Rozprawy doktorskie: „Cancer – Molecular aspects”

1

Fransén, Karin. "Molecular genetic aspects of colorectal cancer development /". Linköping : Univ, 2005. http://www.bibl.liu.se/liupubl/disp/disp2005/med878s.pdf.

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Hubbard, Alexandra Louise. "Some aspects of the molecular pathology of breast cancer". Thesis, University of Edinburgh, 1996. http://hdl.handle.net/1842/20581.

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This thesis examines some aspects of the molecular pathology of breast cancer. Disregulation of the c-erb B2 oncogene was related to several histopathological and biochemical features of breast cancer. Other genes, specifically THRA1 and urokinase plasminogen activator were investigated for disregulation and possible interaction with c-erb B2 in the biology of breast cancer. A differential PCR technique for the detection of c-erb B2 gene amplification, was tested and validated for use on paraffin embedded methacarn fixed breast cancer tissues. Tissues from 314 breast cancers and 43 control samples were assessed for c-erb B2 gene amplification by dPCR. In clinical material the results were not affected by the DNA contribution of normal tissue elements or by cancer DNA ploidy change. C-erb B2 gene amplification was detected in 55% of invasive cancers and in 66% of in situ cancers. C-erb B2 protein overexpression in breast cancer cells, as determined by specific immunohistochemistry, was only detected in 11% of invasive cancers and 43% of in situ cancers. Comparisons show that a substantial number of cancers with c-erb B2 amplification lack detectable protein overexpression. The nature of c-erb B2 gene disregulation in breast cancer appears to be complex and multiple combinations of biological events are suggested. A model for the involvement of c-erb B2 in breast cancer progression is proposed. Mechanisms of c-erb B2 gene amplification and interaction with other cellular proteins are discussed.

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3

黃鳳如 i Fung-yu Huang. "Molecular and cytogenetic analysis of cervical and vulvar cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B26662188.

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4

Kee, Francis, i 紀思思. "Molecular pathology of hepatocellular carcinoma". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40203785.

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5

Webster, Lucy R. "Diagnostic molecular profiling of ductal carcinoma in situ of the breast". Thesis, The University of Sydney, 2007. https://hdl.handle.net/2123/28109.

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The introduction of population-based mammographic screening has led to a dramatic increase in the diagnosis of ductal carcinoma in situ (DCIS) of the breast; with DCIS now accounting for approximately 25-35% of all screen-detected breast cancers. Epidemiological, histopathological and molecular studies have provided compelling evidence to support the notion that DCIS is a direct precursor of invasive cancer; although such data also indicate that DCIS represents a highly heterogeneous group of lesions. Some women with DCIS will develop life-threatening invasive cancer, whereas others may not. Currently, determination of the malignant potential of an individual DCIS lesion is very difficult, making selection of optimal treatment from the range of options available challenging. Histopathology has long been used to classify invasive breast tumours into biologically relevant sub-classes; although for DCIS there is still no universally accepted histological grading system. In recent years, gene expression profiling of invasive breast cancer has demonstrated that superior classification, prognostication and prediction can be achieved. Therefore, the principal aim of this study was to use classic histopathology and contemporary molecular biological methods to better classify DCIS lesions according to their inherent malignant potential. A significant difficulty in studying in situ breast cancer is a lack of rational endpoints against which potential markers can be judged; consequently initial studies were directed at identifying a rational surrogate end-point for use in subsequent molecular studies. Through the examination of a large cohort of screen-detected breast cancers, we demonstrated that the grade of concomitant invasive breast cancer was the best surrogate end-point to examine the malignant potential of in situ disease due to its direct relationship with breast cancer biology and established correlation with breast cancer survival. Another significant limitation to molecular studies of DCIS is the heterogeneity of breast tissue and the small size and limited extent of in situ lesions. Therefore, in this thesis laser capture microdissection and nucleic acid amplification techniques were successfully optimised and applied to a well-characterised cohort of DCIS lesions and adjacent areas of pre-malignant and benign epithelium. Gene expression profiling analysis of this cohort of laser capture microdissected samples was successfully performed on 36K oligonucleotide microarrays. Supervised analysis was used to identify genes differentially expressed between DCIS lesions associated with grade 1 and grade 3 invasive cancer. The “DCIS discriminative gene list” comprised 173 oligonucleotide probes and according to the relative expression of the top 100 genes samples were clustered into two biologically relevant groups. In addition, a gene expression grade index (GGI) was calculated and using a defined cut-point the DCIS lesions were classified into the same “low” and “high” molecular grade groups that had highly significant correlations with histopathologic and biological factors including DCIS nuclear grade, cell polarisation, necrosis, ER, PR, HERZ, p53 and Ki67. Further support for the clinical relevance of the gene expression derived DCIS classification was provided by the strong correlation between the molecular grade groups and both disease-free and overall survival in two independent invasive breast cancer cohorts. lmportantly, work described in this thesis also demonstrated that the gene-expression derived classification can be closely approximated using a combination of routinely available features including DCIS nuclear grade and accurate Ki67 scoring of the in situ component; thus offering a novel, biologically significant and clinically useful DCIS classification system. Results from array-based comparative genomic hybridisation (aCGH) analyses further supported the biological relevance of the gene-expression derived classification and identified potential candidate chromosomal regions underlying the variable malignant potential of in situ breast cancer.

