Rozprawy doktorskie: „Lungs – Cancer”

1

林華杰 i Wah-kit Lam. "A clinical and epidemiological study of carcinoma of lung in HongKong". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1985. http://hub.hku.hk/bib/B31981264.

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Lian, Fuzhi. "The anti-carcinogenic effect of carotenoids against lung cancer /". Thesis, Connect to Dissertations & Theses @ Tufts University, 2006.

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Thesis (Ph.D.)--Tufts University, 2006.
Submitted to the School of Nutrition Science and Policy. Adviser: Xiang-Dong Wang. Includes bibliographical references. Access restricted to members of the Tufts University community. Also available via the World Wide Web;

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3

Lee, Richard. "An improved system for lung cancer diagnosis using lung cell images". Diss., Online access via UMI:, 2006.

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Wong, Pui-sze. "The lived experience of Hong Kong Chinese men undergoing radiotherapy to treat lung cancer /". View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38296251.

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Yip, Tsz-chung. "The role of computed tomography volumetry in the assessment of advanced lung cancer and oesophageal cancer /". Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B25205468.

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Wong, Wing-sze. "Fusion genes in non-small cell lung cancer". Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43781378.

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Lam, Chi-leung David, i 林志良. "Oncogenic mutations as biomarkers and therapeutic targets in lung cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/207610.

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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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Li, Yuanyuan, i 李园园. "The role of autophagy on targeted therapy in lung adenocarcinoma : in vitro and in vivo models". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2015. http://hdl.handle.net/10722/208609.

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Non-small cell lung cancer (NSCLC) causes most of the cancer deaths worldwide. Tyrosine kinase inhibitors (TKIs), like erlotinib and crizotinib, are commonly used as specific treatments targeting epidermal growth factor receptor (EGFR)-mutated and anaplastic lymphoma kinase (ALK)-rearranged NSCLC. Autophagy is a highly conserved cellular process in response to stress. Tumor microenvironment (TME) is composed of both tumor cells and stromal cells. This study aimed to investigate whether autophagy could confer intrinsic and acquired resistance to TKIs in NSCLC, and its role in the presence of TME or in animal models. In the first part of this study, the effect of EGFR TKI or ALK TKI on sensitive NSCLC cells to generate autophagy was investigated, and manipulation of autophagy in these cell lines was performed. Autophagy inhibition was shown to enhance apoptotic effect of TKIs in sensitive NSCLC cells. This part provided strong evidence that TKIs and autophagy inhibitor chloroquine (CQ) work synergistically in sensitive NSCLC cells. Autophagy induction by erlotinib treatment was observed in a HCC827 (lung adenocarcinoma, EGFR exon 19 del) xenograft model, which was in line with the in vitro observation. Correspondingly, the combination of erlotinib (12.5 mg/kg) with CQ (50 mg/kg) in the HCC827 xenograft model achieved greater tumor growth suppression, compared with single drug treatments. In the second part of this study, a model of TME was established to allow study of autophagy under such circumstances. An activated TME with cytokine production, autophagy induction and epithelial-to-mesenchymal transition (EMT) was generated by co-culturing NSCLC cells and human fibroblasts. Sensitivity to TKI under TME was not affected, and combination of chloroquine with TKI under TME remained synergistic compared with single treatments. In the third part of this study, erlotinib-resistant (ER) HCC827 cells were acquired by stepwise exposure to increasing concentrations of erlotinib in cell culture. Common acquired resistance mechanisms to EGFR TKI (EGFR T790M or c-MET amplification) were excluded in this ER HCC827 model, except EMT. Autophagy status in ER HCC827 cells was studied and autophagy manipulation was performed. It was found that CQ and erlotinib worked synergistically to induce cell death even in ER HCC827 cells. In an ER HCC827 xenograft model, significant degree of autophagy and EMT was evident. Interestingly, combining erlotinib (25 mg/kg) with CQ (50 mg/kg) showed better inhibitory effect on tumor growth compared with single treatments. In summary, TKIs induced both apoptosis and autophagy in EGFR-mutated and ALK-rearranged NSCLC cells. Autophagy inhibition by CQ enhanced TKI-induced cell death in sensitive cells. The presence of TME did not confer TKI resistance. Autophagy was highly activated in EGFR-mutated NSCLC cells with acquired resistance to erlotinib. Combination of CQ with erlotinib remained synergistic in the presence of TME and acquired resistance, both in vitro and in vivo.
published_or_final_version
Medicine
Doctoral
Doctor of Philosophy

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9

Tam, Gloria. "Non-small cell lung cancer clinical trials on new medicines". Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41711956.

