Evidence map›Paper›PMID 31400611›Full record

ArticleMolecular therapy. Nucleic acids2019

Genetic Interaction-Based Biomarkers Identification for Drug Resistance and Sensitivity in Cancer Cells.

Yue Han, Chengyu Wang, Qi Dong, Tingting Chen, Fan Yang, Yaoyao Liu, Bo Chen, Zhangxiang Zhao, Lishuang Qi, Wenyuan Zhao and 3 more

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 25 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

13 authors at 2 institutions in 1 country.

Yue HanDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, China.
Chengyu WangDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, China.
Qi DongDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, China.
Tingting ChenDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, China.
Fan YangDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, China.
Yaoyao LiuDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, China.
Bo ChenDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, China.
Zhangxiang ZhaoDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, China.
Lishuang QiDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, China.
Wenyuan ZhaoDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, China.
Haihai LiangDepartment of Pharmacology, College of Pharmacy, Harbin Medical University, Harbin, China.
Zheng GuoDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, China; Key Laboratory of Ministry of Education for Gastrointestinal Cancer, Department of Bioinformatics, Fujian Medical University, Fuzhou, China; Fujian Key Laboratory of Tumor Microbiology, Fujian Medical University, Fuzhou, China. Electronic address: guoz@ems.hrbmu.edu.cn.
Yunyan GuDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, China. Electronic address: guyunyan@ems.hrbmu.edu.cn.
Harbin Medical University · CNFujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells generally harbor hundreds of alterations in the cancer genomes and act as crucial factors in the development and progression of cancer. Gene alterations in the cancer genome form genetic interactions, which affect the response of patients to drugs. We developed an algorithm that mines copy number alteration and whole-exome mutation profiles from The Cancer Genome Atlas (TCGA), as well as functional screen data generated to identify potential genetic interactions for specific cancer types. As a result, 4,529 synthetic viability (SV) interactions and 10,637 synthetic lethality (SL) interactions were detected. The pharmacogenomic datasets revealed that SV interactions induced drug resistance in cancer cells and that SL interactions mediated drug sensitivity in cancer cells. Deletions of HDAC1 and DVL1, both of which participate in the Notch signaling pathway, had an SV effect in cancer cells, and deletion of DVL1 induced resistance to HDAC1 inhibitors in cancer cells. In addition, patients with low expression of both HDAC1 and DVL1 had poor prognosis. Finally, by integrating current reported genetic interactions from other studies, the Cancer Genetic Interaction database (CGIdb) (http://www.medsysbio.org/CGIdb) was constructed, providing a convenient retrieval for genetic interactions in cancer.

Indexed as

biomarkerdrug resistancedrug sensitivitysynthetic lethalitysynthetic viability

Identifiers

PMID31400611
PMCPMC6700431
OpenAlexW2958002629

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.