Evidence map›Paper›PMID 32759058›Full record

ArticleMolecular therapy. Nucleic acids2020

An Improved Anticancer Drug-Response Prediction Based on an Ensemble Method Integrating Matrix Completion and Ridge Regression.

Chuanying Liu, Dong Wei, Ju Xiang, Fuquan Ren, Li Huang, Jidong Lang, Geng Tian, Yushuang Li, Jialiang Yang

Abstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

76 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. PROTACs in cancer therapy: targeted degradation of GPX4, PARP and epigenetic regulators.Journal of enzyme inhibition and medicinal chemistry · 2026
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16 more citing papers are in PubMed but not listed here.

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

9 authors.

Chuanying LiuSchool of Science, Yanshan University, Qinhuangdao, Hebei 066004, China.
Dong WeiSchool of Science, Yanshan University, Qinhuangdao, Hebei 066004, China.
Ju XiangCollege of Information Engineering, Changsha Medical University, Changsha, Hunan 410219, China; School of Information Science and Engineering, Central South University, Changsha 410083, China.
Fuquan RenSchool of Science, Yanshan University, Qinhuangdao, Hebei 066004, China.
Li HuangTianhang Experiment School, Hangzhou, Zhejiang 310004, China.
Jidong LangGeneis Beijing Co., Ltd., Beijing 100102, China.
Geng TianGeneis Beijing Co., Ltd., Beijing 100102, China.
Yushuang LiSchool of Science, Yanshan University, Qinhuangdao, Hebei 066004, China. Electronic address: yushuangli@ysu.edu.cn.
Jialiang YangCollege of Information Engineering, Changsha Medical University, Changsha, Hunan 410219, China; Geneis Beijing Co., Ltd., Beijing 100102, China. Electronic address: yangjl@geneis.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, we proposed an ensemble learning method, simultaneously integrating a low-rank matrix completion model and a ridge regression model to predict anticancer drug response on cancer cell lines. The model was applied to two benchmark datasets, including the Cancer Cell Line Encyclopedia (CCLE) and the Genomics of Drug Sensitivity in Cancer (GDSC). As previous studies suggest, the dual-layer integrated cell line-drug network model was one of the best models by far and outperformed most state-of-the-art models. Thus, we performed a head-to-head comparison between the dual-layer integrated cell line-drug network model and our model by a 10-fold crossvalidation study. For the CCLE dataset, our model has a higher Pearson correlation coefficient between predicted and observed drug responses than that of the dual-layer integrated cell line-drug network model in 18 out of 23 drugs. For the GDSC dataset, our model is better in 26 out of 28 drugs in the phosphatidylinositol 3-kinase (PI3K) pathway and 26 out of 30 drugs in the extracellular signal-regulated kinase (ERK) signaling pathway, respectively. Based on the prediction results, we carried out two types of case studies, which further verified the effectiveness of the proposed model on the drug-response prediction. In addition, our model is more biologically interpretable than the compared method, since it explicitly outputs the genes involved in the prediction, which are enriched in functions, like transcription, Src homology 2/3 (SH2/3) domain, cell cycle, ATP binding, and zinc finger.

Indexed as

anticancer drug responseensemble learning methodfunctional biomarkermatrix completionridge regression

Identifiers

PMID32759058
PMCPMC7403773

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.