Evidence map›Paper›PMID 23470966›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2013

Inhibition of established micrometastases by targeted drug delivery via cell surface-associated GRP78.

Yu Rebecca Miao, Bedrich L Eckhardt, Yuan Cao, Renata Pasqualini, Pedram Argani, Wadih Arap, Robert G Ramsay, Robin L Anderson

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 79 citations in OpenAlex.

  1. Review
  2. Stress-induced translocation of the endoplasmic reticulum chaperone GRP78/BiP and its impact on human disease and therapy.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. 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

8 authors at 3 institutions in 2 countries.

Yu Rebecca MiaoMetastasis Research Laboratory, Peter MacCallum Cancer Centre, Melbourne, Australia.
Bedrich L Eckhardt
Yuan Cao
Renata Pasqualini
Pedram Argani
Wadih Arap
Robert G Ramsay
Robin L Anderson
University of Melbourne · AUPeter MacCallum Cancer Centre · AUThe University of Texas MD Anderson 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
NCI NIH HHS U54 CA151668Worldwide Cancer Research 07-0158
6 · The paper itself

Abstract

purposeThe major cause of morbidity in breast cancer is development of metastatic disease, for which few effective therapies exist. Because tumor cell dissemination is often an early event in breast cancer progression and can occur before diagnosis, new therapies need to focus on targeting established metastatic disease in secondary organs. We report an effective therapy based on targeting cell surface-localized glucose-regulated protein 78 (GRP78). GRP78 is expressed normally in the endoplasmic reticulum, but many tumors and disseminated tumor cells are subjected to environmental stresses and exhibit elevated levels of GRP78, some of which are localized at the plasma membrane. EXPERIMENTAL DESIGN AND

resultsHere, we show that matched primary tumors and metastases from patients who died from advanced breast cancer also express high levels of GRP78. We used a peptidomimetic targeting strategy that uses a known GRP78-binding peptide fused to a proapoptotic moiety [designated bone metastasis targeting peptide 78 (BMTP78)] and show that it can selectively kill breast cancer cells that express surface-localized GRP78. Furthermore, in preclinical metastasis models, we show that administration of BMTP78 can inhibit primary tumor growth as well as prolong overall survival by reducing the extent of outgrowth of established lung and bone micrometastases.

conclusionsThe data presented here provide strong evidence that it is possible to induce cell death in established micrometastases by peptide-mediated targeting of cell surface-localized GRP in advanced breast cancers. The significance to patients with advanced breast cancer of a therapy that can reduce established metastatic disease should not be underestimated.

Indexed as

Amino Acid SequenceAnimalsBreast NeoplasmsCell LineCell Line, TumorCell MembraneCell SurvivalDrug Delivery SystemsEndoplasmic Reticulum Chaperone BiPFemaleHeat-Shock ProteinsHumansImmunohistochemistryLung NeoplasmsMammary Neoplasms, ExperimentalMiceEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsHSPA5 protein, humanHspa5 protein, mousePeptides

Identifiers

PMID23470966
PMCPMC4331071
OpenAlexW2123501897

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.