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柳言樺 i Yin-wah Lau. "Mutation and expression analysis of PTEN in non-small cell lung cancerfrom non-smokers". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41650931.

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Ho, Chung-man. "Non-small cell lung cancer from bench to bedside /". Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39432592.

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McKee, Daniel Wayne. "An end-to-end process for cancer identification from images of lung tissue". Diss., Online access via UMI:, 2006.

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Tam, Yee-san Issan. "Epidermal growth factor receptor (EGFR) mutations and phosphorylation pattern in non-small cell lung cancer (NSCLC)". Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40687673.

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Keller, Elizabeth Greer. "Novel chemotherapeutics against lung and colon cancer". Click here for download, 2010. http://proquest.umi.com.ps2.villanova.edu/pqdweb?did=1961333981&sid=1&Fmt=2&clientId=3260&RQT=309&VName=PQD.

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15

Lau, Yin-wah. "Mutation and expression analysis of PTEN in non-small cell lung cancer from non-smokers". Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41650931.

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16

Wong, Pui-sze, i 黃佩詩. "The lived experience of Hong Kong Chinese men undergoing radiotherapy to treat lung cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B45012155.

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17

譚郭雅欣 i Gloria Tam. "Non-small cell lung cancer clinical trials on new medicines". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41711956.

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18

Wong, Wing-sze, i 黃詠詩. "Fusion genes in non-small cell lung cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43781378.

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19

Tai, Lai-shan. "Molecular genetic characterizations of human non-small cell lung cancer". Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31375315.

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20

田珮芝 i Pui-chi Tin. "Detection of EGFR mutation in lung adenocarcinoma and paired plasma". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40737044.

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Chiu, Siu-hau, i 招兆厚. "A search for optimal radiation therapy technique for lung tumours stereotactic body radiation therapy (SBRT) : dosimetric comparison of 3D conformal radiotherapy, static gantry intensity modulated radiotherapy (IMRT) and volumetric-modulated arc therapy (VMAT) with flattening filter (FF) or flattening filter-free (FFF) beams". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/196549.

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Materials/Methods: Ten patients who underwent thoracic SBRT with primary stage I (T1/2N0) lung cancer or oligometastatic lung lesion, with PTV diameter ≤ 5cm were selected and were immobilized with Easyfoam or Vac-Lock. Planned/treated with inspiratory breath-hold (25 seconds, 70 to 80% of vital capacity) assisted with Active Breathing Control (ABC). Four treatment plans: non-coplanar 3DCRT, coplanar static gantry IMRT, coplanar VMAT (FF) and VMAT (FFF) were generated. Field arrangements, either static fields or partial arcs (duration=20 sec) were used to avoid direct beam entry to contralateral lung. All plans were compared in terms of dosimetric performance included dose to PTV or organs at risk (OAR), high/low dose spillage, integral dose (body and lungs), dose delivery efficiency (MU/Gy) and estimated beam-on time (BOT) with reference to the RTOG 0813 protocol. Results: All plans complied with RTOG 0813 protocol. VMAT (FF/ FFF) techniques improved target coverage and dose conformity, with the highest conformity number (CN > 0.91), compared to IMRT (0.88) and 3DCRT (0.85). The control of high dose spillage (NT>105% and CI) for IMRT (3.04% and 1.08) and VMAT (FF/ FFF) (1.08/ 1.06% and 1.03/ 1.04) techniques were comparable (p > 0.05) and significantly better than 3DCRT (4.22% and 1.11, p < 0.005) technique. In addition, VMAT (FF/ FFF) techniques performed the best in controlling low dose spillage (D2cm and R50%) compared with IMRT (reduction: 4.7%, p=0.036 and >5.9%, p = 0.009) and 3DCRT (reduction: > 16.3%, p < 0.001 and > 10%, p = 0.002). Benefits of rapid and isotropic dose fall-off were shown from superior tissue sparing (reduction ranges from 3.2% up to 67%) of ipsilateral brachial plexus, skin (0-5mm), great vessels and ribs. Also lung V10, V12.5, esophagus and heart tend to receive lower dose with VMAT technique. The relatively lower integral dose to whole body (> 3Gy∙L reduction, p < 0.013) and ipsilateral lung (0.65Gy∙L reduction, p = 0.025) compared with 3DCRT, were associated with lower risk of radiation induced cancers. The MU/Gy and BOT were substantial lower for VMAT (FF) (22.4% and 32.4%) compared with IMRT. Apart from higher (7%) maximum skin dose, dosimetric performance for VMAT (FFF) was comparable with VMAT (FF), with advantages of further reduction of MU/Gy (1.8% lesser), partial arc numbers (from 12-14 arcs down to 8 arcs) and BOT (35% shortened), owing to the increased dose output with flattening filter removal. Conclusions: VMAT (FF and FFF) plans maintained IMRT equivalent plan qualities, simultaneously enhanced the delivery efficiency with shortened BOT. VMAT (FFF) further reduced the required arcs number and BOT, significantly minimized the intra-fraction motions and more tolerable to patient with long SBRT treatment duration.
published_or_final_version
Medicine
Master
Master of Medical Sciences

