Evidence map›Paper›PMID 28825725›Full record

ArticleOncogene2017

S100A7: from mechanism to cancer therapy.

L Padilla, S Dakhel, J Adan, M Masa, J M Martinez, L Roque, T Coll, R Hervas, C Calvis, L Llinas and 5 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 57 citations in OpenAlex.

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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

15 authors at 1 institution in 1 country.

L PadillaBiomed Division, LEITAT Technological Center, Barcelona, Spain.
S DakhelBiomed Division, LEITAT Technological Center, Barcelona, Spain.
J AdanBiomed Division, LEITAT Technological Center, Barcelona, Spain.
M MasaBiomed Division, LEITAT Technological Center, Barcelona, Spain.
J M MartinezBiomed Division, LEITAT Technological Center, Barcelona, Spain.
L RoqueBiomed Division, LEITAT Technological Center, Barcelona, Spain.
T CollBiomed Division, LEITAT Technological Center, Barcelona, Spain.
R HervasBiomed Division, LEITAT Technological Center, Barcelona, Spain.
C CalvisBiomed Division, LEITAT Technological Center, Barcelona, Spain.
L LlinasBiomed Division, LEITAT Technological Center, Barcelona, Spain.
S BuenestadoBiomed Division, LEITAT Technological Center, Barcelona, Spain.
J CastellsagueBiomed Division, LEITAT Technological Center, Barcelona, Spain.
R MesseguerBiomed Division, LEITAT Technological Center, Barcelona, Spain.
F MitjansBiomed Division, LEITAT Technological Center, Barcelona, Spain.
J L HernandezBiomed Division, LEITAT Technological Center, Barcelona, Spain.
Leitat Technological Center · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Within the tumor, malignant and stromal cells support each other by secreting a wide variety of growth factors and cytokines, allowing tumor growth and disease progression. The identification and regulation of those key factors in this crosstalk has opened the opportunity to develop new therapeutic strategies that not only act on the tumor cells but also on the stroma. Among these factors, S100A7 protein has gained interest in the last years. With key roles in cell motility its expression correlates with increased tumor growth, angiogenesis and metastatic potential. This work aims to deepen in the role played by extracellular S100A7 in the tumor microenvironment, offering a new integrative insight of its mechanism of action on each cellular compartment (tumor, endothelial, immune and fibroblast). As a result, we demonstrate its implication in cell migration and invasion, and its important contribution to the formation of a proinflammatory and proangiogenic environment that favors tumor progression and metastasis. Furthermore, we define its possible role in the pre-metastatic niche formation. Considering the relevance of S100A7 in cancer progression, we have developed neutralizing monoclonal antibodies, reporting for the first time the proof of principle of this promising therapeutic strategy for cancer treatment.

Indexed as

Xenograft Model Antitumor AssaysAnimalsAntibodies, MonoclonalAntibodies, NeutralizingCell Line, TumorCell MovementCells, CulturedFemaleHumansMice, Inbred BALB CMice, NudeNeoplasmsNeovascularization, PathologicRecombinant ProteinsS100 Calcium Binding Protein A7Tumor MicroenvironmentAntibodies, MonoclonalAntibodies, NeutralizingRecombinant ProteinsS100 Calcium Binding Protein A7

Identifiers

PMID28825725
OpenAlexW2746605095

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.