<?xml version="1.1" encoding="utf-8"?>
<article xsi:noNamespaceSchemaLocation="http://jats.nlm.nih.gov/publishing/1.1/xsd/JATS-journalpublishing1-mathml3.xsd" dtd-version="1.1" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"><front><journal-meta><journal-id journal-id-type="publisher-id">MRP</journal-id><journal-title-group><journal-title>Medical Research and Practice</journal-title></journal-title-group><issn>2993-9690</issn><eissn>2993-9704</eissn><publisher><publisher-name>Art and Design</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.61369/MRP.2358</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title>基于机器学习的胃腺癌基因诱导药物再利用研究</title><url>https://artdesignp.com/journal/MRP/1/5/10.61369/MRP.2358</url><author>师瑜英</author><pub-date pub-type="publication-year"><year>2023</year></pub-date><volume>1</volume><issue>5</issue><history><date date-type="pub"><published-time>2023-12-20</published-time></date></history><abstract>本研究通过药物再利用，开发了一个基于批量RNA转录组学胃腺癌药物的再利用计算流程。利用基因表达综合数据库（GEO）中的胃癌基因表达数据，我们鉴定出1004个差异表达基因，并将其作为潜在药物靶标的生成依据。此外，本项目从DrugBank中筛选了超过10,000种药物作为候选药物。为了深入探索药物再利用的潜力，我们构建了包括基因-基因相互作用和基因-靶标相互作用在内的多组学网络。这些网络有助于发现核心基因和再利用药物的目标，同时协助对药物进行有效排序。最终，结合药物-靶标相互作用的评分，我们对候选药物进行了综合排名。我们通过对排名靠前的药物在胃癌领域的临床试验证据和研究进行探讨，以验证这些药物的有效性和潜力。</abstract><keywords>药物再利用，机器学习，转录组学，胃癌</keywords></article-meta></front><body/><back><ref-list><ref id="B1" content-type="article"><label>1</label><element-citation publication-type="journal"><p>[1]Gao等，《A Pipeline to Call Multilevel Expression Changes between Cancer and Normal Tissues and Its Applications in Repurposing Drugs Effective for Gastric Cancer》.[2]Rudrapal, J. Khairnar和G. Jadhav, 《Drug Repurposing (DR)》.[3] Dudley, Deshpande 和Butte, 《Exploiting Drug-Disease Relationships for Computational Drug Repositioning》.[4] Rogers 和Hahn, 《Extended-Connectivity Fingerprints》.[5] Wang 等，《Ursolic Acid Inhibits Proliferation and Induces Apoptosis of Cancer Cells in Vitro and in Vivo》.[6] Chen, Li和Pan, 《Geldanamycin Induces Apoptosis in Human Gastric Carcinomas by Affecting Multiple Oncogenic Kinases That Have Synergic Effects with TNF-Related Apoptosis-Inducing Ligand》.[7]Liu等，《Parthenolide Increases the Sensitivity of Gastric Cancer Cells to Chemotherapy》.[8] Lee等，《Selumetinib plus docetaxel as second-line chemotherapy in KRAS mutant, KRAS amplified or MEK signatured gastric cancer patients: First arm of the umbrella trial in GC though the molecular screening, VIKTORY trial.》[9] Kim等，《Tivantinib Inhibits the VEGF Signaling Pathway and Induces Apoptosis in Gastric Cancer Cells with C-MET or VEGFA Amplification》.[10]Yamasaki等，《MEK Inhibition Suppresses Metastatic Progression of KRAS-Mutated Gastric Cancer》.[11]Claerhout 等，《Gene Expression Signature Analysis Identifies Vorinostat as a Candidate Therapy for Gastric Cancer》.</p><pub-id pub-id-type="doi"/></element-citation></ref></ref-list></back></article>
