Evidence map›Paper›PMID 15359289›Full record

ArticleCancer gene therapy2004

Decreased tumorigenic potential of EphA2-overexpressing breast cancer cells following treatment with adenoviral vectors that express EphrinA1.

Loren W Noblitt, Dinesh S Bangari, Shruti Shukla, Deborah W Knapp, Sulma Mohammed, Michael S Kinch, Suresh K Mittal

Abstract read
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In one paragraph

Article in Cancer gene therapy, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

68 citing papers in PubMed, 118 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Identification of potent pan-ephrin receptor kinase inhibitors using DNA-encoded chemistry technology.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. EphrinB2-EphB4 Signaling in Neurooncological Disease.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

8 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

7 authors at 2 institutions in 1 country.

Loren W NoblittLaboratory of Gene Therapy, Purdue University, West Lafayette, Indiana 47907, USA.
Dinesh S Bangari
Shruti Shukla
Deborah W Knapp
Sulma Mohammed
Michael S Kinch
Suresh K Mittal
Purdue University Institute for Cancer ResearchPurdue University West Lafayette · US

Funding

Targeted Intervention Against EphA2 on Cancer CellsU01CA091318 · NCI · PURDUE UNIVERSITY WEST LAFAYETTE · PI KNAPP, DEBORAH W · 2001 to 2004
$919k
NCI NIH HHS U01 CA91318
6 · The paper itself

Abstract

The EphA2 receptor tyrosine kinase is frequently overexpressed in invasive breast cancer cells. Moreover, these malignant cells have unstable cell-cell contacts, which preclude EphA2 from interacting with its ligand, EphrinA1, which is anchored to the membrane of adjacent cells. This defect is important because ligand binding causes EphA2 to transmit signals that negatively regulate tumor cell growth and survival, whereas the absence of ligand binding favors these same behaviors. In our present study, human adenoviral type 5 (HAd) vectors were engineered to express secreted-forms of EphrinA1. These vectors were used to infect MDA-MB-231 human breast cancer cells, or MCF-10A human breast epithelial cells providing matched controls. Infection with HAd-EphrinA1-Fc (HAd vector expressing extracellular domain of human EphrinA1 attached to Fc portion of human IgG1 heavy chain) caused increased EphA2 activation and turnover and consequently decreased tumor cell viability in soft agar assays. Consistent with this observation, infection of MDA-MB-231 cells with HAd-EphrinA1-Fc prevented tumor formation in xenograft models. Furthermore, therapeutic modeling via intratumoral inoculation revealed that HAd-EphrinA1-Fc significantly inhibited subsequent tumor growth as compared to matched controls. These results suggest that targeting of EphA2 with adenoviral vectors may have therapeutic value.

Indexed as

Genetic VectorsAdenoviridaeBreast NeoplasmsCell Line, TumorEphrin-A1HumansInjections, IntralesionalPhosphorylationReceptor, EphA2Ephrin-A1Receptor, EphA2

Identifiers

PMID15359289
OpenAlexW2008259383

What OpenQuestion holds

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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.