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6

Wang, Yue, i 王悦. "Molecular analysis of mitochondrial DNA alterations in endometrial carcinomas". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B32059127.

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7

陳君怡 i Kwan-yi Queeny Chan. "Molecular studies on endometrial and ovarian carcinogenesis". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39634474.

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8

Chan, Kwan-yi Queeny, i 陳君怡. "Molecular study of pi-class glutathione-S-transferase in endometrial carcinoma". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29157717.

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9

Liao, Xiaoyun, i 廖晓耘. "Hedgehog signaling pathway and epigenetic studies in ovarian carcinomas and endometrial carcinomas". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41290367.

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10

Butler, Lisa Maree. "Molecular analysis of the human Fas gene in colorectal cancer /". Title page, contents and summary only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phb9858.pdf.

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11

Ko, Chi-fat, i 高自發. "Molecular regulations of deleted in liver cancer (DLC) protein family". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B41896889.

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12

Mitchell, Irene Patricia. "Clinical, cellular and molecular aspects of carbohydrate metabolising enzymes in human tissues". Thesis, Open University, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294109.

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13

Lam, King-yin Alfred, i 林敬賢. "Pathology and molecular biology of malignant thyroid tumours". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B29867824.

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14

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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15

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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16

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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17

Ng, Oi-lin Irene, i 呂愛蓮. "Allelic and molecular changes in multistep process of hepatocarcinogenesis". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B32058767.

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18

Weichhaus, Michael Georg. "Molecular aspects of the link between obesity, insulin resistance and breast cancer". Thesis, Robert Gordon University, 2010. http://hdl.handle.net/10059/591.

