肺癌病人PAFAH1Bl 基因變異參與癌症惡化

Abstract

旦且全﹒基因體結構變其為腫瘤形成的表彼之一﹒於本實驗室先前的研究，我們針對肺瘋族群進行微矩陣比較基因麓的結交分析(array-CO昀，其結果顯示P品的IBI 基因具有基因種結構擴增的現車﹒因此，我們推測PAF;的IBI 基因為肺瘋有潛力的致瘋基因﹒坐登皇室主:本研究利用即時定量反轉錄PCR (q-RT PCR) 反免疫組織染色法(tH C)對91 位肺瘋族群檢現1 PAFAH1Bl 基因其mRNA 及蛋白層次變其情形﹒盆~:PAFAHIBI 基因於mRNA 層次的過度表現頻率為6 1. 5% •於蛋白層次過度表現頻率為56%· 且此基因於mRNA 及蛋白層次的過度表現皆與病人的晚期具有相關性(mRNA : P=0.001 .蛋白層: P=0.05) • 且屬於腺細胞瘤的病人於蛋白層次的過度表現具有較差的預後(戶。.049) ﹒笙畫畫:其結果顯示PAFAH1BI 基因於肺描族群具有過度表達的變異，且可能季奧肺瘤細胞轉移過程﹒

Rationale and Objectives: Genomic DNA copy number variation is a hallmark of cancer. In our previous array-comparative genomic hybridization (array-CGH) study， we showed that PAFAHJBJ was amplified in lung cancer patients, suggesting that PAFAHJBJ is a potential oncogene in lung cancer Methods: In thiis study, we have determined the mRNA and protein expression level ofPAFAHIBI in 91 lung cancer patients using quantitative reverse transcription polymerase chain reation (qRT-PCR) and immunohistochemistry (IHC). Main Results: The PAFAHIBI mRNA and protein overexpression frequency were 61.5% (56/91) and 56% (51191) in lung cancer patients. The results indicated that mRNA and protein overexpression level of PAFAHJBJ was significantly associated with late stage (mRNA: P=0.001， protein: P=0.05) and poor survival in lung adenocarcinoma (P=0.049). Conclusions: The results revealed the roles of overexpressed PAFAHI BI in tumor progression and poor survival in lung cancer.