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Chan, Ka-heng, i 陳加慶. "Four-dimensional Monte Carlo stereotactic body radiotherapy for lung cancers using image-guided robotic target tracking". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206441.

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Stereotactic body radiotherapy (SBRT) is a promising treatment strategy for early–stage lung cancers. Conventional three–dimensional (3D) SBRT based on a static patient geometry is an insufficient model of reality, posing constraints on accurate Monte Carlo (MC) dose calculation and intensity–modulated radiotherapy (IMRT) optimization. Four–dimensional (4D) radiotherapy explicitly considers temporal anatomical changes by characterizing the organ motion and building a 4D patient model, generating a treatment plan that optimizes the doses to moving tissues, i.e., 4D dose (as opposed to the static 3D dose to tissue), and delivering this plan by synchronizing the radiation with the moving tumor. This thesis focuses on 4D robotic tracking lung SBRT. By recalculating the conventional 3D plan on the 4D patient model using MC simulation, it was found that 4D moving dose distributions could detect increase of normal tissue doses and complication probabilities (NTCP), and decrease of tumor dose and control probability. For one patient, the risk of myelopathy was estimated at 8% and 18% from the 3D equivalent path–length corrected (EPL) and the 4D MC doses, respectively. Such increased NTCP suggests that better estimations of different dosimetric quantities using 4D MC dose calculation are crucial to improve the existing dose–response models. Dosimetric error in 4D robotic tracking SBRT was found to be caused predominately by tissue heterogeneities, as assessed by the comparisons of the 4D moving tissue doses calculated using the conventional EPL and MC algorithms. At 3% tolerance level, our results indicated clinically significant dose prediction errors only in tumor but not in other major normal tissues. Furthermore, 4D tracking radiotherapy was found to have greater ability to limit the normal tissue volume receiving high to medium doses than the other advanced SBRT strategy combining volumetric–arc radiotherapy with 4D cone–beam CT verification. Invariant target motion was found to be an unrealistic assumption of 4D radiotherapy from the analysis of probability motion function (pmf) of motion data. Systematic and random variations of motion amplitude, frequency, and baseline were found to reduce the reproducibility of pmfs, on average, to just 30% for the principal motion of 3400 seconds. Experimental evaluations showed that systematic motion change reduced the gamma passing rate of radiochromic film measurements at 3mm distance–to–agreement and 3% dose difference criteria from 91% for 4D dose calculated with MCand EPL algorithms to 47% and 53% in the static object, respectively,. For moving target object, gamma passing rates of the 4D MC doses hardly changed with reproducible and non–reproducible motion (95% vs. 93%), and barely differed between conventional 3D and 4D MC doses (95% vs. 95% with reproducible, and 96% vs. 93% with non–reproducible motions). Distortions due to image artifacts and registration errors were consistently observed in the 4D dose distributions but not the 3D dose distributions. In conclusion, 4D Monte Carlo planning shall be considered for robotic target tracking only if robustness against uncertainties of patient geometry, and accuracy of 4DCT imaging and deformation registration are significantly improved.
published_or_final_version
Clinical Oncology
Doctoral
Doctor of Philosophy

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23

Ho, Lok-man, i 何樂文. "Evaluation of verification accuracy of two different immobilization methods in stereotactic body radiotherapy of early stage non-small cell lung carcinoma and pulmonary oligometastases". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206609.