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Obesity is a multi-factorial metabolic disease, resulting in increased adipose tissue acquisition by the host. This disease increases the risk for developing co-morbidities, including Metabolic Syndrome and other disorders such as breast cancer. Obesity, and particularly abdominal obesity, is characterised by metabolic changes, including chronically elevated insulin concentrations and aberrant secretion of cytokines released from fat tissue, called adipokines. Epidemiologically, the risk of developing postmenopausal breast cancer is increased in obese individuals. The molecular link between obesity and breast cancer however is not well understood. The study presented here aimed at identifying the molecular mechanisms involved in this link, by testing the hypothesis that high insulin concentration and certain adipokines may promote breast cancer progression and/or breast cancer aetiology. A cell culture system of breast cancer cells and breast epithelial cells was employed to investigate changes in cell proliferation, activation of cell signalling pathways, cell cycle progression and apoptosis after treatment with insulin, leptin, TNF-α, adiponectin and IL-6. In MDA-MB-231 breast cancer cells, insulin treatment did not affect cell proliferation, cell cycle or apoptosis. Conversely, IR-phosphorylation, AKT-phosphorylation and ERK1/2-phosphorylation were all significantly increased. Microarray analysis indicated several important changes in gene expression with insulin treatment. Leptin treatment increased proliferation by 21%. Additional analyses of the effect of leptin indicated that neither the PI3-kinase pathway nor the MAP-kinase pathway was involved in mediating this effect. Treatment with TNF-α increased apoptosis, but did not affect cell proliferation or activation of cell signalling pathways. In MCF-10A breast epithelial cells, cell proliferation increased after insulin treatment by 180%. IR-phosphorylation, AKT-phosphorylation and ERK1/2 phosphorylation were all significantly increased while early apoptosis decreased after insulin treatment. Analysis of cell cycle however did not indicate a change in progression. Microarray analysis indicated that insulin treatment may increase expression of genes related to cancer growth. Leptin treatment increased cell proliferation and also increased ERK1/2-phosphorylation, while AKT-phosphorylation was not affected. Leptin did not change cell cycle progression. TNF-α treatment increased cell proliferation and also increased ERK1/2 phosphorylation, while AKT-phosphorylation was not changed. TNF-α treatment tended to increase apoptosis, the change however was not statistically significant. In SK-BR-3 breast cancer cells, cell proliferation did not change after insulin treatment. IR-phosphorylation and AKT-phosphorylation increased after insulin treatment, while ERK1/2-phosphorylation decreased. Gene expression of cyclin D and cyclin E increased with insulin treatment, while apoptotic rate and cell cycle profile were also not affected. Cell proliferation increased by 115% after treatment with 100 ng/ml leptin. ERK1/2-phosphorylation however decreased, while AKT-phosphorylation tended to increase, but the change was not statistically significant. Cell cycle profile was not affected by leptin treatment, G1-phase however tended to increase, but the change was again not statistically significant. Cell proliferation increased by 59% after 48 h treatment with 10 ng/ml TNF-α. AKT-phosphorylation and ERK1/2-phosphorylation increased with TNF-α treatment. Cell cycle analysis showed a decrease in S-phase and G2-phase, indicative of a decrease in cell cycle progression. These results indicate that none of the examined obesity-related factors is convincingly identified as the main molecular link between obesity and postmenopausal breast cancer. Conversely, all treatments affected each of the cell lines in, at least, one of the examined aspects. This indicates that many of the obesity-related factors may affect breast cancer and that a single breast tumour may utilise a unique combination of those factors to promote growth. All treatments increased proliferation in MCF-10A breast epithelial cells, with additional analysis generally supporting growth promotion. Insulin treatment particularly increased cell proliferation, while leptin and TNF-α increased MAP-kinase signalling. This may indicate that insulin and adipokines may have a higher impact on breast cancer aetiology than on breast cancer progression.

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19

凌明達 i Ming-tat Patrick Ling. "A study of molecular and cell biology of prostate tumorigenesis in cell culture". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31223102.

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20

Ma, Huan, i 马欢. "Molecular analysis of ocular adnexal lymphomas in the search for potential biomarkers". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46921655.

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21

Hu, Yingchuan, i 胡穎川. "Molecular pathogenesis of oesophageal squamous cell carcinoma". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31241797.

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22

Law, Bic-fai Fian, i 羅璧輝. "Molecular genetics of esophageal squamous cell carcinoma". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B3660446X.

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23

Sze, Ivan, i 施綺雯. "Estrogenic effects of isoflavonoids on human breast cancer cells". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B45010894.

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24

Bull, Caroline Joyce. "Molecular and epidemiological aspects of prostate cancer : the impact of LDL-lowering therapy". Thesis, University of Bristol, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.742991.

