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Genomic aberrations in lung cancer: a study with comparative genomic hybridization and analysis of loss ofheterozygosity文詠賢, Man, Wing-yin, Cornelia. January 2003 (has links)
published_or_final_version / Medicine / Master / Master of Philosophy
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Fusion genes in non-small cell lung cancerWong, Wing-sze, 黃詠詩 January 2009 (has links)
published_or_final_version / Pathology / Master / Master of Philosophy
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Analysis of fragile site FRA16D and WWOX gene in non-small cell lung cancerTsang, Hing-wing, 曾慶榮 January 2005 (has links)
published_or_final_version / Medical Sciences / Master / Master of Medical Sciences
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Molecular genetic characterizations of human non-small cell lung cancerTai, Lai-shan., 戴麗珊. January 2005 (has links)
published_or_final_version / abstract / Clinical Oncology / Doctoral / Doctor of Philosophy
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Oncogenic mutations as biomarkers and therapeutic targets in lung cancerLam, Chi-leung, David, 林志良 January 2014 (has links)
Oncogenic mutations in lung cancer further our knowledge about cancer initiation and progression, and may guide personalized treatment. The fact that targeted therapy is most effective in subsets of patients with defined molecular targets indicates the need for classification of clinically-related molecular tumor phenotypes based on the presence of oncogenic mutations, including EGFR mutations and EML4-ALK rearrangements.
The identification of EGFR mutations, in up to half of lung adenocarcinomas in Asians, could predict clinical sensitivity to tyrosine kinase inhibitor (TKI). However, testing for mutations is not always possible due to tumor tissue availability. The therapeutic decision sometimes remains a clinical one especially for elderly lung cancer patients but no known mutation status. We studied the survival outcomes of targeted therapy versus conventional chemotherapy in elderly patients with lung cancer when we did not yet have routine EGFR mutation testing and demonstrated comparable survival outcomes in targeted therapy compared to chemotherapy, implying that survival with targeted therapy could be better if the treatment population could be selected with EGFR mutations.
Though testing for EGFR mutation in tumor biopsy have later become routine practice and remains the accepted reference for therapeutic decision, the detection of EGFR mutations in plasma DNA with high diagnostic performance will be useful adjunct for diagnostic and therapeutic monitoring. Among patients with EGFR mutations in tumor biopsy, the concurrent detection of EGFR mutation in plasma DNA was found to confer a less favorable prognosis in terms of overall survival than those patients with EGFR mutations in tumor biopsy but the corresponding mutation was not detected in plasma.
Other oncogenic mutations with therapeutic implications in lung tumors are yet to be fully explored, like ALK, KRAS, ROS1 or NTRK1 mutations. It is not exactly the tumor – but the mutations in the tumor that need to be explored with reference to clinical behavior. Even with EGFR mutation with well-established clinical implications, further exploration into its mechanistic functions will help in understanding of drug resistance. Lung cancer cell lines established from patients with known mutation profiles could be useful tools for studying the biology of known molecular targets as well as for therapeutic testing. Four new lung adenocarcinoma and one mesothelioma cell lines were established from patients with different clinical characteristics and oncogenic mutation profiles. These cell lines with defined mutation profiles will provide tools for exploration of lung cancer and mesothelioma biology with respect to molecular therapeutic targets.
The Large Tumor Suppressor 2 (LATS2) gene was a differentially expressed gene between EGFR mutant and wildtype lung adenocarcinomas. The differential LATS2 expression levels were predictive of survival in patients with resected lung AD and may modulate tumor growth via different signaling pathways in EGFR mutant and wild-type tumors.
The identification of oncogenic mutations has led to a new paradigm of targeted therapy in lung cancer. Further improvements in outcome of lung cancer management will stem from research into the biology of oncogenic mutations and their clinico-pathological correlations, which would fuel parallel development of clinically efficacious targeted therapies. / published_or_final_version / Medicine / Master / Doctor of Medicine
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Gene expression profiling in non-small cell lung cancerLam, Chi-leung, David., 林志良. January 2007 (has links)
published_or_final_version / abstract / Pathology / Doctoral / Doctor of Philosophy
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DNA copy number and expression analysis of candidate tumour genes in adenocarcinomas of the lungHan, Kam-chu, Beymier., 韓金柱. January 2005 (has links)
published_or_final_version / Medical Sciences / Master / Master of Medical Sciences
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Epidermal growth factor receptor (EGFR) mutations and phosphorylation pattern in non-small cell lung cancer (NSCLC)Tam, Yee-san, Issan., 譚薏珊. January 2008 (has links)
published_or_final_version / Pathology / Doctoral / Doctor of Philosophy
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Epidermal growth factor receptor (EGFR) and phosphoinositide-3-kinase catalytic alpha (PIK3CA) mutations in non-small cell lung cancer(NSCLC) and response to tyrosine kinase inhibitor therapyChoy, Kit-chi., 蔡潔芝. January 2011 (has links)
published_or_final_version / Pathology / Master / Master of Medical Sciences
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Expression of vascular endothelial growth factor and its receptors in tumours張毅, Cheung, Ngai. January 1998 (has links)
published_or_final_version / Pathology / Master / Master of Philosophy
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