therapies. Thus, in this review, we summarize available genetic mouse models for mTORC1 and mTORC2 components, as well as characterized mTOR upstream regulators and downstream targets, and assign a potential oncogenic or tumor suppressive role for each evaluated molecule. Together, our work will not only facilitate the current understanding of mTOR biology and possible future research directions, but more importantly, provide a molecular basis for targeted therapies aiming at key oncogenic members along the mTOR signaling pathway.

Indexed as

CarcinogenesisAdaptor Proteins, Signal TransducingAMP-Activated Protein KinasesAnimalsAutophagyCarrier ProteinsHumansMiceRapamycin-Insensitive Companion of mTOR ProteinRegulatory-Associated Protein of mTORSignal TransductionTOR Serine-Threonine KinasesTuberous Sclerosis Complex 1 ProteinTumor Suppressor ProteinsAdaptor Proteins, Signal TransducingAMP-Activated Protein KinasesCarrier ProteinsMAPKAP1 protein, humanRapamycin-Insensitive Companion of mTOR ProteinRegulatory-Associated Protein of mTORRICTOR protein, humanRPTOR protein, humanTOR Serine-Threonine KinasesTuberous Sclerosis Complex 1 ProteinTumor Suppressor ProteinsMouse modelmTORC1mTORC2mTOR pathwayTumorigenesis

Identifiers

PMID25450580
PMCPMC4261029
OpenAlexW2024578614

What OpenQuestion holds

Textmetadata
LicenceTDM
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.