Evidence map›Paper›PMID 28249168›Full record

ArticleCell reports2017

Autocrine IGF1 Signaling Mediates Pancreatic Tumor Cell Dormancy in the Absence of Oncogenic Drivers.

Nirakar Rajbhandari, Wan-Chi Lin, Barbara L Wehde, Aleata A Triplett, Kay-Uwe Wagner

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.4field-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

47 citing papers in PubMed, 66 citations in OpenAlex.

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  17. A cell cycle centric view of tumour dormancy.British journal of cancer · 2023
    Review
  18. Review
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  20. Oncogenic Addiction of Fibrolamellar Hepatocellular Carcinoma to the Fusion Kinase DNAJB1-PRKACA.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
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 2 institutions in 1 country.

Nirakar RajbhandariEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, 985950 Nebraska Medical Center, Omaha, NE 68198-5950, USA; Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, 985950 Nebraska Medical Center, Omaha, NE 68198-5950, USA.
Wan-Chi LinEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, 985950 Nebraska Medical Center, Omaha, NE 68198-5950, USA.
Barbara L WehdeEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, 985950 Nebraska Medical Center, Omaha, NE 68198-5950, USA.
Aleata A TriplettEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, 985950 Nebraska Medical Center, Omaha, NE 68198-5950, USA.
Kay-Uwe WagnerEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, 985950 Nebraska Medical Center, Omaha, NE 68198-5950, USA; Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, 985950 Nebraska Medical Center, Omaha, NE 68198-5950, USA; Department of Pathology and Microbiology, University of Nebraska Medical Center, 985950 Nebraska Medical Center, Omaha, NE 68198-5950, USA. Electronic address: kuwagner@unmc.edu.
Nebraska Medical Center · USUniversity of Nebraska Medical Center · US

Funding

CHEMICAL CARCINOGENESIS &CANCER BIOLOGYT32CA009476 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Jennifer D. Black · 1988 to 2026
$6.2M
JAK1 Signaling in Pancreatic Cancer Initiation and ProgressionR01CA202917 · NCI · WAYNE STATE UNIVERSITY · PI WAGNER, KAY-UWE · 2017 to 2021
$1.6M
Temporally controlled oncogene expression in a novel pancreatic cancer modelR21CA155175 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI WAGNER, KAY-UWE · 2011 to 2012
$355k
NCI NIH HHS R01 CA202917NCI NIH HHS R21 CA155175NCI NIH HHS T32 CA009476
6 · The paper itself

Abstract

Mutant KRAS and c-MYC are oncogenic drivers and rational therapeutic targets for the treatment of pancreatic cancer. Although tumor growth and homeostasis are largely dependent on these oncogenes, a few residual cancer cells are able to survive the ablation of mutant KRAS and c-MYC. By performing a genome-wide gene expression analysis of in vivo-derived bulk tumor cells and residual cancer cells lacking the expression of mutant KRAS or c-MYC, we have identified an increase in autocrine IGF1/AKT signaling as a common survival mechanism in dormant cancer cells. The pharmacological inhibition of IGF-1R reduces residual disease burden and cancer recurrence, suggesting that this molecular pathway is crucial for the survival of cancer cells in the absence of the primary oncogenic drivers.

Indexed as

AnimalsAutocrine CommunicationCarcinogenesisCell Line, TumorCell ProliferationGene ExpressionGenes, mycHumansInsulin-Like Growth Factor IMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMutationNeoplasm Recurrence, LocalOncogenesInsulin-Like Growth Factor IProto-Oncogene Proteins c-aktProto-Oncogene Proteins p21(ras)Receptor, IGF Type 1AKTcancer dormancyc-MYCgenetic engineeringIGF1 signalingKRASmouse modelsoncogenespancreatic cancer

Identifiers

PMID28249168
PMCPMC5369772
OpenAlexW2592443973

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.