Evidence map›Paper›PMID 22342683›Full record

ArticleCancer letters2012

K-Ras mutation-mediated IGF-1-induced feedback ERK activation contributes to the rapalog resistance in pancreatic ductal adenocarcinomas.

Feng Wei, Yan Liu, Anita C Bellail, Jeffrey J Olson, Shi-Yong Sun, Guoyue Lu, Lijuan Ding, Changji Yuan, Guangyi Wang, Chunhai Hao

Abstract read
In one paragraph

Article in Cancer letters, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. The Role of the Guanosine Nucleotide-Binding Protein in the Corpus Luteum.Animals : an open access journal from MDPI · 2021
    Review
  2. Article
  3. Article
  4. Insulin-Like Growth Factor-1 Receptor Expression and Disease Recurrence and Survival in Patients with Resected Pancreatic Ductal Adenocarcinoma.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2020
    Article
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  6. Oncotarget · 2017
    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

10 authors at 3 institutions in 2 countries.

Feng WeiDepartment of Hepatobiliary & Pancreas Surgery and Hematology & Oncology, The First Hospital, Jilin University, China.
Yan Liu
Anita C Bellail
Jeffrey J Olson
Shi-Yong Sun
Guoyue Lu
Lijuan Ding
Changji Yuan
Guangyi Wang
Chunhai Hao
Emory University · USJilin University · CNFirst Hospital of Jilin University · CN

Funding

Translational Training Grant in Experimental TherapeuticsK12CA133250 · NCI · OHIO STATE UNIVERSITY · PI WILLIAM E. CARSON, Rosa Lapalombella · 2008 to 2026
$15.0M
Enhancing the mTOR-targeted cancer therapyR01CA118450 · NCI · EMORY UNIVERSITY · PI SUN, SHI-YONG · 2006 to 2015
$2.6M
Molecular mechanisms of TRAIL resistance in glioblastomaR01CA129687 · NCI · EMORY UNIVERSITY · PI HAO, CHUNHAI CHARLIE · 2009 to 2013
$1.5M
NCI NIH HHS R01 CA118450NCI NIH HHS R01 CA129687NCI NIH HHS R01 CA133250
6 · The paper itself

Abstract

Mammalian target of rapamycin complex 1 (mTORC1) is frequently activated in human cancers; however, clinical trials of rapalog (the mTORC1 inhibitors) have shown that pancreatic ductal adenocarcinomas (PDACs) resist to the treatment. Rapalog treatment activated the extracellular signal-regulated kinase (ERK) pathway in K-Ras mt PDAC cells. K-Ras knockdown abolished the insulin-like growth factor-1 (IGF-1)-induced ERK pathway in the K-Ras mt PDAC cells and enhanced the therapeutic efficacy of everolimus in treating K-Ras mt PDAC cells-derived mouse xenografts. The results indicate that targeting of K-Ras mutation may lead to the development of therapies that overcome rapalog resistance in PDAC.

Indexed as

MutationAdenocarcinomaAnimalsAntineoplastic AgentsBenzenesulfonatesCarcinoma, Pancreatic DuctalCell Line, TumorDrug Resistance, NeoplasmEnzyme ActivationEverolimusExtracellular Signal-Regulated MAP KinasesFeedback, PhysiologicalFemaleHumansInsulin-Like Growth Factor IMAP Kinase Signaling SystemAntineoplastic AgentsBenzenesulfonatesEverolimusExtracellular Signal-Regulated MAP KinasesInsulin-Like Growth Factor IKRAS protein, humanMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesNiacinamideNVP-AEW541Phenylurea CompoundsProteinsProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)PyridinesPyrimidinesPyrrolesras ProteinsSirolimusSorafenibTOR Serine-Threonine Kinases

Identifiers

PMID22342683
PMCPMC3361568
OpenAlexW2017913000

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.