Evidence map›Paper›PMID 25815697›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2015

Blocking the adhesion cascade at the premetastatic niche for prevention of breast cancer metastasis.

Shin-Ae Kang, Nafis Hasan, Aman P Mann, Wei Zheng, Lichao Zhao, Lynsie Morris, Weizhu Zhu, Yan D Zhao, K Stephen Suh, William C Dooley and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.2field-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

38 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
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  6. Premetastatic niche mechanics and organotropism in breast cancer.npj biological physics and mechanics · 2025
    Review
  7. The origin of brain malignancies at the blood-brain barrier.Cellular and molecular life sciences : CMLS · 2023
    Review
  8. The Brain Pre-Metastatic Niche: Biological and Technical Advancements.International journal of molecular sciences · 2023
    Review
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  10. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 5 institutions in 1 country.

Shin-Ae KangDepartment of Pathology, Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Nafis HasanDepartment of Pharmaceutical Sciences, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.
Aman P MannInstitute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Wei ZhengDepartment of Pathology, Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Lichao ZhaoDepartment of Pathology, Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Lynsie MorrisDepartment of Pathology, Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Weizhu ZhuDepartment of Pathology, Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Yan D ZhaoDepartment of Pathology, Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
K Stephen SuhJohn Theurer Cancer Center, Hackensack University Medical Center, Hackensack, New Jersy, USA.
William C DooleyDepartment of Pathology, Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
David VolkInstitute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas, USA.
David G GorensteinInstitute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Massimo CristofanilliDepartment of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.
Hallgeir RuiDepartment of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.
Takemi TanakaDepartment of Pathology, Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA. Electronic address: takemi-tanaka@ouhsc.edu.
University of Oklahoma Health Sciences Center · USThe University of Texas Health Science Center at Houston · USThomas Jefferson University · USHackensack University Medical Center · USSidney Kimmel Cancer Center · US

Funding

Texas Center for Cancer NanomedicineU54CA151668 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI FERRARI, MAURO · 2010 to 2014
$12.4M
Biodefense Proteomics CollaboratoryU01AI054827 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI GORENSTEIN, DAVID G · 2003 to 2007
$6.1M
Subcellular localization of nanoparticlesRC2GM092599 · NIGMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI CHIU, WAH, DECUZZI, PAOLO · 2009 to 2010
$3.0M
Nanovectors for Characterization and Destruction of Breast Tumor VasculatureR01CA128797 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI FERRARI, MAURO · 2007 to 2010
$1.7M
Anti-Migration Therapy for Prevention and Treatment of Breast TumorR01CA160271 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI TANAKA, TAKEMI · 2012 to 2016
$1.6M
NCI NIH HHS 1R01CA160271-01A1NCI NIH HHS R01 CA128797NCI NIH HHS R01 CA160271NCI NIH HHS U54 CA151668NCI NIH HHS U54CA151668NIAID NIH HHS U01 AI054827
6 · The paper itself

Abstract

Shear-resistant adhesion and extravasation of disseminated cancer cells at the target organ is a crucial step in hematogenous metastasis. We found that the vascular adhesion molecule E-selectin preferentially promoted the shear-resistant adhesion and transendothelial migration of the estrogen receptor (ER)(-)/CD44(+) hormone-independent breast cancer cells, but not of the ER(+)/CD44(-/low) hormone-dependent breast cancer cells. Coincidentally, CD44(+) breast cancer cells were abundant in metastatic lung and brain lesions in ER(-) breast cancer, suggesting that E-selectin supports hematogenous metastasis of ER(-)/CD44(+) breast cancer. In an attempt to prevent hematogenous metastasis through the inhibition of a shear-resistant adhesion of CD44(+) cancer cells to E-selectin-expressing blood vessels on the premetastatic niche, an E-selectin targeted aptamer (ESTA) was developed. We demonstrated that a single intravenous injection of ESTA reduced metastases to a baseline level in both syngeneic and xenogeneic forced breast cancer metastasis models without relocating the site of metastasis. The effect of ESTA was absent in E-selectin knockout mice, suggesting that E-selectin is a molecular target of ESTA. Our data highlight the potential application of an E-selectin antagonist for the prevention of hematogenous metastasis of ER(-)/CD44(+) breast cancer.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsAptamers, NucleotideBreast NeoplasmsCell AdhesionCell Line, TumorEndothelial CellsE-SelectinFemaleGenetic TherapyHumansMCF-7 CellsMiceMice, Inbred BALB CNeoplasm MetastasisReceptors, EstrogenAptamers, NucleotideE-SelectinReceptors, Estrogen

Identifiers

PMID25815697
PMCPMC4817749
OpenAlexW2081148792

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.