Evidence map›Paper›PMID 27019623›Full record

ArticleInternational journal of biological sciences2016

Targeting Oncogenes into a Defined Subset of Mammary Cells Demonstrates That the Initiating Oncogenic Mutation Defines the Resulting Tumor Phenotype.

Kimberly R Holloway, Vidya C Sinha, Wen Bu, Michael Toneff, Jie Dong, Yi Peng, Yi Li

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
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  9. Effect of glycosides ofNeural regeneration research · 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

7 authors at 2 institutions in 2 countries.

Kimberly R Holloway1. Lester & Sue Smith Breast Center, Baylor College of Medicine, Houston, TX, USA;
Vidya C Sinha1. Lester & Sue Smith Breast Center, Baylor College of Medicine, Houston, TX, USA;; 2. Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA.
Wen Bu1. Lester & Sue Smith Breast Center, Baylor College of Medicine, Houston, TX, USA;; 2. Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA.
Michael Toneff2. Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA.
Jie Dong2. Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA.
Yi Peng3. National Center for International Research of Biological Targeting Diagnosis and Therapy, Guangxi Medical University, Nanning, Guangxi 530021, China;; 4. Guangxi Key Laboratory of Biological Targeting Diagnosis and Therapy Research, Guangxi Medical University, Nanning, Guangxi 530021, China.
Yi Li1. Lester & Sue Smith Breast Center, Baylor College of Medicine, Houston, TX, USA;; 2. Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA.
Baylor College of Medicine · USGuangxi Medical University · CN

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
TUMOR SUPPRESSOR GENES IN BREAST CANCER DEVELOPMENTP50CA058183 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI OSBORNE, C KENT · 1992 to 2012
$30.9M
The Core of the Computational BiologyU54CA149196 · NCI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI WONG, STEPHEN TC · 2010 to 2015
$10.6M
CELL &MOLECULAR BIOLOGY OF AGINGT32AG000183 · NIA · BAYLOR COLLEGE OF MEDICINE · PI DONEHOWER, LAWRENCE A. · 1989 to 2015
$3.7M
Oncogene susceptibility: physiological state & breast cell differentiationR01CA124820 · NCI · BAYLOR COLLEGE OF MEDICINE · PI LI, YI · 2010 to 2014
$1.5M
NCI NIH HHS CA124820NCI NIH HHS P30 CA125123NCI NIH HHS P30CA125123NCI NIH HHS P50 CA058183NCI NIH HHS P50-CA058183NCI NIH HHS R01 CA124820NCI NIH HHS U54 CA149196NCI NIH HHS U54CA149196NIA NIH HHS T32 AG000183NIA NIH HHS T32AG000183
6 · The paper itself

Abstract

Breast cancers exhibit high intertumoral heterogeneity in genetic alterations as well as histopathological and other phenotypic characteristics. The contribution of the initiating oncogenic mutation to tumor phenotype remains controversial, largely due to the technical difficulties in delivering genetic alterations into well-defined subsets of mammary epithelial cells. To examine how different initiating oncogenes drive tumor phenotype, we somatically delivered two oncogenes (ErbB2, PyMT) into a narrow and distinct subset of the mouse mammary epithelium defined by the expression of the progenitor marker keratin 6a (Krt6a), and compared the phenotypes of the resulting mammary tumors. While PyMT-induced tumors were well-differentiated and displayed glandular and papillary features, ErbB2-induced tumors were poorly differentiated and exhibited epithelial-to-mesenchymal transition as well as β-catenin activation. These in vivo data demonstrate that the initiating oncogene plays a key role in driving mammary tumor phenotype.

Indexed as

Animalsbeta CateninCell Transformation, NeoplasticEpithelial-Mesenchymal TransitionErb-b2 Receptor Tyrosine KinasesFemaleKeratin-6Mammary Glands, AnimalMammary Neoplasms, ExperimentalMiceMice, TransgenicMutationbeta CateninErb-b2 Receptor Tyrosine KinasesKeratin-6Breast CancerErbB2Keratin 6aPyMTRCAStva

Identifiers

PMID27019623
PMCPMC4807158
OpenAlexW2316514528

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.