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25

徐智 i Zhi Xu. "Yes associated protein (YAP) in hepatocellular carcinoma: oncogenic functions and molecular targeting". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43278589.

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26

Li, Shao Ying. "Study of the role of DNA methylation and PIK3CA mutations in human breast cancer". University of Western Australia. School of Surgery and Pathology, 2006. http://theses.library.uwa.edu.au/adt-WU2006.0031.

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[Truncated abstract] Introduction: Breast cancer is a heterogeneous disease, resulting in very different outcomes for women with apparently similar tumour characteristics. In order for patients to have optimal treatment, a better understanding of the molecular nature of their disease is required. Aims: The aims of this thesis were: 1) To determine whether methylation of RARβ2, ER, CDH1, BRCA1, CCND2, p16 and TWIST genes are associated with phenotypic features of breast cancer and the prognostic significance of methylation of these genes. 2) To investigate for possible associations between the frequency of methylation at RARβ2, CDH1, ER, BRCA1, CCND2, p16 and TWIST genes and the presence of germ-line variants in the TS, MTHFR, MS, CBS, MTHFD1 and DNMT3B genes, as well as for possible correlations between these polymorphisms and clincopathological features of breast cancer including patient outcome. 3) To determine whether PIK3CA mutations determined clinical phenotype and the prognostic significance of PIK3CA mutations in a large and well characterized cohort of breast cancer patients. Methods: A large and well characterized series of primary breast tumours were selected for methylation of RARβ2, ER, CDH1, BRCA1, CCND2, p16 and TWIST genes using MSP, and for polymorphisms in TS, MTHFR, MS, CBS, MTHFD1 and DNMT3B genes using PCR, PCR-RFLP and PCR-SSCP. Mutations to PIK3CA were detected using F-SSCP. Results and Conclusions: Methylation frequencies ranged from 11% for CCND2 to 84% for ER. More frequent hypermethylation was observed in tumours with poor histological differentiation compared to those with well/moderate differentiation, as well as trends for association with larger tumour size and mutant TP53. Tumours with ER and CDH1 methylation were associated with significantly lower hormone receptor levels, younger age at diagnosis and the presence of mutant p53. TWIST methylation is firstly reported to be associated with significantly older patient age at diagnosis and larger tumour size. Our data suggests that gene methylation may be linked to various pathological features of breast cancer. However, there appears to be little support for a distinctive CpG island methylator phenotype in breast cancer.

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陳國龍 i Kok-lung Chan. "Molecular alterations on chromosome 8 in hepatocellular carcinoma". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31225676.

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Chan, Yan-yan, i 陳茵茵. "The role of cyclin E1 in hepatocellular carcinoma". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/208041.

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Hepatocellular carcinoma (HCC) accounts for 70-85% of liver cancer, which is the sixth most common cancer in the world. Prognosis of HCC is dismal with little chance of complete recovery after diagnosis. It is of essence to discover the key molecules involved in the tumor progression. This could help earlier detection of HCC and establish targeted molecular therapies. Cyclin E1 (CCNE1) is a cyclin molecule responsible for the transition from G1 to S phase of the cell cycle and is often dysregulated in human cancers. CCNE1 is reported with overexpression in about 30-70% of HCC cases. It expresses in tumor cells as a ladder of proteins and as low molecular weight CCNE1. The study is aimed to investigate the role of CCNE1 in HCC. From the local cohort of HCC patients, 6 out of 13 patients (46.2%) of HCC tumor tissues were found with CCNE1 overexpression compared with the non-tumor tissues by western blotting. The presence of three CCNE1 isoforms in HCC was detected. The expression of total CCNE1 and each isoform varied independently among the studied HCC cell lines, with HepG2 having the highest expression and 97L the lowest. To extend our study on the regulation of CCNE1 expression, the expression of selected four genes associating with the CCNE1 expression and functions was studied by quantitative PCR (qPCR). F-box and WD repeat domain containing 7, E3 ubiquitin protein ligase (FBXW7) and cullin 3 (CUL3), the two genes responsible for CCNE1 degradation, had increased expression in the HCC cell lines with higher CCNE1 expression. Cyclin A (CCNA2), the downstream cyclin molecule of CCNE1, also had higher expression in these cell lines. In contrast, the expression of cyclin dependent kinase 2 (CDK2), the catalytic partner of CCNE1, had the least difference among the six HCC cell lines compared to other three genes. To characterize the role of CCNE1 isoforms in HCC, CCNE1 isoform 1, 2, and 3 were overexpressed in PLC cells and such overexpression remained even after 8 passages in culture. In flow cytometric analysis, GFP signal in cell culture population was viewed to observe the transduction efficiency. The vector control showed the strongest GFP signal, followed by CCNE1 isoform 3 showing dim signal. CCNE1 isoform 1 and 2 almost showed no signal. In the functional studies, the overexpression of CCNE1 isoform 3 could increase proliferation and migration of HCC cells. In summary, CCNE1 could promote proliferation and migration of HCC cells through elevated expression of CCNE1 isoform 3.
published_or_final_version
Surgery
Master
Master of Philosophy

