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An Integrated Approach For Uncovering Novel DNA Methylation Biomarkers For Non-small Cell Lung Carcinoma

為了解決電腦 更新中 如何 停止的問題，作者VAIBHAV KUMAR SUNKARIA 這樣論述：

Introduction - Lung cancer is one of primal and ubiquitous cause of cancer related fatalities in the world. Leading cause of these fatalities is non-small cell lung cancer (NSCLC) with a proportion of 85%. The major subtypes of NSCLC are Lung Adenocarcinoma (LUAD) and Lung Small Cell Carcinoma (LUS

C). Early-stage surgical detection and removal of tumor offers a favorable prognosis and better survival rates. However, a major portion of 75% subjects have stage III/IV at the time of diagnosis and despite advanced major developments in oncology survival rates remain poor. Carcinogens produce wide

spread DNA methylation changes within cells. These changes are characterized by globally hyper or hypo methylated regions around CpG islands, many of these changes occur early in tumorigenesis and are highly prevalent across a tumor type.Structure - This research work took advantage of publicly avai

lable methylation profiling resources and relevant comorbidities for lung cancer patients extracted from meta-analysis of scientific review and journal available at PubMed and CNKI search which were combined systematically to explore effective DNA methylation markers for NSCLC. We also tried to iden

tify common CpG loci between Caucasian, Black and Asian racial groups for identifying ubiquitous candidate genes thoroughly. Statistical analysis and GO ontology were also conducted to explore associated novel biomarkers. These novel findings could facilitate design of accurate diagnostic panel for

practical clinical relevance.Methodology - DNA methylation profiles were extracted from TCGA for 418 LUAD and 370 LUSC tissue samples from patients compared with 32 and 42 non-malignant ones respectively. Standard pipeline was conducted to discover significant differentially methylated sites as prim

ary biomarkers. Secondary biomarkers were extracted by incorporating genes associated with comorbidities from meta-analysis of research articles. Concordant candidates were utilized for NSCLC relevant biomarker candidates. Gene ontology annotations were used to calculate gene-pair distance matrix fo

r all candidate biomarkers. Clustering algorithms were utilized to categorize candidate genes into different functional groups using the gene distance matrix. There were 35 CpG loci identified by comparing TCGA training cohort with GEO testing cohort from these functional groups, and 4 gene-based pa

nel was devised after finding highly discriminatory diagnostic panel through combinatorial validation of each functional cluster.Results – To evaluate the gene panel for NSCLC, the methylation levels of SCT(Secritin), FOXD3(Forkhead Box D3), TRIM58(Tripartite Motif Containing 58) and TAC1(Tachikinin

1) were tested. Individually each gene showed significant methylation difference between LUAD and LUSC training cohort. Combined 4-gene panel AUC, sensitivity/specificity were evaluated with 0.9596, 90.43%/100% in LUAD; 0.949, 86.95%/98.21% in LUSC TCGA training cohort; 0.94, 85.92%/97.37 in GEO 66

836; 0.91,89.17%/100% in GEO 83842 smokers; 0.948, 91.67%/100% in GEO83842 non-smokers independent testing cohort. Our study validates SCT, FOXD3, TRIM58 and TAC1 based gene panel has great potential in early recognition of NSCLC undetermined lung nodules. The findings can yield universally accurate

and robust markers facilitating early diagnosis and rapid severity examination.

透過基於基因本體之整合性分析識別卵巢上皮性腫瘤發病機轉的失調基因功能體

為了解決電腦 更新中 如何 停止的問題，作者蘇國銘 這樣論述：

上皮性卵巢癌（EOCs）在晚期或復發的婦科惡性腫瘤中常是致命的和頑固的，其中漿液性佔絕大多數而卵巢清亮細胞癌（OCCC）是僅次於漿液性上皮性卵巢癌的第二常見的上皮性卵巢癌。即便經過腫瘤減積手術後加上化學藥物治療後仍有不少的患者有著較差的預後或是復發，故整體而言，對於卵巢癌的治療仍是一個相當大的挑戰。此外，邊緣性卵巢腫瘤(BOT)，包括漿液性 BOT與黏液性BOT，是屬於介於良性與惡性之間的卵巢疾病，雖然大部分的預後不差但是也有與卵巢癌不同的組織病理學特性。本研究使用以基因本體(GO)為基礎加上機器學習輔助運算的綜合分析去探討卵巢清亮細胞癌以及漿液性卵巢腫瘤包含漿液性邊緣性卵巢腫瘤與漿液性卵巢

癌的GEO資料庫中失調的基因體、功能途徑，藉以去識別重要的差異表達基因(DEG)。首先在卵巢清亮細胞癌的整合性分析中，發現無論是早期抑或是晚期，與免疫功能相關尤其是活化補體系統的替代途徑的功能失調在腫瘤發生佔有相當重要的關聯性，而補體C3與補體C5也影響了疾病無惡化存活期(Progression-free survival, PFS)和整體存活率(Overall survival, OS)且免疫染色結果是有意義的。而在漿液性卵巢腫瘤的分析中發現，SRC基因和功能失調的芳烴受體(AHR)結合路徑(Binding pathway)確實影響PFS和OS，而且與上皮細胞間質轉化(Epithelial-

mesenchymal transition, EMT)相關的鋅指蛋白SNAI2在腫瘤發生過程中有重要角色，並顯示出從漿液性 BOT 到卵巢癌有著逐漸上升的影響趨勢。未來，標靶治療可以專注於這些有意義的生物標誌並結合精確監測，以提高治療效果和患者存活率。