Evidence map›Paper›PMID 35524261›Full record

ArticleCancer cell international2022

TNFRSF13B is a potential contributor to prostate cancer.

Chia-Yang Li, Shu-Pin Huang, Yei-Tsung Chen, Hsin-En Wu, Wei-Chung Cheng, Chao-Yuan Huang, Chia-Cheng Yu, Victor C Lin, Jiun-Hung Geng, Te-Ling Lu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

8 citing papers in PubMed, 10 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 6 institutions in 1 country.

Chia-Yang Li *Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, 807, Taiwan.
Shu-Pin Huang *Department of Urology, Kaohsiung Medical University Hospital, Kaohsiung, 807, Taiwan.
Yei-Tsung ChenDepartment of Life Sciences, Institute of Genome Sciences, National Yang Ming Chiao Tung University, Taipei, 112, Taiwan.
Hsin-En WuGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, 807, Taiwan.
Wei-Chung ChengGraduate Institute of Biomedical Science, China Medical University, Taichung, 40403, Taiwan.
Chao-Yuan HuangDepartment of Urology, College of Medicine, National Taiwan University Hospital, National Taiwan University, Taipei, 100, Taiwan.
Chia-Cheng YuDivision of Urology, Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, 813, Taiwan.
Victor C LinDepartment of Urology, E-Da Hospital, Kaohsiung, 824, Taiwan.
Jiun-Hung GengDepartment of Urology, Kaohsiung Medical University Hospital, Kaohsiung, 807, Taiwan.
Te-Ling LuDepartment of Pharmacy, China Medical University, 100 Jingmao Road Section 1, Taichung, 406, Taiwan.
Bo-Ying BaoDepartment of Pharmacy, China Medical University, 100 Jingmao Road Section 1, Taichung, 406, Taiwan. bao@mail.cmu.edu.tw.ORCID http://orcid.org/0000-0001-5510-6513
Kaohsiung Medical University · TWChina Medical University · TWNational Yang Ming Chiao Tung University · TWAsia University · TWE-Da Hospital · TWNational Taiwan University Hospital · TW

Funding

China Medical University, Taiwan CMU109-MF-65China Medical University, Taiwan CMU109-SR-64China Medical University, Taiwan CMU110-MF-59Kaohsiung Medical University KMU-DK(A)111003Kaohsiung Medical University NHRIKMU-111-I002Kaohsiung Medical University Chung-Ho Memorial Hospital KMUH105-5R42Kaohsiung Medical University Chung-Ho Memorial Hospital KMUH108-8R53Kaohsiung Medical University Chung-Ho Memorial Hospital KMUH108-8R55Kaohsiung Medical University Chung-Ho Memorial Hospital KMUH108-8R55, KMUH109-9R63, and KMUH109-9R64Kaohsiung Medical University Chung-Ho Memorial Hospital KMUH109-9R63Kaohsiung Medical University Chung-Ho Memorial Hospital KMUH109-9R63, and KMUH109-9R64Kaohsiung Medical University Chung-Ho Memorial Hospital KMUH109-9R64Kaohsiung Medical University Research Center KMU-TC108A04-4Ministry of Science and Technology, Taiwan 108-2314-B-037-026-MY2Ministry of Science and Technology, Taiwan 108-2314-B-037-029Ministry of Science and Technology, Taiwan 108-2320-B-039-050-MY3Ministry of Science and Technology, Taiwan 109-2314-B-037-106-MY3Ministry of Science and Technology, Taiwan 109-2314-B-037-108-MY2Ministry of Science and Technology, Taiwan 109-2320-B-037-007-MY3
6 · The paper itself

Abstract

backgroundImmunodeficiencies are genetic diseases known to predispose an individual to cancer owing to defective immunity towards malignant cells. However, the link between immunodeficiency and prostate cancer progression remains unclear. Therefore, the aim of this study was to evaluate the effects of common genetic variants among eight immunodeficiency pathway-related genes on disease recurrence in prostate cancer patients treated with radical prostatectomy.

methodsGenetic and bioinformatic analyses on 19 haplotype-tagging single-nucleotide polymorphisms in eight immunodeficiency pathway-related genes were conducted in 458 patients with prostate cancer after receiving radical prostatectomy. Furthermore, the TNFRSF13B was knocked down in 22Rv1 and PC-3 human prostate cancer cell lines via transfecting short hairpin RNAs and cell proliferation and colony formation assays were performed. The molecular mechanisms underlying the effects of TNFRSF13B were further explored by microarray gene expression profiling.

resultsTNFRSF13B rs4792800 was found to be significantly associated with biochemical recurrence even after adjustment for clinical predictors and false discovery rate correction (adjusted hazard ratio 1.78, 95% confidence interval 1.16-2.71, p = 0.008), and the G allele was associated with higher TNFRSF13B expression (p = 0.038). Increased TNFRSF13B expression suggested poor prognosis in four independent prostate cancer datasets. Furthermore, silencing TNFRSF13B expression resulted in decreased colony formation of 22Rv1 and PC-3 cells through modulating the cell cycle and p53 signalling pathways.

conclusionsThe present study suggests the potential role of immunodeficiency pathway-related genes, primarily TNFRSF13B, in prostate cancer progression.

Indexed as

Biochemical recurrenceBiomarkerImmunodeficiencyPrognosisProstate cancerTNFRSF13B

Identifiers

PMID35524261
PMCPMC9074181
OpenAlexW4229016870

What OpenQuestion holds

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LicenceCC BY
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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.