Evidence map›Paper›PMID 25573952›Full record

ArticleMolecular cancer research : MCR2015

Mutant p53 Amplifies Epidermal Growth Factor Receptor Family Signaling to Promote Mammary Tumorigenesis.

Alisha R Yallowitz, Dun Li, Anthony Lobko, Daniel Mott, Alice Nemajerova, Natalia Marchenko

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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  4. Clustering subtypes of breast cancer by combining immunohistochemistry profiles and metabolism characteristics measured using FDG PET/CT.Cancer imaging : the official publication of the International Cancer Imaging Society · 2021
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  8. Article
  9. Article
  10. p53 balances between tissue hierarchy and anarchy.Journal of molecular cell biology · 2019
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
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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

6 authors at 1 institution in 1 country.

Alisha R YallowitzDepartment of Pathology, School of Medicine, Stony Brook University, Stony Brook, New York.
Dun LiDepartment of Pathology, School of Medicine, Stony Brook University, Stony Brook, New York.
Anthony LobkoDepartment of Pathology, School of Medicine, Stony Brook University, Stony Brook, New York.
Daniel MottDepartment of Pathology, School of Medicine, Stony Brook University, Stony Brook, New York.
Alice NemajerovaDepartment of Pathology, School of Medicine, Stony Brook University, Stony Brook, New York.
Natalia MarchenkoDepartment of Pathology, School of Medicine, Stony Brook University, Stony Brook, New York. natalia.marchenko@stonybrook.edu.
Stony Brook University · US

Funding

TRAINING PROGRAM IN ORGANOGENESIST32HD007505 · NICHD · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PASCA DI MAGLIANO, MARINA, SPENCE, JASON · 1997 to 2021
$6.9M
NICHD NIH HHS T32 HD007505
6 · The paper itself

Abstract

unlabelledThe EGFR family (ErbB2/Her2 and EGFR/ErbB1/Her1) often modulates the transcriptional program involved in promoting mammary tumorigenesis. In humans, the majority of ErbB2-positive sporadic breast cancers harbor p53 mutations, which correlate with poor prognosis. Also, the extremely high incidence of ErbB2-positive breast cancer in women with p53 germline mutations (Li-Fraumeni syndrome) suggests a key role of mutant p53 specifically in ErbB2-mediated mammary tumorigenesis. To examine the role of mutant p53 during ErbB2-mediated mammary tumorigenesis, a mutant p53 allele (R172H) was introduced into the (MMTV)-ErbB2/Neu mouse model system. Interestingly, we show in heterozygous p53 mice that mutant p53 R172H is a more potent activator of ErbB2-mediated mammary tumorigenesis than simple loss of p53. The more aggressive disease in mutant p53 animals was reflected by earlier tumor onset, increased mammary tumor multiplicity, and shorter survival. These in vivo and in vitro data provide mechanistic evidence that mutant p53 amplifies ErbB2 and EGFR signaling to promote the expansion of mammary stem cells and induce cell proliferation. IMPLICATIONS: This study identifies mutant p53 as an essential player in ErbB2 and EGFR-mediated mammary tumorigenesis and indicates the potential translational importance of targeting mutant p53 in this subset of patients with breast cancer.

Indexed as

MutationSignal TransductionAnimalsBreast NeoplasmsCarcinoma, Ductal, BreastCell Line, TumorCell ProliferationErb-b2 Receptor Tyrosine KinasesErbB ReceptorsFemaleHumansMammary Neoplasms, ExperimentalMiceNeoplastic Stem CellsSurvival AnalysisTumor Suppressor Protein p53EGFR protein, mouseErbb2 protein, mouseErb-b2 Receptor Tyrosine KinasesErbB ReceptorsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID25573952
PMCPMC4824060
OpenAlexW2139353479

What OpenQuestion holds

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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.