Evidence map›Paper›PMID 25071152›Full record

ArticleMolecular and cellular biology2014

p66ShcA promotes breast cancer plasticity by inducing an epithelial-to-mesenchymal transition.

Jesse Hudson, Jacqueline R Ha, Valerie Sabourin, Ryuhjin Ahn, Rachel La Selva, Julie Livingstone, Lauren Podmore, Jennifer Knight, Laura Forrest, Nicole Beauchemin and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

19 citing papers in PubMed, 22 citations in OpenAlex.

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  16. Insights into the Shc Family of Adaptor Proteins.Journal of molecular signaling · 2017
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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

13 authors at 3 institutions in 1 country.

Jesse HudsonLady Davis Institute for Medical Research, Montreal, Quebec, Canada.
Jacqueline R HaLady Davis Institute for Medical Research, Montreal, Quebec, Canada.
Valerie SabourinLady Davis Institute for Medical Research, Montreal, Quebec, Canada.
Ryuhjin AhnLady Davis Institute for Medical Research, Montreal, Quebec, Canada.
Rachel La SelvaLady Davis Institute for Medical Research, Montreal, Quebec, Canada.
Julie LivingstoneGoodman Cancer Research Centre, Montreal, Quebec, Canada.
Lauren PodmoreLady Davis Institute for Medical Research, Montreal, Quebec, Canada.
Jennifer KnightGoodman Cancer Research Centre, Montreal, Quebec, Canada.
Laura ForrestLady Davis Institute for Medical Research, Montreal, Quebec, Canada Goodman Cancer Research Centre, Montreal, Quebec, Canada.
Nicole BeaucheminGoodman Cancer Research Centre, Montreal, Quebec, Canada Department of Oncology, McGill University, Montreal, Quebec, Canada Department of Biochemistry, McGill University, Montreal, Quebec, Canada.
Michael HallettGoodman Cancer Research Centre, Montreal, Quebec, Canada Department of Biochemistry, McGill University, Montreal, Quebec, Canada.
Morag ParkGoodman Cancer Research Centre, Montreal, Quebec, Canada Department of Oncology, McGill University, Montreal, Quebec, Canada Department of Biochemistry, McGill University, Montreal, Quebec, Canada.
Josie Ursini-SiegelLady Davis Institute for Medical Research, Montreal, Quebec, Canada Department of Oncology, McGill University, Montreal, Quebec, Canada giuseppina.ursini-siegel@mcgill.ca.
Jewish General Hospital · CAMcGill University · CAOccupational Cancer Research Centre · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Breast cancers are stratified into distinct subtypes, which influence therapeutic responsiveness and patient outcome. Patients with luminal breast cancers are often associated with a better prognosis relative to that with other subtypes. However, subsets of patients with luminal disease remain at increased risk of cancer-related death. A critical process that increases the malignant potential of breast cancers is the epithelial-to-mesenchymal transition (EMT). The p66ShcA adaptor protein stimulates the formation of reactive oxygen species in response to stress stimuli. In this paper, we report a novel role for p66ShcA in inducing an EMT in HER2(+) luminal breast cancers. p66ShcA increases the migratory properties of breast cancer cells and enhances signaling downstream of the Met receptor tyrosine kinase in these tumors. Moreover, Met activation is required for a p66ShcA-induced EMT in luminal breast cancer cells. Finally, elevated p66ShcA levels are associated with the acquisition of an EMT in primary breast cancers spanning all molecular subtypes, including luminal tumors. This is of high clinical relevance, as the luminal and HER2 subtypes together comprise 80% of all newly diagnosed breast cancers. This study identifies p66ShcA as one of the first prognostic biomarkers for the identification of more aggressive tumors with mesenchymal properties, regardless of molecular subtype.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsBiomarkers, TumorBreast NeoplasmsCell Line, TumorCell MovementErb-b2 Receptor Tyrosine KinasesFemaleGene Expression Regulation, NeoplasticHumansMammary Neoplasms, ExperimentalMiceMice, SCIDProto-Oncogene Proteins c-metShc Signaling Adaptor ProteinsSignal TransductionBiomarkers, TumorERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesMET protein, humanProto-Oncogene Proteins c-metSHC1 protein, humanShc Signaling Adaptor ProteinsSrc Homology 2 Domain-Containing, Transforming Protein 1

Identifiers

PMID25071152
PMCPMC4187732
OpenAlexW2325623142

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.