Evidence map›Paper›PMID 19805309›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

Genetic heterogeneity of Myc-induced mammary tumors reflecting diverse phenotypes including metastatic potential.

Eran R Andrechek, Robert D Cardiff, Jeffrey T Chang, Michael L Gatza, Chaitanya R Acharya, Anil Potti, Joseph R Nevins

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

60 citing papers in PubMed, 87 citations in OpenAlex.

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  19. How to Choose a Mouse Model of Breast Cancer, a Genomic Perspective.Journal of mammary gland biology and neoplasia · 2019
    Review
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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 4 institutions in 1 country.

Eran R AndrechekDuke Institute for Genome Sciences and Policy, Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC 27710, USA.
Robert D Cardiff
Jeffrey T Chang
Michael L Gatza
Chaitanya R Acharya
Anil Potti
Joseph R Nevins
Duke University Hospital · USDuke Medical Center · USDuke University · USUniversity of California, Davis · US

Funding

Integration of Oncogenic Networks in Cancer PhenotypesU54CA112952 · NCI · DUKE UNIVERSITY · PI NEVINS, JOSEPH R · 2004 to 2009
$12.4M
Mechanisms of breast cancer progressionU01CA105490 · NCI · UNIVERSITY OF PENNSYLVANIA · PI CHODOSH, LEWIS A · 2004 to 2013
$6.7M
The Center for Translational Genomic PhenotypingU01CA141582 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CARDIFF, ROBERT D, CHERRY, SIMON R · 2009 to 2013
$3.5M
Molecular Mechanisms of E2F SpecificityR01CA104663 · NCI · DUKE UNIVERSITY · PI NEVINS, JOSEPH R · 2003 to 2012
$3.4M
Oncogenic Gene Regulatory NetworksR01CA106520 · NCI · DUKE UNIVERSITY · PI CHI, JEN-TSAN ASHLEY · 2005 to 2014
$2.9M
Functional Components of the Rb/E2F and p53 PathwaysR00LM009837 · NLM · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI CHANG, JEFFREY T · 2010 to 2012
$699k
NCI NIH HHS 2R01CA104663-06NCI NIH HHS 5R01CA106520-04NCI NIH HHS 5U54CA112952-05NCI NIH HHS R01 CA104663NCI NIH HHS R01 CA106520NCI NIH HHS U01 CA105490NCI NIH HHS U01 CA141582NCI NIH HHS U54 CA112952NLM NIH HHS R00 LM009837
6 · The paper itself

Abstract

Human cancers result from a complex series of genetic alterations, resulting in heterogeneous disease states. Dissecting this heterogeneity is critical for understanding underlying mechanisms and providing opportunities for therapeutics matching the complexity. Mouse models of cancer have generally been used to reduce this complexity and focus on the role of single genes. Nevertheless, our analysis of tumors arising in the MMTV-Myc model of mammary carcinogenesis reveals substantial heterogeneity, seen in both histological and expression phenotypes. One contribution to this heterogeneity is the substantial frequency of activating Ras mutations. Additionally, we show that these Myc-induced mammary tumors exhibit even greater heterogeneity, revealed by distinct histological subtypes as well as distinct patterns of gene expression, than many other mouse models of tumorigenesis. Two of the major histological subtypes are characterized by differential patterns of cellular signaling pathways, including beta-catenin and Stat3 activities. We also demonstrate that one of the MMTV-Myc mammary tumor subgroups exhibits metastatic capacity and that the signature derived from the subgroup can predict metastatic potential of human breast cancer. Together, these data reveal that a combination of histological and genomic analyses can uncover substantial heterogeneity in mammary tumor formation and therefore highlight aspects of tumor phenotype not evident in the population as a whole.

Indexed as

ActinsAnimalsCluster AnalysisGene Expression ProfilingGene Expression Regulation, NeoplasticGenetic HeterogeneityImmunohistochemistryKeratin-18Mammary Neoplasms, ExperimentalMiceMice, TransgenicMuscle, SmoothNeoplasm MetastasisOligonucleotide Array Sequence AnalysisOncogene Proteins v-mybReverse Transcriptase Polymerase Chain ReactionActinsKeratin-18Oncogene Proteins v-mybVimentin

Identifiers

PMID19805309
PMCPMC2752567
OpenAlexW2026433475

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.