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Purpose: The aim of the study is to compare the positioning accuracy of two immobilization systems commonly used in stereotactic body radiation therapy (SBRT) of non–small cell lung carcinoma (NSCLC) and lung oligometastases, Polyurethane Foam Cradles (PFC) and the BodyFIX System (BFS) with 2D and 3D image guidance. Both the interfraction and intrafractional positional errors were analyzed. Methods and Materials: 189 CBCT scans from 44 patients with NSCLC or lung oligometastases who received SBRT between August 2008 and April 2014 were analyzed retrospectively. Of these, 20 and 24 patients were immobilized with a Polyurethane Foam Cradle (PFC) and the BodyFIX System (BFS) respectively. The results of on board imaging (OBI) and pre-treatment cone-beam computed tomography (CBCT) at initial setup and after correction were registered to planning CT for online matching. The positional errors in anteroposterior (AP), superior-inferior (SI) and medial-lateral (ML) directions were analyzed. Post-treatment CBCT were used to assess intrafraction tumour displacement for 19 patients. The planning target volume margins were calculated using the van Herk’s formula. Other possible factors contributing to setup uncertainty were also analyzed. Result: By using skin mark as a reference, the mean setup errors were 0.09, -0.10 and 0.02 cm for PFC and 0.04, -0.19 and -0.10 cm for BFS in AP, SI and ML directions respectively. The mean setup errors were decreased to 0.04, 0.02 and 0.04 cm for PFC; and -0.04, -0.04 and -0.02 cm for BFS after the application of OBI. The errors were further decreased to below 0.02 cm in all directions after the application of first pre-treatment CBCT in both immobilization methods. Statistically significant difference (p < 0.05 ) was only found in the comparison of AP error between the two devices, when OBI was used as the verification method. For PFC, the 3D vector errors of skin mark, OBI and first pre-treatment CBCT were 6.4 mm, 2.9 mm and 0.5 mm, respectively cases. For BFS, the errors were 7.1 mm, 3.0 mm and 0.4 mm, respectively. Smaller PTV margins in various directions were needed in BFS when using CBCT as the verification method. Positioning errors of skin mark setup in AP and SI directions had major contributions to all the setup errors; gender and tumour location might significantly affect the setup uncertainties. Comparatively large intrafractional errors were found in the post-treatment CBCT results of PFC. Conclusion: When employing the CBCT-based final couch position as the benchmark, the setup errors of skin mark, OBI and first CBCT results were compared relatively. The positioning accuracies of PFC and BFS were similar. Apart from the vertical error (AP direction) found in the OBI verification, there was no significant difference between the positioning accuracy of both immobilization devices. Both imaging guided RT techniques were superior to skin mark. OBI and CBCT online correction improved the positioning accuracy of lung SBRT and substantially reduces required target margins and normal tissue irradiation.
published_or_final_version
Diagnostic Radiology
Master
Master of Medical Sciences

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24

Zhou, Xing Zhi. "Cationic polypeptide-based micelles for camptothecin delivery in lung cancer therapy". Thesis, University of Macau, 2018. http://umaclib3.umac.mo/record=b3952141.

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25

Stordal, Britta. "Regrowth resistance in platinum-drug resistant small cell lung cancer cells". Connect to full text, 2006. http://hdl.handle.net/2123/2467.

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Thesis (Ph. D.)--University of Sydney, 2007.
Title from title screen (viewed 10 June 2008). Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the Discipline of Medicine, Faculty of Medicine. Degree awarded 2007; thesis submitted 2006. Includes bibliographical references. Also available in print form.

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26

Yip, Tsz-chung, i 葉子仲. "The role of computed tomography volumetry in the assessment of advanced lung cancer and oesophageal cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B29725239.

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Lam, Chi-leung David. "Gene expression profiling in non-small cell lung cancer". Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38585777.

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Chan, Ching Eunice. "Pathogenetic role of aberrant promoter methylation in lung cancer". Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39557819.

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Tsang, Hing-wing. "Analysis of fragile site FRA16D and WWOX gene in non-small cell lung cancer /". View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B34829416.

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Wong, Kit-man Sunny, i 王傑民. "Isolation and characterization of cancer stem cells in non-small cell lung cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47250665.

