Evidence map›Paper›PMID 31390566›Full record

ArticleCell reports2019

A Spontaneous Aggressive ERα+ Mammary Tumor Model Is Driven by Kras Activation.

Katie M Campbell, Kathleen A O'Leary, Debra E Rugowski, William A Mulligan, Erica K Barnell, Zachary L Skidmore, Kilannin Krysiak, Malachi Griffith, Linda A Schuler, Obi L Griffith

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Review
  3. Rat Models of Hormone Receptor-Positive Breast Cancer.Journal of mammary gland biology and neoplasia · 2024
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Prolactin: The Third Hormone in Breast Cancer.Frontiers in endocrinology · 2022
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
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

10 authors at 3 institutions in 1 country.

Katie M CampbellMcDonnell Genome Institute, Washington University School of Medicine, St. Louis, MO 63108, USA.
Kathleen A O'LearyDepartment of Comparative Biosciences, University of Wisconsin-Madison, Madison, WI 53706, USA.
Debra E RugowskiDepartment of Comparative Biosciences, University of Wisconsin-Madison, Madison, WI 53706, USA.
William A MulliganDepartment of Comparative Biosciences, University of Wisconsin-Madison, Madison, WI 53706, USA.
Erica K BarnellMcDonnell Genome Institute, Washington University School of Medicine, St. Louis, MO 63108, USA.
Zachary L SkidmoreMcDonnell Genome Institute, Washington University School of Medicine, St. Louis, MO 63108, USA.
Kilannin KrysiakMcDonnell Genome Institute, Washington University School of Medicine, St. Louis, MO 63108, USA; Division of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63108, USA.
Malachi GriffithMcDonnell Genome Institute, Washington University School of Medicine, St. Louis, MO 63108, USA; Division of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63108, USA; Department of Genetics, Washington University School of Medicine, St. Louis, MO 63108, USA; Siteman Cancer Center, Washington University School of Medicine, St. Louis, MO 63108, USA.
Linda A SchulerDepartment of Comparative Biosciences, University of Wisconsin-Madison, Madison, WI 53706, USA; University of Wisconsin Comprehensive Cancer Center, University of Wisconsin-Madison, Madison, WI 53706, USA. Electronic address: linda.schuler@wisc.edu.
Obi L GriffithMcDonnell Genome Institute, Washington University School of Medicine, St. Louis, MO 63108, USA; Division of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63108, USA; Department of Genetics, Washington University School of Medicine, St. Louis, MO 63108, USA; Siteman Cancer Center, Washington University School of Medicine, St. Louis, MO 63108, USA. Electronic address: obigriffith@wustl.edu.
James S. McDonnell Foundation · USUniversity of Wisconsin–Madison · USWashington University in St. Louis · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Justine Yang Bruce · 1985 to 2026
$142.6M
Matrix density promotes pro-tumorigenic hormone actions in breast cancerR01CA179556 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI PONIK, SUZANNE MARIE, SCHULER, LINDA A. · 2014 to 2024
$4.9M
Genomic and Functional Identification of Chemotherapy Resistance Mechanisms in Small Cell Lung CancerU01CA231844 · NCI · WASHINGTON UNIVERSITY · PI GOVINDAN, RAMASWAMY, GRIFFITH, OBI L. · 2018 to 2022
$3.1M
Prolactin: mammary progenitors and tumor initiating cells in luminal carcinomasR01CA157675 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI SCHULER, LINDA A. · 2011 to 2015
$1.5M
DEVELOPMENT OF INFORMATICS RESOURCES FOR INTERPRETATION OF CLINICALLY ACTIONABLE VARIANTS IN CANCERU01CA209936 · NCI · WASHINGTON UNIVERSITY · PI GRIFFITH, OBI L. · 2016 to 2018
$1.0M
Integrated Analysis & Interpretation of Whole Genome Exome & Transcriptome SequenR00HG007940 · NHGRI · WASHINGTON UNIVERSITY · PI GRIFFITH, MALACHI · 2017 to 2019
$724k
DEFINING THE REGULATORY, NON-CODING, MUTATIONAL LANDSCAPE OF BREAST CANCERK22CA188163 · NCI · WASHINGTON UNIVERSITY · PI GRIFFITH, OBI L. · 2014 to 2016
$515k
NCI NIH HHS K22 CA188163NCI NIH HHS P30 CA014520NCI NIH HHS R01 CA157675NCI NIH HHS R01 CA179556NCI NIH HHS U01 CA209936NCI NIH HHS U01 CA231844NHGRI NIH HHS R00 HG007940
6 · The paper itself

Abstract

The NRL-PRL murine model, defined by mammary-selective transgenic rat prolactin ligand rPrl expression, establishes spontaneous ER+ mammary tumors in nulliparous females, mimicking the association between elevated prolactin (PRL) and risk for development of ER+ breast cancer in postmenopausal women. Whole-genome and exome sequencing in a discovery cohort (n = 5) of end-stage tumors revealed canonical activating mutations and copy number amplifications of Kras. The frequent mutations in this pathway were validated in an extension cohort, identifying activating Ras alterations in 79% of tumors (23 of 29). Transcriptome analyses over the course of oncogenesis revealed marked alterations associated with Ras activity in established tumors compared with preneoplastic tissues; in cell-intrinsic processes associated with mitosis, cell adhesion, and invasion; as well as in the surrounding tumor environment. These genomic analyses suggest that PRL induces a selective bottleneck for spontaneous Ras-driven tumors that may model a subset of aggressive clinical ER+ breast cancers.

Indexed as

AgingAnimalsCarcinogenesisDatasets as TopicEstrogen Receptor alphaFemaleGene Expression ProfilingHumansMammary Neoplasms, ExperimentalMiceProlactinProto-Oncogene Proteins p21(ras)RatsSignal TransductionTransgenesEstrogen Receptor alphaHras protein, mouseKRAS protein, humanKras protein, ratProlactinProto-Oncogene Proteins p21(ras)breast cancerER+ breast cancergenomic analysesmouse modelsprolactinRas mutations

Identifiers

PMID31390566
PMCPMC6713291
OpenAlexW2965972967

What OpenQuestion holds

Textmetadata
LicenceTDM
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.