Article(id=1291753177402069444, tenantId=1146029695717560320, journalId=1291416913693474840, issueId=1291753151179280707, articleNumber=PA20260408_h937kb6D, orderNo=null, doi=10.3969/j.issn.1671-7856.2026.06.006, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1755792000000, receivedDateStr=2025-08-22, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785907557107, onlineDateStr=2026-08-05, pubDate=1774800000000, pubDateStr=2026-03-30, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785907557106, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785907557106, creator=admin, updateTime=1785907557106, updator=admin, issue=Issue{id=1291753151179280707, tenantId=1146029695717560320, journalId=1291416913693474840, year='2026', volume='36', issue='6', pageStart='1', pageEnd='144', issueExtLink='null', onlineDate='null', pubDate='1774800000000', pubDateStr='2026-03-30', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1785907550854, creator='ztmeta', updateTime=1786331902788, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1293533012289941791, tenantId=1146029695717560320, journalId=1291416913693474840, issueId=1291753151179280707, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1293533012289941792, tenantId=1146029695717560320, journalId=1291416913693474840, issueId=1291753151179280707, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=51, endPage=68, ext={EN=ArticleExt(id=1291753192480592326, articleId=1291753177402069444, tenantId=1146029695717560320, journalId=1291416913693474840, language=EN, title=Preliminary study on selection of CD19 and CD79A as factors for lung adenocarcinoma microenvironment remodeling and prognosis using the programmed cell death genome in combination with The Cancer Genome Atlas database, columnId=1292760394137887571, journalTitle=Chinese Journal of Comparative Medicine, columnName=Reseaech Reports, runingTitle=null, highlight=null, articleAbstract=
Objective Lung adenocarcinoma (LUAD) has a poor prognosis. This study aimed to screen core genes associated with the tumor microenvironment (TME) and programmed cell death (PCD) to provide new prognostic markers and therapeutic targets for LUAD, and to validate their cross-species conservation. Methods Based on RNA-seq data for LUAD and normal lung tissue in The Cancer Genome Atlas (TCGA) database, we assessed the TME and screened for differentially expressed genes (DEGs) using the ESTIMATE algorithm. Functional enrichment analysis (Gene Ontology/Kyoto Encyclopedia of Genes and Genomes), protein-protein interaction (PPI) networks, and univariate Cox regression analysis were performed on the DEGs. Cross-screening combining PPI networks, univariate Cox regression, and the PCD genome was employed to identify core prognostic genes, and their prognostic value and TME association were validated by survival analysis, gene set enrichment analysis (GSEA), and immune infiltration (CIBERSORT) analysis.
Results High immune/ESTIMATE scores were significantly associated with prolonged patient survival. The selected shared DEGs were primarily enriched in immune-related pathways. Cross-analysis identified CD19 and CD79A as core prognostic genes associated with PCD. Clinical-feature analysis showed that CD19 and CD79A expression were significantly higher in LUAD tumors than in normal lung tissues, but their expression levels decreased significantly with advancing TNM staging, closely associated with advanced staging, distant metastasis, and poor prognosis. Patients with high CD19/CD79A expression had significantly longer overall survival than those with low expression. Animal-model validation confirmed the cross-species conserved role of CD19/CD79A in tumor progression. GSEA indicated that the high-CD19/CD79Aexpression group was significantly enriched in immune activation pathways (e. g. , allograft rejection, complement response), while the low-expression group was enriched in metabolic (glycolysis, oxidative phosphorylation) and oncogenic pathways. CIBERSORT analysis confirmed that their expression levels were significantly positively correlated with TME immune activity. Conclusions CD19 and CD79A are overexpressed in LUAD tumor tissues, but their expression levels decrease with disease progression. High expression of CD19/CD79A is closely associated with a favorable prognosis and immune-activated TME, while low expression suggests a poor prognosis and immune suppression/oncogenic states. As genes associated with PCD, CD19/CD79A may serve as potential protective prognostic biomarkers and immunotherapeutic targets in LUAD, thereby providing a basis for understanding the immune mechanisms of LUAD and guiding the development of B cell-targeted therapeutic strategies.