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Tumor heterogeneity has long been observed and recognized as a challenge to cancer therapy. The cancer stem cell (CSC) model is one of the hypotheses proposed to explain such a phenomenon. A specific cancer stem cell marker has not been determined for non-small cell lung cancers (NSCLC), preventing the definitive evaluation of whether the biology of NSCLC is governed by the CSC model. This study aimed to analyze the expression of candidate CSC markers and using the identified putative marker, to isolate CSC and determine the applicability of the CSC model in NSCLC. The expression or activities of four putative stem cell markers, CD24, CD44, CD133 and aldehyde dehydrogenase 1 (ALDH1) were measured by flow cytometry in eight NSCLC cell lines before and after chemotherapy for 24 hours. Markers with increased expression after treatment were considered potential CSC markers and used for isolating tumor cell subpopulations from the untreated cell lines by fluorescence-activated cell sorting (FACS). Confirmatory analyses using widely acceptable methodology were performed to test for CSC properties in the marker+ and marker- subpopulations. Isolated subpopulations were further characterized by functional and phenotypic studies. Flow cytometry showed amongst the 4 markers, only ALDH1 expression was significantly enhanced by chemotherapeutic treatment, suggesting ALDH1 could be a CSC marker. Untreated ALDH1+ cells formed significantly more and larger cell spheres in non-adherent, serum-free conditions than ALDH1- cells. Likewise, higher in vitro tumorigenic ability was observed in ALDH1+ subset using colony formation assay. Furthermore, a higher resistance to cytotoxic drugs was observed in ALDH1+ compared to ALDH1- cells. In vivo studies also showed ALDH1+ cells showed higher tumorigenicity than ALDH1- cells; as few as 2,500 ALDH1+ cells formed tumor in SCID mice which were serially transplantable to 2nd and 3rd recipients, while no tumor was formed from ALDH- cells with even ten times the number of cells. Also, expression analysis revealed higher expression of the pluripotency genes, OCT4, NANOG, BMI1 and SOX9, in ALDH1+ cells. In view of previous studies reporting CD44 as a CSC marker in lung cancer, double marker selection of putative CSC was performed to compare ALDH1+CD44+ and ALDH1-CD44+ subpopulations. Results of the spheroid body formation assay and cisplatin treatment experiments revealed the ALDH1+CD44+ subpopulation possessed higher self-renewal ability and chemo-resistance. Cell migration and invasion assays showed differences between the ALDH1+CD44+ and ALDH1- CD44+ subpopulations. The significance of these observations require further investigation. In conclusion, the result showed that ALDH1 could be a marker for NSCLC stem cells as evidenced by enhanced self-renewal and differentiation abilities in ALDH1+ subpopulation. Furthermore, this study observed the presence of at least two potential stem cell subpopulations in NSCLC cells with differential selfrenewal, chemotherapy resistance and cell mobility properties. Further investigations are required to validate these observations and to investigate the underlying mechanisms. Better understanding of these issues would help to solve the challenges brought by tumor heterogeneity in lung cancer therapy.
published_or_final_version
Pathology
Master
Master of Philosophy

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31

Yang, Zhiyi. "Mass spectrometry-based metabolomic and lipidomic characterization of esophageal cancer and lung cancer". HKBU Institutional Repository, 2020. https://repository.hkbu.edu.hk/etd_oa/819.

