Evidence map›Paper›PMID 27169614›Full record

ReviewInternational journal of hematology2016

Endoplasmic-reticulum stress pathway-associated mechanisms of action of proteasome inhibitors in multiple myeloma.

Masaki Ri

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in International journal of hematology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

75 citing papers in PubMed, 123 citations in OpenAlex.

  1. Review
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  14. Targeting Acetyl-CoA Carboxylase Suppresses De Novo Lipogenesis and Tumor Cell Growth in Multiple Myeloma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Targeting apoptotic pathways for cancer therapy.The Journal of clinical investigation · 2024
    Review

15 more citing papers are in PubMed but not listed here.

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.

Masaki RiDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-chou, Mizuho-ku, Nagoya, Aichi, 467-8601, Japan. rrmasaki@ybb.ne.jp.
Nagoya City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bortezomib (BTZ), a proteasome inhibitor, was initially reported as an inhibitor of the NF-κB pathway, which plays a critical role in the pathogenesis of multiple myeloma (MM). The NF-κB activity of MM cells is mediated via two distinct pathways, canonical and non-canonical, which show opposing activity after BTZ treatment in MM cells. Recent studies of proteasome inhibition in MM cells reveal that the accumulation of unfolded proteins in the endoplasmic reticulum (ER), referred to as ER stress, triggered the activity of several pro-apoptotic factors and sources of cell stress, such as the accumulation of reactive oxygen species (ROS), which is considered to be the main mechanism of action of BTZ-induced apoptosis. Several factors associated with ER stress and unfolded protein response (UPR) have been identified with the sensitivity of BTZ treatment. Low levels of XBP1, ATF3, and ATF4, which regulate UPR and ER stress-induced apoptosis, have been observed in poor responders to BTZ treatment, and three other genes, KLF9, Nampt, and CDK5, are associated with response to BTZ-containing therapy. These findings contribute to a better understanding of the mechanisms underlying BTZ-induced apoptosis in MM cells; however, further study is needed to develop potential predictive biomarkers of efficacy of BTZ-containing therapy.

Indexed as

ApoptosisBortezomibEndoplasmic Reticulum StressHumansMultiple MyelomaProteasome InhibitorsUnfolded Protein ResponseBortezomibProteasome InhibitorsBortezomibER stressMechanism of actionMultiple myelomaNF-κB

Identifiers

PMID27169614
OpenAlexW2354070186

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.