Evidence map›Paper›PMID 24362522›Full record

ArticleOncogene2015

HER2/Neu tumorigenesis and metastasis is regulated by E2F activator transcription factors.

E R Andrechek

Abstract read
In one paragraph

Article in Oncogene, 2015. 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
2.8field-weighted citation impact, top 9% 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, 76 citations in OpenAlex.

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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

1 author at 1 institution in 1 country.

E R AndrechekDepartment of Physiology, Michigan State University, East Lansing, MI, USA.
Michigan State University · US

Funding

Dissecting Tumor Heterogeneity by Analyzing Signaling Pathway Requirements.R01CA160514 · NCI · MICHIGAN STATE UNIVERSITY · PI ANDRECHEK, ERAN ROBERT · 2012 to 2016
$1.5M
NCI NIH HHS 1R01CA160514NCI NIH HHS R01 CA160514
6 · The paper itself

Abstract

HER2/Neu is amplified and overexpressed in a large proportion of human breast cancers, but the signaling pathways that contribute to tumor development and metastatic progression are not completely understood. Using gene expression data and pathway signatures, we predicted a role for activator E2F transcription factors in Neu-induced tumors. This was genetically tested by interbreeding Neu transgenics with knockouts of the three activator E2Fs. Loss of any E2F delayed Neu-induced tumor onset. E2F1 loss accelerated tumor growth, while E2F2 and E2F3 loss did not. Strikingly, it was observed that loss of E2F1 or E2F2 significantly reduced the metastatic capacity of the tumor and this was associated with a reduction in circulating tumor cells in the E2F2 knockout. Gene expression analysis between the tumors in the various E2F-mutant backgrounds revealed that there was extensive compensation by other E2F family members in the individual knockouts, underscoring the importance of the E2Fs in HER2/Neu-induced tumors. Extension to HER2-positive (HER2+) human breast cancer revealed a number of HER2+ subtypes based on E2F activity with differences in relapse-free survival times. Taken together, these data demonstrate that the E2F transcription factors are integral to HER2+ tumor development and progression.

Indexed as

AnimalsBreast NeoplasmsCarcinogenesisDisease Models, AnimalE2F Transcription FactorsErb-b2 Receptor Tyrosine KinasesFemaleHumansMammary Neoplasms, ExperimentalMiceMice, KnockoutMice, NudeNeoplasm MetastasisNeoplastic Cells, CirculatingSignal TransductionE2F Transcription FactorsERBB2 protein, humanErbb2 protein, mouseErb-b2 Receptor Tyrosine Kinases

Identifiers

PMID24362522
PMCPMC4067469
OpenAlexW2045244782

What OpenQuestion holds

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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.