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Esophageal cancer and lung cancer are among the most common cancers worldwide with millions of new cases annually. Esophageal cancer patients at an advanced stage suffer from a poor five-year survival rate. However, only fewer than 30% of esophageal cancer cases were diagnosed at an early stage. For lung cancer, malignant pleural effusion (MPE) is an important hallmark for late-stage patients with metastasis. However, other causes of pleural effusions including tuberculosis bring difficulties in the diagnosis of MPE. It is necessary to develop novel diagnostic biomarkers and elucidate the pathological mechanism of esophageal cancer and lung cancer. Metabolic reprogramming is an emerging hallmark of cancer. It has been clear that metabolites play a critical role in cancer development and impose vulnerabilities that could be targeted for cancer therapy. The overall objective of this study is to comprehensively characterize the metabolic dysregulation in esophageal cancer and lung cancer for biomarker discovery and pathological elucidation, by using liquid chromatography--mass spectrometry (LC-MS)-based metabolomics and lipidomics. Paired tumors and normal adjacent tissues from esophageal squamous-cell carcinoma (ESCC) patients were first analyzed through global metabolomic and lipidomic profiling. Tumors were clearly separated from the normal tissues based on the partial least-square discriminant analysis (PLS-DA) model (R2Y >0.85 and Q2Y >0.79 in metabolomic profiling and R2Y >0.70 and Q2Y >0.67 in lipidomic profiling). A preliminary list of 41 polar metabolites and 65 lipids were identified to be significantly perturbed in tumor tissues. Kynurenine, spermidine, citicoline, as well as several glucosylceramides and phosphatidylcholines (PC) showed excellent predictive potential with area under curve (AUC) values better than 0.95 in receiver operating characteristic (ROC) models. Major elevated metabolic pathways were polyamine biosynthesis, glycerophospholipid metabolism, methionine mechanism, arginine and proline mechanism, and kynurenine metabolism, suggesting active amino acid biosynthesis and lipid biosynthesis in ESCC. The potential biomarkers and dysregulated pathways discovered above in ESCC tissue was further validated using targeted metabolomic, lipidomic and proteomic profiling. Polyamine biosynthesis was found to be activated in ESCC through the overexpression of tumor promoting ornithine decarboxylase and spermidine/spermine synthases. Upregulated levels of S-adenosylmethionine and DNA (cytosine-5)-methyltransferase 1 implied DNA hypermethylation in ESCC. Elevated purines in tumors were generated through the overexpression of methylenetetrahydrofolate dehydrogenases. Active phospholipid biosynthesis in tumors was promoted by overexpression of choline transporters and synthase of citicoline, which may accelerate the tumor growth. Dysregulation of coenzyme A species with different fatty acyl chains showed the same trend as of phospholipids, implying the specific activation of relevant acyltransferases in the phospholipid remodeling pathway. Moreover, essential amino acids exhibited a higher upregulation trends in patients with high-grade tumor or with cancer recurrence. Collectively, this study revealed the detailed metabolic dysregulations in ESCC tumor tissues, discovered potential metabolite biomarkers and identified therapeutic targets of ESCC. In order to explore the clinical application of the discovered biomarkers, metabolomic and lipidomic profiling was further performed on ESCC plasma samples. Eight metabolites were found to be simultaneously upregulated in ESCC tumors and plasma samples, indicating their potential as tumor-derived plasma biomarkers. Among them, a panel of five tumor-derived plasma biomarkers consisting of arginine, acetylspermidine, methylguanosine, dimethylguanosine and cystine showed good diagnostic potential in the cross validation. These biomarkers are related with polyamine biosynthesis and purine metabolism, which are critical to support tumor growth. For lung cancer, MPE from lung adenocarcinoma patients were investigated by LC-MS/MS-based metabolomic and lipidomic profiling. In PLS-DA models, the MPE samples were clearly separated from benign pleural effusion samples from pulmonary tuberculosis patients. A group of 17 polar metabolites and 45 lipids were identified to be significantly perturbed in MPE. For diagnostic purposes, ether lipid biomarkers, including PCs, lyso-PCs and phosphatidylethanolamines, showed an excellent predictive ability with the highest AUC value of 0.953 in ROC models. Furthermore, downregulated ether lipids and upregulated oxidized polyunsaturated fatty acids in MPE reflected the elevated oxidative stress and peroxisome disorder in lung cancer patients, which offers deeper understanding in lung cancer pathology.

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32

Gupta, Gaorav. "Breast cancer metastasis to the lungs : from genes to mechanisms /". Access full-text from WCMC :, 2007. http://proquest.umi.com/pqdweb?did=1456287491&sid=10&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Meraviglia, Martha Gene. "The mediating effects of meaning in life and prayer on the physical and psychological responses of people experiencing lung cancer /". Full text (PDF) from UMI/Dissertation Abstracts International, 2001. http://wwwlib.umi.com/cr/utexas/fullcit?p3008392.

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Xiang, Cao Wen. "Chelerythrine induces apoptosis in lung cancer cells via a mutual regulation between MLKL and PERK eIF2α". Thesis, University of Macau, 2018. http://umaclib3.umac.mo/record=b3952184.

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Tam, Yee-san Issan, i 譚薏珊. "Epidermal growth factor receptor (EGFR) mutations and phosphorylation pattern in non-small cell lung cancer (NSCLC)". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40687673.

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Brena, Romulo Martin. "Aberrant DNA methylation in human non-small cell lung cancer". Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1172083621.

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文詠賢 i Wing-yin Cornelia Man. "Genomic aberrations in lung cancer: a study with comparative genomic hybridization and analysis of loss ofheterozygosity". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31227697.

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Chu, Ka-wan Kevin, i 朱嘉運. "High-throughput molecular characterization of human non-small cell lung carcinoma". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B4501288X.

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Maguire, Roma. "Where is the person in symptom cluster research? : the experience of symptom clusters in patients with advanced lung cancer". Thesis, University of Stirling, 2011. http://hdl.handle.net/1893/3423.

