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Drug-induced cell viability prediction from LINCS-L1000 through WRFEN-XGBoost algorithm

BACKGROUND: Predicting the drug response of the cancer diseases through the cellular perturbation signatures under the action of specific compounds is very important in personalized medicine. In the process of testing drug responses to the cancer, traditional experimental methods have been greatly h...

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Detalles Bibliográficos
Autores principales: Lu, Jiaxing, Chen, Ming, Qin, Yufang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7788947/
https://www.ncbi.nlm.nih.gov/pubmed/33407085
http://dx.doi.org/10.1186/s12859-020-03949-w
Descripción
Sumario:BACKGROUND: Predicting the drug response of the cancer diseases through the cellular perturbation signatures under the action of specific compounds is very important in personalized medicine. In the process of testing drug responses to the cancer, traditional experimental methods have been greatly hampered by the cost and sample size. At present, the public availability of large amounts of gene expression data makes it a challenging task to use machine learning methods to predict the drug sensitivity. RESULTS: In this study, we introduced the WRFEN-XGBoost cell viability prediction algorithm based on LINCS-L1000 cell signatures. We integrated the LINCS-L1000, CTRP and Achilles datasets and adopted a weighted fusion algorithm based on random forest and elastic net for key gene selection. Then the FEBPSO algorithm was introduced into XGBoost learning algorithm to predict the cell viability induced by the drugs. The proposed method was compared with some new methods, and it was found that our model achieved good results with 0.83 Pearson correlation. At the same time, we completed the drug sensitivity validation on the NCI60 and CCLE datasets, which further demonstrated the effectiveness of our method. CONCLUSIONS: The results showed that our method was conducive to the elucidation of disease mechanisms and the exploration of new therapies, which greatly promoted the progress of clinical medicine.