Evidence map›Paper›PMID 30229281›Full record

ReviewDer Pathologe2018

[Regulator proteins of actin dynamics as possible targets of antineoplastic therapies].

K Steinestel

Abstract readReview
PubMed Publisher
In one paragraph

Review in Der Pathologe, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 87% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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.

K SteinestelInstitut für Pathologie und Molekularpathologie, Bundeswehrkrankenhaus Ulm, Oberer Eselsberg 40, 89081, Ulm, Deutschland. konradsteinestel@bundeswehr.org.
Bundeswehrkrankenhaus · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe ability of tumor cells to leave the primary tumor is prerequisite for metastatic spread. In previous studies, we identified regulator proteins of actin reorganization with essential functions in both synaptogenesis and tumor cell migration.

objectiveThe aim of the studies summarized in this article is to identify signaling pathways associated with actin-related proteins that might represent potential molecular targets for antiinvasive and/or antineoplastic therapies. MATERIALS AND

methodsWe used immunohistochemical analyses of protein expression as well as in vitro techniques (cell culture, fluorescence microscopy, RNAi-based knockdown of protein expression, protein biochemistry and in vivo animal experiment substitutes).

resultsWe show that phosphorylation of Abelson interactor 1 (Abi1) is essential for the adhesion and invasion of colorectal carcinoma cells and might be targeted by the tyrosine kinase inhibitor STI571/Glivec®. HnRNP K, a protein interaction partner of Abi1, is upregulated in malignant melanoma in response to ionizing radiation; this upregulation is impaired upon application of the MEK inhibitor PD98059, enhancing radiosensivity of melanoma. Edelfosin, an alkyl-lipid blocker of the Abi1 interaction partner SK3, inhibits invasion of urothelial carcinoma cells.

conclusionThe studies summarized in this overview confirm a central role for the investigated proteins in tumor cell invasion and resistance to antineoplastic therapies and identify possible molecular targets for novel therapeutic compounds.

Indexed as

Colorectal NeoplasmsActinsAnimalsAntineoplastic AgentsCell Line, TumorCell MovementPhosphorylationSignal TransductionActinsAntineoplastic AgentsCell migrationInvasionMetastasisRadioresistanceSynaptogenesis

Identifiers

PMID30229281
OpenAlexW2890749315

What OpenQuestion holds

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Registered trials

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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.