Evidence map›Paper›PMID 30397214›Full record

ArticleScientific reports2018

Proteomic approach for understanding milder neurotoxicity of Carfilzomib against Bortezomib.

Betul Karademir, Gulce Sari, Ayse Tarbin Jannuzzi, Sravani Musunuri, Grzegorz Wicher, Tilman Grune, Jia Mi, Husniye Hacioglu-Bay, Karin Forsberg-Nilsson, Jonas Bergquist and 1 more

Abstract read
In one paragraph

Article in Scientific reports, 2018. 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
–field-weighted citation impact
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.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Pathological Mechanisms of Bortezomib-Induced Peripheral Neuropathy.International journal of molecular sciences · 2021
    Review
  11. Review
  12. Review
  13. Article
  14. Effect of Bortezomib on Global Gene Expression in PC12-Derived Nerve Cells.International journal of molecular sciences · 2020
    Article
  15. Chemotherapy-Induced Peripheral Neuropathy and Changes in Cytoskeleton.International journal of molecular sciences · 2019
    Review
  16. 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

11 authors.

Betul KarademirDepartment of Biochemistry, School of Medicine/Genetic and Metabolic Diseases Research and Investigation Center, Marmara University, Istanbul, Turkey. betulkarademir@marmara.edu.tr.
Gulce SariDepartment of Biochemistry, School of Medicine/Genetic and Metabolic Diseases Research and Investigation Center, Marmara University, Istanbul, Turkey.
Ayse Tarbin JannuzziDepartment of Pharmaceutical Toxicology, Faculty of Pharmacy, Istanbul University, Istanbul, Turkey.
Sravani MusunuriDepartment of Chemistry - BMC, Analytical Chemistry, Uppsala University, Uppsala, Sweden.
Grzegorz WicherDepartment of Immunology, Genetics and Pathology, Neuro-Oncology, Uppsala University, Uppsala, Sweden.
Tilman GruneDepartment of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558, Nuthetal, Germany.
Jia MiDepartment of Chemistry - BMC, Analytical Chemistry, Uppsala University, Uppsala, Sweden.
Husniye Hacioglu-BayDepartment of Anatomy, School of Medicine, Marmara University, Istanbul, Turkey.
Karin Forsberg-NilssonDepartment of Immunology, Genetics and Pathology, Neuro-Oncology, Uppsala University, Uppsala, Sweden.
Jonas BergquistDepartment of Chemistry - BMC, Analytical Chemistry, Uppsala University, Uppsala, Sweden.ORCID http://orcid.org/0000-0002-4597-041X
Tobias JungDepartment of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558, Nuthetal, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The proteasomal system is responsible for the turnover of damaged proteins. Because of its important functions in oncogenesis, inhibiting the proteasomal system is a promising therapeutic approach for cancer treatment. Bortezomib (BTZ) is the first proteasome inhibitor approved by FDA for clinical applications. However neuropathic side effects are dose limiting for BTZ as many other chemotherapeutic agents. Therefore second-generation proteasome inhibitors have been developed including carfilzomib (CFZ). Aim of the present work was investigating the mechanisms of peripheral neuropathy triggered by the proteasome inhibitor BTZ and comparing the pathways affected by BTZ and CFZ, respectively. Neural stem cells, isolated from the cortex of E14 mouse embryos, were treated with BTZ and CFZ and mass spectrometry was used to compare the global protein pool of treated cells. BTZ was shown to cause more severe cytoskeletal damage, which is crucial in neural cell integrity. Excessive protein carbonylation and actin filament destabilization were also detected following BTZ treatment that was lower following CFZ treatment. Our data on cytoskeletal proteins, chaperone system, and protein oxidation may explain the milder neurotoxic effects of CFZ in clinical applications.

Indexed as

ProteomicsActinsBortezomibCell LineGene Expression RegulationHSP70 Heat-Shock ProteinsHumansNeural Stem CellsNeurotoxinsOligopeptidesProteasome InhibitorsProtein CarbonylationUbiquitinationActinsBortezomibcarfilzomibHSP70 Heat-Shock ProteinsNeurotoxinsOligopeptidesProteasome Inhibitors

Identifiers

PMID30397214
PMCPMC6218500

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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.