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Where is the Person in Symptom Cluster Research? The Experience of Symptom Clusters in Patients with Advanced Lung Cancer This thesis describes a three-year qualitative study which aimed to explore the experience of symptom clusters in patients with advanced lung cancer. The study employed a patient-focused approach utilising Interpretative Phenomenological Analysis (IPA) (Smith et al. 2009a). This methodology (IPA), informed by a contextual constructionist stance, was selected to explore the experience of symptom clusters, for its focus on the lived experience, the context and meanings which surround such experiences and its idiographic approach. Ten patients (a sample size which is the upper limit of the number of participants advocated for studies employing IPA (Smith et al. 2009b;Reid et al. 2005;Smith and Osborn 2004)) with advanced lung cancer took part in the study and data were collected using unstructured, in-depth interviews at two time points: on recruitment and three to five weeks later. Data were analysed using Interpretative Phenomenological Analysis, within the framework advocated by Smith and Osborn (2003). The study generated interesting and significant findings. The experience of symptom clusters in patients with advanced lung cancer was characterised by two super-ordinate themes: ‘The lived experience of symptom clusters and the role of context and meaning’ and ‘Symptom clusters and loss of sense of self’. The super-ordinate theme of ‘The lived experience of symptom clusters and the role of context and meaning’ in the first instance, illustrates that the participants in this study were experiencing symptom clusters and providing detail on the components, nature and patterning of the symptom clusters reported, particularly the way that one or two salient symptoms were commonly highlighted from all the other symptoms experienced. This super-ordinate theme also demonstrates the core role that context and meaning play in the lived experience of symptom clusters, with many of the participants in this study framing their experiences of symptom clusters within a fear of death, stigma and loss of sense of self. The second super-ordinate theme informing this thesis is ‘Symptom clusters and loss of sense of self’. This super-ordinate theme illustrates the impact of symptom clusters on the participants’ lives, and how this, in turn, impacted on their sense of self in a number of different ways. For some, their sense of self was compromised by the concurrent symptoms that they were experiencing, as they prevented them from undertaking roles and activities that they were accustomed to in the past. This super-ordinate theme also highlights the role of the body relative to the self, and describes how the participants’ sense of self was transiently lost during periods when they experienced symptom clusters of high severity. The findings presented also demonstrate the knock-on effect of loss of sense of self experienced, with the participants feeling like they were a burden due to their incapacitation, and at times hiding the multiple symptoms that they were experiencing, in a bid to protect their loved ones from their illness. In light of the loss of sense of self experienced, this super-ordinate theme also demonstrates how the participants employed various strategies in a bid to try and maintain a coherent and valued sense of self. The findings presented illustrate how the use of IPA facilitated the collection of data that provided an in-depth understanding of the complexity of the experience of symptom clusters in patients with advanced lung cancer, adding a unique contribution to this body of knowledge. The results of this study highlight the limitations of definitions that currently underpin the study of symptom clusters in patients with cancer and the current empirical base to date, particularly the way that they do not acknowledge the core role that context and meaning play in the lived experience of this phenomenon. This lack of recognition of these core elements of the patient experience of symptom clusters poses the risk of this body of research producing data that have limited relevance to the patient and therefore clinical practice. It is therefore proposed that the study of symptom clusters in patients with cancer needs to move away from the reductionist approach which currently dominates and to broaden its scope, to one that acknowledges the complexity of the experience of symptom clusters, the core role that context and meaning play in such experiences, and contributions that patient experience can make in advancing this important and emerging body of research.

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Neustein, Michelle Elizabeth Schauer Caroline L. Wheatley Margaret A. "Polymer thin film colorimetric gas sensor for lung cancer analytes /". Philadelphia, Pa. : Drexel University, 2005. http://dspace.library.drexel.edu/handle/1860/488.

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Weber, Anika Maria. "Targeting ATM/ATR signalling in lung cancer". Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:3117219f-5273-4dc7-9a28-c531c708663f.

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Cells respond to the induction of DNA damage with activation of the DNA damage response (DDR), a complex signalling network which orchestrates cell cycle arrest and DNA repair in order to maintain genomic stability and cell viability. Activation of these signalling pathways enables cancer cells to survive DNA damaging chemo- or radiotherapy and contributes to the development of therapy resistance. Therefore, components of the DDR have become attractive targets for chemo- or radiosensitisation. Furthermore, cancer cells frequently exhibit defects in certain DDR components and may, as a consequence, become highly dependent on remaining DDR pathways to survive DNA damage. Two apical mediators of the DDR are the serine/threonine protein kinases ATM and ATR. ATM is frequently mutated in non-small cell lung cancer (NSCLC), and defects in ATM may render the tumour cells dependent on ATR signalling for survival. In this study, we characterised the functional consequences of ATM mutations in NSCLC cell lines and established an immunohistochemistry-based assay to identify patients with loss of ATM expression. As a single agent, pharmacological ATR inhibition (ATRi) was selectively cytotoxic for cells deficient in both ATM and p53. Furthermore, ATRi in combination with either ATM or PARP inhibition selectively killed tumour cells with mutant p53. We show that following ATR inhibition, ATM and p53 perform critical cell cycle checkpoint functions, independently of each other. Our results suggest that while retained function in any of these pathways is sufficient to maintain cell viability, functional loss of ATM, ATR and p53 results in premature mitotic entry, chromosome fragmentation and mitotic catastrophe. We conclude that in NSCLC the functional status of both ATM and p53 determines the cellular response to ATR inhibition, and propose that a combination of ATR inhibition with ATM or PARP inhibition may have broad utility for the treatment of p53-mutated NSCLC.

