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Home > Medicine & Health Science textbooks > Medical specialties, branches of medicine > Pathology > Genetic and Expression Analysis of Candidate Tumor Loci in Non-Small Cell Lung Cancer
Genetic and Expression Analysis of Candidate Tumor Loci in Non-Small Cell Lung Cancer

Genetic and Expression Analysis of Candidate Tumor Loci in Non-Small Cell Lung Cancer


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This dissertation, "Genetic and Expression Analysis of Candidate Tumor Loci in Non-small Cell Lung Cancer" by Hong, Zhu, 朱紅, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: Abstract of thesis entitled Genetic and Expression Analysis of Candidate Tumor Loci in Non-Small Cell Lung Cancer Submitted by ZHU Hong For the degree of Doctor of Philosophy at the University of Hong Kong in August 2005 Lung cancer is a common malignancy with high mortality in Hong Kong and worldwide. Although risk factors are well known, the underlying molecular mechanisms are unclear. Non-small cell lung cancer (NSCLC) exhibits multiple chromosome aberrations. Genomic and transcriptional abnormalities of genes encompassed within these aberrant loci could constitute underlying mechanisms for cancer development. The aim of this study was to detect genomic imbalances in lung adenocarcinoma (AD), and to identify cancer-related genes within these altered loci. The strategy consisted of screening by array-based comparative genomic hybridization (array-CGH), followed by comparison with expression microarray data to identify genes with concordant genomic and expression changes. Integration of these results with known data on gene functions was then employed for selection of potential cancer-related gene targets. An array comprising BAC and PAC clones spanning the entire genome at an average of 1 Mb interval was used. Three lung adenocarcinoma cell lines established from local patients and 36 clinical primary lung AD samples were analyzed. Conventional metaphase CGH was performed on the cell lines and 14 of the AD for comparison. The results showed general agreement between chromosome profiles analyzed by CGH and array-CGH. From the cancer cell lines, recurrent genomic gains were found at lp36.33- p36.32, lq, 7, 8q21.13-q21.3, 8q24.13-q24.21, 8q24.3, 17q, 20q and loss at Ip33-pl2, 3p, 3qll.2-ql2.1, 8p23.3-pl2, 9p, 12q24.32, 17p, 18, 19ql3.43. In the clinical samples, recurrent genomic aberrations were found in segmental or focal distribution. The most frequently gained loci were within segments 5pl5.33-pl5.31, 20ql3.31- 20ql3.33 and 16pl3.3-pl3.12, followed by lp36.32, lq32.1 and 17q25.3, while the commonest deleted loci were 9p23, followed by 6ql6.3 and 10q21.1. Many of these segmental aberrations could be matched to minimal overlapping regions according to CGH analysis. Additional alterations involving interstitial short DNA fragments or focal sites spanned by dispersed BAC clones were also identified by array-CGH. Selective loci of gain at 7p, 8q, 20q and loss at 9p were verified by fluorescent in-situ hybridization (FISH) analysis. Comparison with clinicopathological parameters showed more genetic alterations in the more advanced tumors, consistent with the concept that tumour progression was associated with increasing genetic abnormalities. Cancer cells derived from a smoker showed more numerous aberrations than those from non-smokers. Aberrations associated with different types of smoking history were also identified in clinical tumours. By integrated analysis of results from expression array and array-CGH, 25 genes showing concordant gene dosage and transcriptional changes were chosen. Expression analysis by real-time PCR validated the results by microarray analysis. The highest expression was found for EEF1A2 (20q), DDR1 (6p), CHI3L1 (lq), FOXA1 (14q) and CHC1 (lp) with genomic gain; the 2 least expressed genes in deleted regions were MYH10 (17p) and COPEB (lOp). Allelic loss at 3p21 was common and RASSF1A located in this region showed decreased expression. A high proportion of cases s


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Product Details
  • ISBN-13: 9781361235812
  • Publisher: Open Dissertation Press
  • Publisher Imprint: Open Dissertation Press
  • Height: 279 mm
  • No of Pages: 212
  • Weight: 780 gr
  • ISBN-10: 1361235810
  • Publisher Date: 26 Jan 2017
  • Binding: Hardback
  • Language: English
  • Spine Width: 13 mm
  • Width: 216 mm


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