, authors=Jiaheng YU
1, 3, Yunqi CHU
1, 3, Chaojin HONG
1, 3, Xingzi LIN
1, 3, Shengxia XU
2, 3, Yuehuan LIU
3, *, authorsList=Jiaheng YU, Yunqi CHU, Chaojin HONG, Xingzi LIN, Shengxia XU, Yuehuan LIU, authorCompany=null, correspAuthors=Yuehuan LIU, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1291753190488297925, articleId=1291753177402069444, tenantId=1146029695717560320, journalId=1291416913693474840, language=CN, title=程序性死亡基因组结合TCGA数据库筛选CD19和CD79A作为肺腺癌微环境重塑和预后因子的初步研究, columnId=1292760394347606213, journalTitle=中国比较医学杂志, columnName=研究报告, runingTitle=null, highlight=null, articleAbstract=
目的 肺腺癌(LUAD)预后不佳,本研究旨在筛选与肿瘤微环境(TME)和程序性细胞死亡(PCD)相关的核心预后基因,为LUAD提供新的预后标志物和治疗靶点,并验证其跨物种保守性。
方法 基于TCGA数据库LUAD和正常肺组织RNA-seq数据,利用ESTIMATE算法评估TME并筛选差异表达基因(DEGs)。对DEGs进行功能富集(GO/KEGG)、蛋白质互作(PPI)网络和单变量COX回归分析。联合PPI网络、单变量COX回归与PCD基因组进行交叉筛选,以确定核心预后基因。通过生存分析、基因组富集(GSEA)和免疫浸润(CIBERSORT)分析验证其预后价值和TME关联。
结果 高免疫/ESTIMATE评分与患者生存期延长显著相关。筛选出的共享DEGs主要富集于免疫相关通路。交叉分析确定CD19和CD79A为与PCD相关的核心预后基因。临床特征分析显示,CD19和CD79A在LUAD肿瘤组织中的表达显著高于正常肺组织,但其表达水平随TNM分期进展而显著下降,与晚期分期、远处转移及不良预后密切相关。生存分析表明,CD19/CD79A高表达的LUAD患者总生存期显著长于低表达患者。动物模型验证了CD19/CD79A在肿瘤进展中的跨物种保守作用。GSEA分析表明,CD19/CD79A高表达组显著富集于免疫激活通路(如异体移植排斥、补体反应),而低表达组则富集于代谢(糖酵解、氧化磷酸化)及促癌通路。免疫浸润(CIBERSORT)分析进一步证实其表达水平与TME免疫活性呈显著正相关。结论CD19和CD79A在LUAD肿瘤组织中表达升高,但其表达水平随疾病进展而降低。高表达CD19/CD79A与良好预后及免疫激活的TME密切相关,而低表达则提示不良预后并与免疫抑制/促癌状态相关。CD19和CD79A是PCD相关基因,可作为LUAD潜在的保护性预后生物标志物和免疫治疗靶点,为理解LUAD免疫机制及开发B细胞靶向治疗策略提供依据。
, authors=虞家恒
1, 3, 褚云起
1, 3, 洪超金
1, 3, 林幸子
1, 3, 徐圣霞
2, 3, 刘月环
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1.School of Clinical Medicine, Hangzhou Medical College, Hangzhou 310053, China
3.Hangzhou Medical College, Zhejiang Center of Laboratory animals , Hangzhou 310013, bio=null, bioImg=null, bioContent=null, aboutCorrespAuthor=null), CN=AuthorExt(id=1292760407966507941, tenantId=1146029695717560320, journalId=1291416913693474840, articleId=1291753177402069444, authorId=1292760407811318689, language=CN, stringName=虞家恒, firstName=null, middleName=null, lastName=null, prefix=null, suffix=null, authorComment=null, nameInitials=null, affiliation=null, department=null, xref=
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1.杭州医学院临床医学院,杭州 310053
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虞家恒(2003—),男,本科,研究方向:实验动物模型标准化与中医药科学化基础。E-mail: 1290090906@qq.com
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虞家恒(2003—),男,本科,研究方向:实验动物模型标准化与中医药科学化基础。E-mail: 1290090906@qq.com
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1.School of Clinical Medicine, Hangzhou Medical College, Hangzhou 310053, China
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1.杭州医学院临床医学院,杭州 310053
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1.School of Clinical Medicine, Hangzhou Medical College, Hangzhou 310053, China
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1.杭州医学院临床医学院,杭州 310053
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1.School of Clinical Medicine, Hangzhou Medical College, Hangzhou 310053, China
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1.杭州医学院临床医学院,杭州 310053
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