Evidence map›Paper›PMID 14578451›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2003

Id-1 as a molecular target in therapy for breast cancer cell invasion and metastasis.

Sylvia Fong, Yoko Itahana, Tomoki Sumida, Jarnail Singh, Jean-Philippe Coppe, Yong Liu, Peter C Richards, James L Bennington, Nancy M Lee, Robert J Debs and 1 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

91 citing papers in PubMed, 204 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Telomere Maintenance and Oncogenesis.International journal of molecular sciences · 2025
    Review
  5. Observational
  6. Article
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  9. Article
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  14. Review
  15. Article
  16. Article
  17. Inhibitor of Differentiation 1 (Id1) in Cancer and Cancer Therapy.International journal of medical sciences · 2020
    Review
  18. Article
  19. Article
  20. Review

31 more citing papers are in PubMed but not listed here.

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

11 authors at 2 institutions in 1 country.

Sylvia FongCalifornia Pacific Medical Center, Cancer Research Institute, San Francisco, CA 94115, USA.
Yoko Itahana
Tomoki Sumida
Jarnail Singh
Jean-Philippe Coppe
Yong Liu
Peter C Richards
James L Bennington
Nancy M Lee
Robert J Debs
Pierre-Yves Desprez
Cancer Research Institute · USCalifornia Pacific Medical Center · US

Funding

Application of Novel Antigens and Integrated Microfluidics for Leprosy DiagnosisR01AI082575 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MODLIN, ROBERT L · 2009 to 2013
$1.7M
SYSTEMIC ANTIANGIOGENIC GENE THERAPY FOR BREAST CANCERR01CA082575 · NCI · CALIFORNIA PACIFIC MED CTR RES INSTITUTE · PI DEBS, ROBERT J · 1999 to 2002
$916k
ID-1 EXPRESSION IN BREAST EPITHELIAL CELLSR01CA082548 · NCI · CALIFORNIA PACIFIC MED CTR RES INSTITUTE · PI DESPREZ, PIERRE-YVES · 1999 to 2002
$644k
NCI NIH HHS R01 CA082548NCI NIH HHS R01 CA82548NCI NIH HHS R01 CA82575NIAID NIH HHS R01 AI082575
6 · The paper itself

Abstract

Mammary epithelial cells constitutively expressing Id-1 protein are unable to differentiate, acquire the ability to proliferate, and invade the extracellular matrix. In addition, Id-1 is aberrantly over-expressed in aggressive and metastatic breast cancer cells, as well as in human breast tumor biopsies from infiltrating carcinomas, suggesting Id-1 might be an important regulator of breast cancer progression. We show that human metastatic breast cancer cells become significantly less invasive in vitro and less metastatic in vivo when Id-1 is down-regulated by stable transduction with antisense Id-1. Expression of the matrix metalloproteinase MT1-MMP is decreased in proportion to the decrease in Id-1 protein levels, representing a potential mechanism for the reduction of invasiveness. Further, to more accurately recapitulate the biology of and potential therapeutic approaches to tumor metastasis, we targeted Id-1 expression systemically in tumor-bearing mice by using a nonviral approach. We demonstrate significant reduction of both Id-1 and MT1-MMP expressions as well as the metastatic spread of 4T1 breast cancer cells in syngeneic BALB/c mice. In conclusion, our studies have identified Id-1 as a critical regulator of breast cancer progression and suggest the feasibility of developing novel therapeutic approaches to target Id-1 expression to reduce breast cancer metastasis in humans.

Indexed as

Repressor ProteinsAnimalsBlotting, NorthernBlotting, WesternBreast NeoplasmsCell Line, TumorDisease ProgressionDown-RegulationExtracellular MatrixGenetic TherapyGenetic VectorsHumansImmunohistochemistryInhibitor of Differentiation Protein 1Lung NeoplasmsMatrix Metalloproteinase 14ID1 protein, humanIdb1 protein, mouseInhibitor of Differentiation Protein 1Matrix Metalloproteinase 14Matrix Metalloproteinases, Membrane-AssociatedMetalloendopeptidasesMmp14 protein, mouseOligonucleotides, AntisenseRepressor ProteinsTranscription Factors

Identifiers

PMID14578451
PMCPMC263850
OpenAlexW2081673344

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.