Evidence map›Paper›PMID 38287309›Full record

ArticleBMC medical genomics2024

Integrated analysis identifies GABRB3 as a biomarker in prostate cancer.

Jun-Yan Chen, Chi-Fen Chang, Shu-Pin Huang, Chao-Yuan Huang, Chia-Cheng Yu, Victor C Lin, Jiun-Hung Geng, Chia-Yang Li, Te-Ling Lu, Bo-Ying Bao

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC medical genomics, 2024. 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
1.3field-weighted citation impact, top 22% 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, 3 citations in OpenAlex.

  1. Article
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

10 authors at 7 institutions in 1 country.

Jun-Yan Chen *Department of Pharmacy, China Medical University, 100 Jingmao Road Section 1, 406, Taichung, Taiwan.
Chi-Fen Chang *Department of Anatomy, School of Medicine, China Medical University, 406, Taichung, Taiwan.
Shu-Pin Huang *Department of Urology, Kaohsiung Medical University Hospital, 807, Kaohsiung, Taiwan.
Chao-Yuan HuangDepartment of Urology, College of Medicine, National Taiwan University Hospital, National Taiwan University, 100, Taipei, Taiwan.
Chia-Cheng YuDivision of Urology, Department of Surgery, Kaohsiung Veterans General Hospital, 813, Kaohsiung, Taiwan.
Victor C LinDepartment of Urology, E-Da Hospital, 824, Kaohsiung, Taiwan.
Jiun-Hung GengDepartment of Urology, Kaohsiung Medical University Hospital, 807, Kaohsiung, Taiwan.
Chia-Yang LiGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, 807, Kaohsiung, Taiwan.
Te-Ling LuDepartment of Pharmacy, China Medical University, 100 Jingmao Road Section 1, 406, Taichung, Taiwan.
Bo-Ying BaoDepartment of Pharmacy, China Medical University, 100 Jingmao Road Section 1, 406, Taichung, Taiwan. bao@mail.cmu.edu.tw.
China Medical University · TWE-Da Hospital · TWKaohsiung Medical University · TWKaohsiung Medical University Chung-Ho Memorial Hospital · TWNational Sun Yat-sen University · TWNational Taiwan University Hospital · TWTajen University · TW

Funding

China Medical University, Taiwan CMU111-MF-09China Medical University, Taiwan CMU111-TC-08Kaohsiung Medical University NHRIKMU-111-I002National Science and Technology Council 111-2218-E-037-001National Science and Technology Council 111-2320-B-039-021-MY3National Science and Technology Council 112-2311-B-039-001
6 · The paper itself

Abstract

backgroundTreatment failure following androgen deprivation therapy (ADT) presents a significant challenge in the management of advanced prostate cancer. Thus, understanding the genetic factors influencing this process could facilitate the development of personalized treatments and innovative therapeutic strategies. The phosphoinositide 3-kinase (PI3K)/AKT signaling pathway plays a pivotal role in controlling cell growth and tumorigenesis. We hypothesized that genetic variants within this pathway may affect the clinical outcomes of patients undergoing ADT for prostate cancer.

methodsWe genotyped 399 single-nucleotide polymorphisms (SNPs) across 28 core PI3K/AKT pathway genes in a cohort of 630 patients with prostate cancer undergoing ADT. We assessed the potential association of the SNPs with patient survival. Functional analyses of the implicated genes were also performed to evaluate their effects on prostate cancer.

resultsAfter multivariate Cox regression analysis and multiple testing correction, GABRB3 rs12591845 exhibited the most significant association with both overall and cancer-specific survivals (P < 0.003). A comprehensive pooled analysis of 16 independent gene expression datasets revealed elevated expression of GABRB3 in prostate cancer tissues compared to that in normal tissues (P < 0.001). Furthermore, gene set enrichment analysis unveiled differential enrichment of pathways such as myogenesis, interferon γ and α responses, and the MYC proto-oncogene pathway in tumors with elevated GABRB3 expression, implying a role for GABRB3 in prostate cancer.

conclusionOur results suggest that rs12591845 could potentially serve as a valuable prognostic indicator for patients undergoing ADT. The potential role of GABRB3 in promoting prostate tumorigenesis is also highlighted.

Indexed as

Prostatic NeoplasmsAndrogen AntagonistsBiomarkersCarcinogenesisHumansMalePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, GABA-AAndrogen AntagonistsBiomarkersGABRB3 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, GABA-AGABRB3Gene set enrichment analysisPI3K/AKT pathwayProstate cancerSurvival

Identifiers

PMID38287309
PMCPMC10826114
OpenAlexW4391304187

What Socratic 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 Socratic graph.