Evidence map›Paper›PMID 25774632›Full record

ArticleCancer biology & therapy2015

Arginine deprivation by arginine deiminase of Streptococcus pyogenes controls primary glioblastoma growth in vitro and in vivo.

Tomas Fiedler, Madlen Strauss, Silvio Hering, Ulrike Redanz, Doreen William, Yvonne Rosche, Carl Friedrich Classen, Bernd Kreikemeyer, Michael Linnebacher, Claudia Maletzki

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.9field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 60 citations in OpenAlex.

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  6. Amino acid metabolism in health and disease.Signal transduction and targeted therapy · 2023
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  14. Novel molecules as the emerging trends in cancer treatment: an update.Medical oncology (Northwood, London, England) · 2022
    Review
  15. Review
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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

10 authors at 4 institutions in 5 countries.

Tomas Fiedlera Institute for Medical Microbiology, Virology, and Hygiene; Rostock University Medical Centre ; Rostock , Germany.
Madlen Strauss
Silvio Hering
Ulrike Redanz
Doreen William
Yvonne Rosche
Carl Friedrich Classen
Bernd Kreikemeyer
Michael Linnebacher
Claudia Maletzki
University of Rostock · DEInstitute of Medical Microbiology and Hygiene · DEMolecular Oncology (United States) · USUniwersytecki Szpital Dziecięcy · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arginine auxotrophy constitutes a weak point of several tumors, among them glioblastoma multiforme (GBM). Hence, those tumors are supposed to be sensitive for arginine-depleting substances, such as arginine deiminase (ADI). Here we elucidated the sensitivity of patient-individual GBM cell lines toward Streptococcus pyogenes-derived ADI. To improve therapy, ADI was combined with currently established and pre-clinical cytostatic drugs. Additionally, effectiveness of local ADI therapy was determined in xenopatients. Half of the GBM cell lines tested responded well toward ADI monotherapy. In those cell lines, viability decreased significantly (up to 50%). Responding cell lines were subjected to combination therapy experiments to test if any additive or even synergistic effects may be achieved. Such promising results were obtained in 2/3 cases. In cell lines HROG02, HROG05 and HROG10, ADI and Palomid 529 combinations were most effective yielding more than 70% killing after 2 rounds of treatment. Comparable boosted antitumoral effects were observed after adding chloroquine to ADI (>60% killing). Apoptosis, as well as cell cycle dysregulation were found to play a minor role. In some, but clearly not all cases, (epi-) genetic silencing of arginine synthesis pathway genes (argininosuccinate synthetase 1 and argininosuccinate lyase) explained obtained results. In vivo, ADI as well as the combination of ADI and SAHA efficiently controlled HROG05 xenograft growth, whereas adding Palomid 529 to ADI did not further increase the strong antitumoral effect of ADI. The cumulative in vitro and in vivo results proved ADI as a very promising candidate therapeutic, especially for development of adjuvant GBM combination treatments.

Indexed as

Xenograft Model Antitumor AssaysAnimalsAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsArginineArgininosuccinate LyaseArgininosuccinate SynthaseBenzopyransCell Line, TumorCell ProliferationChloroquineDNA MethylationGene Expression Regulation, NeoplasticGlioblastomaHumansHydrolasesAntineoplastic AgentsArgininearginine deiminaseArgininosuccinate LyaseArgininosuccinate SynthaseBenzopyransChloroquineHydrolasesHydroxamic Acidspalomid 529Recombinant ProteinsVorinostatADI, arginine deiminasearginine-catabolizing enzymesArg, L-ArginineASL, argininosuccinate lyasecellular metabolismcombination therapyGBM, Glioblastoma multiforme, ASS1, argininosuccinate synthetase 1patient-derived GBM cell linesSAHA, suberoylanilide hydroxamic acidxenopatient

Identifiers

PMID25774632
PMCPMC4623118
OpenAlexW1590754958

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.