Evidence map›Paper›PMID 24276238›Full record

ArticleOncogene2014

Scrib heterozygosity predisposes to lung cancer and cooperates with KRas hyperactivation to accelerate lung cancer progression in vivo.

I A Elsum, L L Yates, H B Pearson, T J Phesse, F Long, R O'Donoghue, M Ernst, C Cullinane, P O Humbert

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

36 citing papers in PubMed, 59 citations in OpenAlex.

  1. Changes in the transcriptome and synthetic lethal dependencies followingProceedings of the National Academy of Sciences of the United States of America · 2026
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  16. Drosophila Models of Cell Polarity and Cell Competition in Tumourigenesis.Advances in experimental medicine and biology · 2019
    Review
  17. Review
  18. Article
  19. Emerging roles for LPP in metastatic cancer progression.Journal of cell communication and signaling · 2018
    Review
  20. BioMed research international · 2018
    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

9 authors at 2 institutions in 1 country.

I A ElsumCell Cycle and Cancer Genetics, Research Division, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia.
L L YatesCell Cycle and Cancer Genetics, Research Division, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia.
H B Pearson1] Cell Cycle and Cancer Genetics, Research Division, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia [2] The Sir Peter MacCallum Department of Oncology, Melbourne, Victoria, Australia.
T J PhesseCell Signaling and Cell Death Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
F LongCell Cycle and Cancer Genetics, Research Division, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia.
R O'DonoghueCell Signaling and Cell Death Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
M ErnstCell Signaling and Cell Death Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
C Cullinane1] The Sir Peter MacCallum Department of Oncology, Melbourne, Victoria, Australia [2] Translational Research Laboratory, Cancer Therapeutics Program, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia.
P O Humbert1] Cell Cycle and Cancer Genetics, Research Division, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia [2] The Sir Peter MacCallum Department of Oncology, Melbourne, Victoria, Australia [3] Department of Pathology, University of Melbourne, Parkville, Victoria, Australia [4] Department of Molecular Biology and Biochemistry, University of Melbourne, Parkville, Victoria, Australia.
Peter MacCallum Cancer Centre · AUWalter and Eliza Hall Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the leading cause of cancer deaths worldwide with non small-cell lung cancer (NSCLC) accounting for 80% of all lung cancers. Although activating mutations in genes of the RAS-MAPK pathway occur in up to 30% of all NSCLC, the cooperating genetic lesions that are required for lung cancer initiation and progression remain poorly understood. Here we identify a role for the cell polarity regulator Scribble (Scrib) in NSCLC. A survey of genomic databases reveals deregulation of SCRIB in human lung cancer and we show that Scrib(+/-) mutant mice develop lung cancer by 540 days with a penetrance of 43%. To model NSCLC development in vivo, we used the extensively characterized LSL-KRas(G12D) murine model of NSCLC. We show that loss of Scrib and activated oncogenic KRas cooperate in vivo, resulting in more aggressive lung tumors, likely due to a synergistic elevation in RAS-MAPK signaling. Finally, we provide data consistent with immune infiltration having an important role in the acceleration of tumorigenesis in KRas(G12D) lung tumors following Scrib loss.

Indexed as

AnimalsCarcinoma, Non-Small-Cell LungCell Transformation, NeoplasticDisease Models, AnimalDisease ProgressionEnzyme ActivationGene DosageHeterozygoteHumansImmunoblottingImmunohistochemistryIntracellular Signaling Peptides and ProteinsLoss of HeterozygosityLung NeoplasmsMembrane ProteinsMiceHras protein, mouseIntracellular Signaling Peptides and ProteinsKRAS protein, humanMembrane ProteinsProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsSCRIB protein, humanscrib protein, mouseTumor Suppressor Proteins

Identifiers

PMID24276238
OpenAlexW2095370559

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.