Evidence map›Paper›PMID 25394974›Full record

ReviewDer Pathologe2014

[Inflammation as molecular target in chondrosarcoma].

T Kalinski

Abstract readEnglish AbstractReview
PubMed Publisher
In one paragraph

Review in Der Pathologe, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact, top 99% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. IL-1RA suppresses esophageal cancer cell growth by blocking IL-1α.Journal of clinical laboratory analysis · 2019
    Article
  3. 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

1 author at 1 institution in 1 country.

T KalinskiInstitut für Pathologie, Otto-von-Guericke-Universität, Leipziger Str. 44, 39120, Magdeburg, Deutschland, kalinski@med.ovgu.de.
Otto-von-Guericke University Magdeburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation is a hallmark in the development and progression of malignant tumors. In chondrosarcoma the inflammatory changes are relatively discrete; however, tumor-associated macrophages (TAM) may exert tumor-promoting effects. Interleukin (IL)-1 is an inflammatory cytokine which is produced by TAMs and which leads to the expression of NF-κB-regulated genes in chondrosarcoma cells, such as vascular endothelial growth factor A (VEGF-A). Through IL-1 antagonists and substances, such as curcumin IL-1-induced VEGF-A expression and angiogenesis can be blocked; therefore, IL-1-blockade provides an interesting therapy target for chondrosarcoma.

Indexed as

Molecular Targeted TherapyAntineoplastic AgentsBone NeoplasmsChondrosarcomaGene Expression Regulation, NeoplasticHumansInflammationInterleukin-1MacrophagesNF-kappa BVascular Endothelial Growth Factor AAntineoplastic AgentsInterleukin-1NF-kappa BVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID25394974
OpenAlexW302268905

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.