Evidence map›Paper›PMID 37039914›Full record

ArticleInternational journal of hematology2023

Mechanisms of preferential bone formation in myeloma bone lesions by proteasome inhibitors.

Emiko Nakaue, Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Takeshi Harada, Asuka Oda, Yusuke Inoue, So Shimizu, Yoshiki Higa, Kimiko Sogabe and 8 more

Open access · hybridAbstract read
In one paragraph

Article in International journal of hematology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

1 citing paper in PubMed, 5 citations in OpenAlex.

  1. Supportive care in myeloma-when treating the clone alone is not enough.Hematology. American Society of Hematology. Education Program · 2024
    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

18 authors at 2 institutions in 1 country.

Emiko NakaueDepartment of Orthodontics and Dentofacial Orthopedics, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Jumpei TeramachiDepartment of Oral Function and Anatomy, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University Graduate School, 2-5-1 Shikata, Okayama, 700-8525, Japan. jumptera@okayama-u.ac.jp.ORCID http://orcid.org/0000-0001-8722-5488
Hirofumi TenshinDepartment of Orthodontics and Dentofacial Orthopedics, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Masahiro HiasaDepartment of Orthodontics and Dentofacial Orthopedics, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Takeshi HaradaDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan.
Asuka OdaDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan.
Yusuke InoueDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan.
So ShimizuDepartment of Orthodontics and Dentofacial Orthopedics, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Yoshiki HigaDepartment of Orthodontics and Dentofacial Orthopedics, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Kimiko SogabeDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan.
Masahiro OuraDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan.
Tomoyo HaraDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan.
Ryohei SumitaniDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan.
Tomoko MaruhashiDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan.
Hiroki YamagamiDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan.
Itsuro EndoDepartment of Bioregulatory Sciences, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Eiji TanakaDepartment of Orthodontics and Dentofacial Orthopedics, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Masahiro AbeDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan. masabe@tokushima-u.ac.jp.
Tokushima University · JPOkayama University · JP

Funding

Japanese Society of Hematology 20247JSPS KAKENHI JP17KK0169JSPS KAKENHI JP20K18784JSPS KAKENHI JP21H03111JSPS KAKENHI JP22H03104JSPS KAKENHI JP22K08455JSPS KAKENHI JP22K19626University of Tokushima 1803003University of Tokushima 2202003
6 · The paper itself

Abstract

Proteasome inhibitors (PIs) can preferentially restore bone in bone-defective lesions of patients with multiple myeloma (MM) who respond favorably to these drugs. Most prior in vitro studies on PIs used continuous exposure to low PI concentrations, although pharmacokinetic analysis in patients has shown that serum concentrations of PIs change in a pulsatile manner. In the present study, we explored the effects of pulsatile treatment with PIs on bone metabolism to simulate in vivo PI pharmacokinetics. Pulsatile treatment with bortezomib, carfilzomib, or ixazomib induced MM cell death but only marginally affected the viability of osteoclasts (OCs) with F-actin ring formation. Pulsatile PI treatment suppressed osteoclastogenesis in OC precursors and bone resorption by mature OCs. OCs robustly enhanced osteoblastogenesis in cocultures with OCs and MC3T3-E1 pre-osteoblastic cells, indicating OC-mediated coupling to osteoblastogenesis. Importantly, pulsatile PI treatment did not impair robust OC-mediated osteoblastogenesis. These results suggest that PIs might sufficiently reduce MM cell-derived osteoblastogenesis inhibitors to permit OC-driven bone formation coupling while suppressing OC differentiation and activity in good responders to PIs. OC-mediated coupling to osteoblastogenesis appears to be a predominant mechanism for preferential occurrence of bone regeneration at sites of osteoclastic bone destruction in good responders.

Indexed as

Multiple MyelomaProteasome InhibitorsBortezomibHumansOsteoclastsOsteogenesisBortezomibProteasome InhibitorsMultiple myelomaOsteoblastOsteoclastProteasome inhibitorPulsatile treatment

Identifiers

PMID37039914
PMCPMC10284934
OpenAlexW4364352872

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.