Evidence map›Paper›PMID 32864713›Full record

ArticleInternational journal of hematology2021

The clonal evolution during long-term clinical course of multiple myeloma.

Yuko Mishima, Yuji Mishima, Yuko Shirouchi, Noriko Nishimura, Masahiro Yokoyama, Takashi Okabe, Norihito Inoue, Hideki Uryu, Takanori Fukuta, Kiyohiko Hatake and 1 more

Abstract readCase Reports
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In one paragraph

Article in International journal of hematology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

4 citing papers in PubMed, 3 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Yuko MishimaDepartment of Hematology Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto-ku, Tokyo, 135-8550, Japan. yuko.mishima@jfcr.or.jp.ORCID http://orcid.org/0000-0002-9742-8470
Yuji MishimaDivision of Clinical Research, The Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo, Japan.
Yuko ShirouchiDepartment of Hematology Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto-ku, Tokyo, 135-8550, Japan.
Noriko NishimuraDepartment of Hematology Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto-ku, Tokyo, 135-8550, Japan.
Masahiro YokoyamaDepartment of Hematology Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto-ku, Tokyo, 135-8550, Japan.
Takashi OkabeDepartment of Hematology Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto-ku, Tokyo, 135-8550, Japan.
Norihito InoueDepartment of Hematology Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto-ku, Tokyo, 135-8550, Japan.
Hideki UryuDepartment of Hematology Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto-ku, Tokyo, 135-8550, Japan.
Takanori FukutaDepartment of Hematology Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto-ku, Tokyo, 135-8550, Japan.
Kiyohiko HatakeDepartment of Hematology, International University of Health and Welfare, School of Medicine, Mita Hospital, Tokyo, Japan.
Yasuhito TeruiDepartment of Hematology Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto-ku, Tokyo, 135-8550, Japan.
The Cancer Institute Hospital · JPMita Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Somatic gene mutations related to acceleration disease and clonal evolution in multiple myeloma strongly influence severe clinical outcomes. In this study, we traced the transition of somatic mutations during the clinical course of myeloma patients over a long-term follow-up period (8.5 year average). Seven myeloma cases treated with immuno-chemotherapy at our institution were analyzed with clinical courses and the results of FISH and G-band analyses. Furthermore, the target sequences in regard to 121 genes, related to driver mutations or acceleration of disease in myeloma, were performed using bone marrow myeloma samples by next-generation sequencing, Ion Proton™ System. We detected a relationship between an increase in the dominant mutated gene (e.g., TP53, DIS3, FAM46C, KDM6B, and EGR1) and poor prognosis. In particular, clonal escalation of the TP53 mutation could not be overcome by any treatment. The selection of a combination treatment conducted in conjunction with the monitoring of gene mutations is appropriate for long-term survival. Our data demonstrate that long-term follow-up of somatic gene mutations during the clinical course of myeloma is helpful in the development of an effective treatment strategy.

Indexed as

Clonal EvolutionDisease SusceptibilityAgedBiomarkers, TumorCell Transformation, NeoplasticCombined Modality TherapyComputational BiologyDatabases, GeneticDisease ProgressionFemaleFollow-Up StudiesGenetic Predisposition to DiseaseGenetic TestingGenetic VariationHumansMiddle AgedBiomarkers, TumorClonal evolutionGene mutationMultiple myelomaResistance for therapySomatic gene mutation analysis

Identifiers

PMID32864713
OpenAlexW3082868445

What OpenQuestion holds

Textmetadata
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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.