Evidence map›Paper›PMID 28212608›Full record

ArticleBMC genomics2017

Transcriptomic dynamics of breast cancer progression in the MMTV-PyMT mouse model.

Ying Cai, Ruben Nogales-Cadenas, Quanwei Zhang, Jhih-Rong Lin, Wen Zhang, Kelly O'Brien, Cristina Montagna, Zhengdong D Zhang

Abstract read
In one paragraph

Article in BMC genomics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
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

30 citing papers in PubMed.

  1. Article
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  6. Leveraging preclinical models of metastatic breast cancer.Biochimica et biophysica acta. Reviews on cancer · 2024
    Review
  7. Article
  8. Article
  9. A PDE Model of Breast Tumor Progression in MMTV-PyMT Mice.Journal of personalized medicine · 2022
    Article
  10. Article
  11. Article
  12. Interrelated Oncogenic Viruses and Breast Cancer.Frontiers in molecular biosciences · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. 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

8 authors.

Ying CaiDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA.ORCID 0000-0001-6550-1373
Ruben Nogales-CadenasDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA.
Quanwei ZhangDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA.
Jhih-Rong LinDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA.
Wen ZhangDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA.
Kelly O'BrienDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA.
Cristina MontagnaDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA.
Zhengdong D ZhangDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA. zhengdong.zhang@eisntein.yu.edu.

Funding

WORD PROCESSORP30CA013330 · NCI · YESHIVA UNIVERSITY · PI THOMAS E ROHAN · 1985 to 2026
$111.2M
Gene regulation in metastasis and new methods to analyze its microarray profilesR00LM009770 · NLM · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI ZHANG, ZHENGDONG · 2010 to 2012
$727k
NCI NIH HHS P30 CA013330NLM NIH HHS R00 LM009770
6 · The paper itself

Abstract

backgroundMalignant breast cancer with complex molecular mechanisms of progression and metastasis remains a leading cause of death in women. To improve diagnosis and drug development, it is critical to identify panels of genes and molecular pathways involved in tumor progression and malignant transition. Using the PyMT mouse, a genetically engineered mouse model that has been widely used to study human breast cancer, we profiled and analyzed gene expression from four distinct stages of tumor progression (hyperplasia, adenoma/MIN, early carcinoma and late carcinoma) during which malignant transition occurs.

resultsWe found remarkable expression similarity among the four stages, meaning genes altered in the later stages showed trace in the beginning of tumor progression. We identified a large number of differentially expressed genes in PyMT samples of all stages compared with normal mammary glands, enriched in cancer-related pathways. Using co-expression networks, we found panels of genes as signature modules with some hub genes that predict metastatic risk. Time-course analysis revealed genes with expression transition when shifting to malignant stages. These may provide additional insight into the molecular mechanisms beyond pathways.

conclusionsThus, in this study, our various analyses with the PyMT mouse model shed new light on transcriptomic dynamics during breast cancer malignant progression.

Indexed as

Disease ProgressionGene Expression ProfilingAnimalsAntigens, Polyomavirus TransformingDisease Models, AnimalFemaleGene ExpressionGene Regulatory NetworksHumansMammary Neoplasms, ExperimentalMammary Tumor Virus, MouseMiceNeoplasm MetastasisNeoplasm StagingAntigens, Polyomavirus TransformingBreast cancerPyMT mouse modelRNA-sequencing

Identifiers

PMID28212608
PMCPMC5316186

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LicenceCC BY
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Registered trials

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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.