Evidence map›Paper›PMID 23291982›Full record

ArticleCancer biology & therapy2013

Alterations of EGFR, p53 and PTEN that mimic changes found in basal-like breast cancer promote transformation of human mammary epithelial cells.

Maira M Pires, Benjamin D Hopkins, Lao H Saal, Ramon E Parsons

Open access · hybridAbstract read
In one paragraph

Article in Cancer biology & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.7field-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

21 citing papers in PubMed, 32 citations in OpenAlex.

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  4. Evaluation of twoMolecular therapy. Methods & clinical development · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 2 countries.

Maira M PiresInstitute for Cancer Genetics, Herbert Irving Cancer Center, Columbia University, New York, NY, USA
Benjamin D Hopkins
Lao H Saal
Ramon E Parsons
Cancer Genetics (United States) · US

Funding

The role of PTEN in basal-like breast cancerP01CA097403 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BAER, RICHARD J · 2003 to 2013
$18.2M
TRAINING IN CELLULAR, MOLECULAR AND BIOPHYSICAL STUDIEST32GM008224 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI LIEM, RONALD K. · 1987 to 2021
$9.9M
NCI NIH HHS P01 CA097403NCI NIH HHS P01CA97403NIGMS NIH HHS T32 GM008224
6 · The paper itself

Abstract

Breast cancer can be classified into different molecular subtypes with varying clinical and pathological characteristics. The basal-like breast cancer subtype represents one of the most aggressive and lethal types of breast cancer, and due to poor mechanistic understanding, it lacks targeted therapy. Many basal-like breast cancer patient samples display alterations of established drivers of cancer development, including elevated expression of EGFR, p53 inactivating mutations and loss of expression of the tumor suppressor PTEN; however, their contribution to human basal-like breast cancer pathogenesis remains ill-defined. Using non-transformed human mammary epithelial cells, we set out to determine whether altering EGFR, p53 and PTEN in different combinations could contribute to basal-like breast cancer progression through transformation of cells. Altering PTEN in combination with either p53 or EGFR in contrast to any of the single alterations caused increased growth of transformed colonies in soft agar. Concomitantly modifying all three genes led to the highest rate of cellular proliferation and the greatest degree of anchorage-independent colony formation. Results from our effort to engineer a model of BBC expressing alterations of EGFR, p53 and PTEN suggest that these changes are cooperative and likely play a causal role in basal-like breast cancer pathogenesis. Consideration should be given to targeting EGFR and restoring p53 and PTEN signaling simultaneously as a strategy for treatment of this subtype of breast cancer.

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorCell ProliferationCell Transformation, NeoplasticEpidermal Growth FactorErbB ReceptorsFemaleGene ExpressionGene Expression Regulation, NeoplasticGene Knockout TechniquesHumansMiceModels, BiologicalNeoplasms, Basal CellPTEN PhosphohydrolaseEpidermal Growth FactorErbB ReceptorsPTEN PhosphohydrolaseTumor Suppressor Protein p53basal-like breast cancerdominant-negativeEGFRMCF10Aoncogenep53PTENsoft agartransformationtumor suppressor

Identifiers

PMID23291982
PMCPMC3595307
OpenAlexW2171564712

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.