Evidence map›Paper›PMID 28719033›Full record

ArticleMolecular oncology2017

Identification of driver copy number alterations in diverse cancer types and application in drug repositioning.

Wenbin Zhou, Zhangxiang Zhao, Ruiping Wang, Yue Han, Chengyu Wang, Fan Yang, Ya Han, Haihai Liang, Lishuang Qi, Chenguang Wang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

14 citing papers in PubMed, 21 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

12 authors at 1 institution in 1 country.

Wenbin ZhouDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, China.
Zhangxiang ZhaoDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, China.
Ruiping WangDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, China.
Yue HanDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, China.
Chengyu WangDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, China.
Fan YangDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, China.
Ya HanDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, China.
Haihai LiangDepartment of Pharmacology, Harbin Medical University, China.
Lishuang QiDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, China.
Chenguang WangDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, China.
Zheng GuoDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, China.
Yunyan GuDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, China.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Results from numerous studies suggest an important role for somatic copy number alterations (SCNAs) in cancer progression. Our work aimed to identify the drivers (oncogenes or tumor suppressor genes) that reside in recurrently aberrant genomic regions, including a large number of genes or non-coding genes, which remain a challenge for decoding the SCNAs involved in carcinogenesis. Here, we propose a new approach to comprehensively identify drivers, using 8740 cancer samples involving 18 cancer types from The Cancer Genome Atlas (TCGA). On average, 84 drivers were revealed for each cancer type, including protein-coding genes, long non-coding RNAs (lncRNA) and microRNAs (miRNAs). We demonstrated that the drivers showed significant attributes of cancer genes, and significantly overlapped with known cancer genes, including MYC, CCND1 and ERBB2 in breast cancer, and the lncRNA PVT1 in multiple cancer types. Pan-cancer analyses of drivers revealed specificity and commonality across cancer types, and the non-coding drivers showed a higher cancer-type specificity than that of coding drivers. Some cancer types from different tissue origins were found to converge to a high similarity because of the significant overlap of drivers, such as head and neck squamous cell carcinoma (HNSC) and lung squamous cell carcinoma (LUSC). The lncRNA SOX2-OT, a common driver of HNSC and LUSC, showed significant expression correlation with the oncogene SOX2. In addition, because some drivers are common in multiple cancer types and have been targeted by known drugs, we found that some drugs could be successfully repositioned, as validated by the datasets of drug response assays in cell lines. Our work reported a new method to comprehensively identify drivers in SCNAs across diverse cancer types, providing a feasible strategy for cancer drug repositioning as well as novel findings regarding cancer-associated non-coding RNA discovery.

Indexed as

DNA Copy Number VariationsDrug RepositioningGene Expression Regulation, NeoplasticGenomicsHumansMicroRNAsNeoplasmsOncogenesRNA, Long NoncodingMicroRNAsRNA, Long Noncodingcopy number alterationsdriverdrug repositioninglncRNAs

Identifiers

PMID28719033
PMCPMC5623819
OpenAlexW2739366076

What OpenQuestion 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 OpenQuestion graph.