Evidence map›Paper›PMID 32698506›Full record

ReviewInternational journal of molecular sciences2020

ADAM-Mediated Signalling Pathways in Gastrointestinal Cancer Formation.

Neele Schumacher, Stefan Rose-John, Dirk Schmidt-Arras

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  5. Article
  6. Article
  7. Review
  8. Article
  9. ADAM10 and ADAM17-Novel Players in Retinoblastoma Carcinogenesis.International journal of molecular sciences · 2022
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
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

3 authors at 1 institution in 1 country.

Neele SchumacherInstitute of Biochemistry, Christian-Albrechts-University, 24118 Kiel, Germany.
Stefan Rose-JohnInstitute of Biochemistry, Christian-Albrechts-University, 24118 Kiel, Germany.ORCID 0000-0002-7519-3279
Dirk Schmidt-ArrasInstitute of Biochemistry, Christian-Albrechts-University, 24118 Kiel, Germany.
Christian-Albrechts-Universität zu Kiel · DE

Funding

Deutsche Forschungsgemeinschaft Cluster of Excellence 'Precision Medicine'Deutsche Forschungsgemeinschaft SFB841, project C1Deutsche Forschungsgemeinschaft SFB877, project A1
6 · The paper itself

Abstract

Tumour growth is not solely driven by tumour cell-intrinsic mechanisms, but also depends on paracrine signals provided by the tumour micro-environment. These signals comprise cytokines and growth factors that are synthesized as trans-membrane proteins and need to be liberated by limited proteolysis also termed ectodomain shedding. Members of the family of A disintegrin and metalloproteases (ADAM) are major mediators of ectodomain shedding and therefore initiators of paracrine signal transduction. In this review, we summarize the current knowledge on how ADAM proteases on tumour cells but also on cells of the tumour micro-environment contribute to the formation of gastrointestinal tumours, and discuss how these processes can be exploited pharmacologically.

Indexed as

Signal TransductionADAM ProteinsAnimalsCytokinesDrug DiscoveryEnzyme InhibitorsErbB ReceptorsGastrointestinal NeoplasmsHumansMolecular Targeted TherapyTumor MicroenvironmentADAM ProteinsCytokinesEnzyme InhibitorsErbB ReceptorsADAMEGFRIL-6Notchproteasetumour micro-environment

Identifiers

PMID32698506
PMCPMC7404302
OpenAlexW3043706166

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.