Evidence map›Paper›PMID 33195193›Full record

ArticleFrontiers in cell and developmental biology2020

Identification of Prognostic Model and Biomarkers for Cancer Stem Cell Characteristics in Glioblastoma by Network Analysis of Multi-Omics Data and Stemness Indices.

Jianyang Du, Xiuwei Yan, Shan Mi, Yuan Li, Hang Ji, Kuiyuan Hou, Shuai Ma, Yixu Ba, Peng Zhou, Lei Chen and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.3field-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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

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  9. Cuprotosis clusters predict prognosis and immunotherapy response in low-grade glioma.Apoptosis : an international journal on programmed cell death · 2024
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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

12 authors at 3 institutions in 1 country.

Jianyang DuDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Xiuwei YanDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Shan MiDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Yuan LiDepartment of Pharmacology (The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, China.
Hang JiDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Kuiyuan HouDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Shuai MaDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Yixu BaDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Peng ZhouDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Lei ChenDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Rui XieDepartment of Digestive Internal Medicine, Harbin Medical University Cancer Hospital, Harbin, China.
Shaoshan HuDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Harbin Medical University · CNSecond Affiliated Hospital of Harbin Medical University · CNFirst Affiliated Hospital of Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The progression of most human cancers mainly involves the gradual accumulation of the loss of differentiated phenotypes and the sequential acquisition of progenitor and stem cell-like features. Glioblastoma multiforme (GBM) stem cells (GSCs), characterized by self-renewal and therapeutic resistance, play vital roles in GBM. However, a comprehensive understanding of GBM stemness remains elusive. Two stemness indices, mRNAsi and EREG-mRNAsi, were employed to comprehensively analyze GBM stemness. We observed that mRNAsi was significantly related to multi-omics parameters (such as mutant status, sample type, transcriptomics, and molecular subtype). Moreover, potential mechanisms and candidate compounds targeting the GBM stemness signature were illuminated. By combining weighted gene co-expression network analysis with differential analysis, we obtained 18 stemness-related genes, 10 of which were significantly related to survival. Moreover, we obtained a prediction model from both two independent cancer databases that was not only an independent clinical outcome predictor but could also accurately predict the clinical parameters of GBM. Survival analysis and experimental data confirmed that the five hub genes (CHI3L2, FSTL3, RPA3, RRM2, and YTHDF2) could be used as markers for poor prognosis of GBM. Mechanistically, the effect of inhibiting the proliferation of GSCs was attributed to the reduction of the ratio of CD133 and the suppression of the invasiveness of GSCs. The results based on an

Indexed as

connectivity mapglioblastomamachine learning methodsprognostic modelstemnesstumor immune environment

Identifiers

PMID33195193
PMCPMC7604309
OpenAlexW3093193313

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.