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Ramroth, Johanna Rankin. "Radiotherapy dose-fractionations and outcomes in cancer patients". Thesis, University of Oxford, 2017. http://ora.ox.ac.uk/objects/uuid:8c5a99de-7d8c-4b19-9a91-e6cf4efa7bd2.

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Radiotherapy cures many cancers, but the optimum total doses and fractionations used to treat different cancer types remain uncertain. While conventional fractionation (≈2 Gy per fraction) is common in many countries, UK practice has been highly variable. This thesis compared different curative-intent radiotherapy dose-fractionations used in non-small cell lung and breast cancer. These two cancers together make up over a quarter of UK cancer incidence and mortality, and radiotherapy can increase cure rates of both cancers. Two studies were conducted: (A) A meta-analysis of randomised radiotherapy trials in non-small cell lung cancer and (B) A cohort study of non-small cell lung and breast cancer radiotherapy in the Thames Valley. For the meta-analysis, a systematic search was conducted. Eligible studies were randomised comparisons of two or more radiotherapy regimens. Median survival ratios were calculated for each comparison and pooled. 3,795 patients in 25 randomised comparisons of radiotherapy dose were studied. When radiotherapy was given alone, the higher dose within-trial resulted in increased survival (median survival ratio 1.13, 95% confidence interval 1.04-1.22). When radiotherapy was given with concurrent chemotherapy, the higher dose within-trial resulted in decreased survival (median survival ratio 0.83, 95% confidence interval 0.71-0.97). For the cohort study, multiple Public Health England data sources were combined to obtain information on radiotherapy, patient characteristics, and outcomes. Multivariable Cox regressions were conducted separately by cancer site. 324 non-small cell lung, 8,879 invasive breast, and 477 ductal carcinoma in situ patients were studied. In analyses of both non-small cell lung and invasive breast cancer, increasing radiotherapy dose was associated with improved survival in some treatment centres, while in other centres the opposite was true. These opposite trends by treatment centre were unlikely to be explained by chance, and they suggest that differences in patient selection were driving results. There were insufficient events among ductal carcinoma in situ patients to assess associations. Findings from the meta-analysis support consideration of further radiotherapy dose escalation trials, making use of modern methods to reduce toxicity. Findings from the cohort study suggest that it is not possible to use observational studies to examine causal effects of radiotherapy dose-fractionation. This thesis therefore shows the continued importance of conducting sufficiently large randomised trials to ascertain optimal dose-fractionation in radiotherapy.

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Chan, Ching Eunice, i 陳清. "Pathogenetic role of aberrant promoter methylation in lung cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39557819.

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Yeung, Shuk-chun Debbie. "Psychological factors predicting quality of life among Hong Kong Chinese with lung cancer /". View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B36403210.

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Li, Tung-ching Kathy. "Hypermethylation of tumor suppressor genes in non-small cell lung cancer". Click to view the E-thesis via HKUTO, 2003. http://sunzi.lib.hku.hk/hkuto/record/B31971180.

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46

Davidson, Scott M. "Analysis of prognostic and drug resistance markers in lung cancer". Connect to e-thesis, 2007. http://theses.gla.ac.uk/101/.

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Thesis (M.D.) - University of Glasgow, 2007.
M.D. thesis submitted to the Centre for Oncology and Applied Pharmacology, Cancer Research UK Beatson Laboratories, University of Glasgow, 2007. Includes bibliographical references. Print version also available.

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47

Zhang, Qing Frankowski Ralph. "An empirical evaluation of the random forests classifier models for variable selection in a large-scale lung cancer case-control study /". See options below, 2006. http://proquest.umi.com/pqdweb?did=1324365481&sid=1&Fmt=2&clientId=68716&RQT=309&VName=PQD.

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Choi, Kim-ching Janie. "Vascular patterns and expression of angiogenesis-related molecules in non-small cell lung cancer". Click to view the E-thesis via HKUTO, 2003. http://sunzi.lib.hku.hk/hkuto/record/B31970953.

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49

Tai, Lai-shan, i 戴麗珊. "Molecular genetic characterizations of human non-small cell lung cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B31375315.

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50

Choy, Kit-chi, i 蔡潔芝. "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 therapy". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46632426.

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