Evidence map›Paper›PMID 32781708›Full record

ArticleCancers2020

Aberrant BUB1 Overexpression Promotes Mitotic Segregation Errors and Chromosomal Instability in Multiple Myeloma.

Yuto Fujibayashi, Reiko Isa, Daichi Nishiyama, Natsumi Sakamoto-Inada, Norichika Kawasumi, Junko Yamaguchi, Saeko Kuwahara-Ota, Yayoi Matsumura-Kimoto, Taku Tsukamoto, Yoshiaki Chinen and 6 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 27 citations in OpenAlex.

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  16. The Role of Non-Coding RNAs in Chromosomal Instability in Cancer.The Journal of pharmacology and experimental therapeutics · 2023
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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

16 authors at 2 institutions in 1 country.

Yuto FujibayashiDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Reiko IsaDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Daichi NishiyamaDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Natsumi Sakamoto-InadaDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Norichika KawasumiDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Junko YamaguchiDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Saeko Kuwahara-OtaDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Yayoi Matsumura-KimotoDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Taku TsukamotoDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Yoshiaki ChinenDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Yuji ShimuraDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Tsutomu KobayashiDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Shigeo HoriikeDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Masafumi TaniwakiDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Hiroshi HandaDepartment of Hematology, Gunma University Graduate School of Medicine, Gunma 371-8511, Japan.ORCID 0000-0003-3753-9862
Junya KurodaDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.ORCID 0000-0001-6130-1550
Kyoto Prefectural University of Medicine · JPGunma University · JP

Funding

Japan Agency for Medical Research and Development JP16ck0106077h003, JP17ck0106348h0001, JP18ck0106348h0002 and JP19ck0106348h0003Japanese Society for Myeloma Research Award N.A.Ministry of Education, Culture, Sports, Science and Technology of Japan MEXT KAKENHI 16K09856, MEXT KAKENHI 18K08367Ministry of Health, Labour and Welfare of Japan H26-kakushin-teki-gan-ippan-074National Cancer Center Research and Development Funds 26-A-4, 29-A-3
6 · The paper itself

Abstract

Chromosome instability (CIN), the hallmarks of cancer, reflects ongoing chromosomal changes caused by chromosome segregation errors and results in whole chromosomal or segmental aneuploidy. In multiple myeloma (MM), CIN contributes to the acquisition of tumor heterogeneity, and thereby, to disease progression, drug resistance, and eventual treatment failure; however, the underlying mechanism of CIN in MM remains unclear. Faithful chromosomal segregation is tightly regulated by a series of mitotic checkpoint proteins, such as budding uninhibited by benzimidazoles 1 (BUB1). In this study, we found that BUB1 was overexpressed in patient-derived myeloma cells, and BUB1 expression was significantly higher in patients in an advanced stage compared to those in an early stage. This suggested the involvement of aberrant BUB1 overexpression in disease progression. In human myeloma-derived cell lines (HMCLs), BUB1 knockdown reduced the frequency of chromosome segregation errors in mitotic cells. In line with this, partial knockdown of BUB1 showed reduced variations in chromosome number compared to parent cells in HMCLs. Finally, BUB1 overexpression was found to promote the clonogenic potency of HMCLs. Collectively, these results suggested that enhanced BUB1 expression caused an increase in mitotic segregation errors and the resultant emergence of subclones with altered chromosome numbers and, thus, was involved in CIN in MM.

Indexed as

BUB1chromosomal instabilitychromosome segregation errorclonogenicitymultiple myeloma

Identifiers

PMID32781708
PMCPMC7464435
OpenAlexW3047389418

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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.