Evidence map›Paper›PMID 31807007›Full record

ArticleOncoTargets and therapy2019

Clinical Significance And Integrative Analysis Of Kinesin Family Member 18B In Lung Adenocarcinoma.

Yonglong Zhong, Lingyu Jiang, Xiaomao Long, Yifan Zhou, Shen Deng, Hui Lin, Xiangwei Li

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. International journal of molecular sciences · 2026
    Article
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  3. A competing TMPO-AS1-let-7b-5p-kinesin superfamily RNA network predicts poor lung cancer patient survival.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2026
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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

7 authors at 1 institution in 1 country.

Yonglong Zhong *Department of Thoracic Cardiovascular Surgery, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, People's Republic of China.
Lingyu Jiang *Intensive Care Unit, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, People's Republic of China.
Xiaomao LongDepartment of Thoracic Cardiovascular Surgery, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, People's Republic of China.
Yifan ZhouDepartment of Thoracic Cardiovascular Surgery, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, People's Republic of China.
Shen DengDepartment of Thoracic Cardiovascular Surgery, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, People's Republic of China.
Hui LinDepartment of Thoracic Cardiovascular Surgery, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, People's Republic of China.
Xiangwei LiDepartment of Thoracic Cardiovascular Surgery, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, People's Republic of China.
The People's Hospital of Guangxi Zhuang Autonomous Region · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKinesin family member 18B (KIF18B) is a member of the kinesin-8 superfamily, and functions as an oncogene in human cancers. However, its expression profile and role in lung adenocarcinoma (LUAD) remain unclear. MATERIALS AND

methodsWe examined the expression profile of KIF18B using quantitative real-time reverse transcription polymerase chain reaction and immunohistochemistry in fresh clinical samples. Using data downloaded from the Cancer Genome Atlas database and Gene Expression Omnibus, we explored the clinical significance of KIF18B, potential mechanisms of its dysregulation and its underlying biological function in LUAD.

resultsKIF18B was significantly over-expressed in LUAD tissues relative to normal tissues. High KIF18B expression was associated with smoking history, positive nodal invasion, advanced clinical stage, death status and poorer prognosis. Cox regression analyses revealed that KIF18B overexpression was an independent prognostic biomarker for poor overall survival (OS) and recurrence-free survival in LUAD. In addition, KIF18B mutation was observed in 2.2% of LUAD cases. DNA copy number variation was correlated with upregulated expression of KIF18B in LUAD tissues and cell lines. The methylation level of some KIF18B DNA CpG sites was negatively associated with its mRNA expression. KIF18B was predictively targeted by miR-125a-5p, which was downregulated in LUAD tissues, inversely correlated with KIF18B mRNA expression and significantly associated with poor OS. Furthermore, gene set enrichment analysis revealed that genes positively co-expressed with KIF18B were mainly enriched in cell cycle signaling pathways.

conclusionOur results indicate that KIF18B is a promising prognostic biomarker for LUAD. DNA amplification, hypomethylation as well as miR-125a-5p downregulation may be involved in the mechanism of KIF18B dysregulation in LUAD. KIF18B might function as a novel oncogene through cell cycle regulation pathways in LUAD.

Indexed as

bioinformatic analysiskinesinlung adenocarcinomamiR-125a-5pprognosis

Identifiers

PMID31807007
PMCPMC6842302
OpenAlexW2987823993

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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.