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29

Li, Cuilan, i 李翠兰. "Functional role of AMPK-{221}1 expression in ovarian cancer progression". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46678530.

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Yuen, Siu-tsan Thomas, i 袁兆燦. "Molecular genetics of colorectal cancer and its relevance to epidemiology in Chinese population". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B26627449.

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31

Drake, Jeremy. "The expression and function of secreted frizzled-related protein 4 in human serous ovarian carcinoma". University of Western Australia. School of Anatomy and Human Biology, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0072.

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[Truncated abstract] Ovarian cancer is currently the leading cause of death from gynaecological malignancies in women from developed countries. Serous ovarian cancer is the most prevalent type of all ovarian cancers, with the majority diagnosed in an advanced stage where treatment efficacy is reduced and patient survival is poor. Because of this fact, the development of improved detection and treatment strategies are necessary, with much research focussing on the complex molecular pathways involved in ovarian tumour growth as one potential avenue for intervention. Apoptosis, or programmed cell death, is one such area of investigation because currently successful cancer treatments induce apoptosis in tumour cells. Molecular analysis of apoptosis in both normal tissue and tumours has established a positive relationship between increased expression of secreted frizzled-related protein 4 (SFRP4) and apoptosis, however to date, very little research has focussed on the role of this gene in the ovary . . . An examination of SFRP4 and β-catenin expression in 163 primary serous ovarian carcinomas revealed high SFRP4 expression was associated with low β-catenin expression and conversely, low SFRP4 was associated with high β-catenin expression in the majority of the ovarian tumours analysed, reinforcing the inverse relationship observed in the ovarian cell lines. A positive trend was observed between cancer stage and the expression level of these proteins, with increased SFRP4 expression and reduced β-catenin expression as cancer stage increased. Additionally, patient survival revealed a trend towards increased survival among ovarian cancer patients who had tumours expressing low levels of SFRP4. Taken together, the novel findings of this study indicate that the increased expression of SFRP4 observed in a large proportion of serous ovarian cancers is a cellular response to down-regulate the level of β-catenin, and thus an attempt to maintain cellular homeostasis by counteracting the excessive proliferating signals present in these tumour cells.

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32

Iddawela, Mahesh Yasantha Bandara. "Genome wide copy number and gene expression profiling using archived tissue for molecular marker studies in breast cancer". Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609626.

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33

Zhu, Rui, i 朱睿. "Liver-intestine cadherin (CDH17) in hepatocellular carcinoma: molecular analysis and clinicalimplications". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43703793.

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34

Leung, Suet-yi, i 梁雪兒. "Epstein-Barr virus-associated carcinoma arising outside the nasopharynx: a clinico-pathological andmolecular study". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31981641.

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35

Kwan, Pak-shing, i 關百誠. "Roles of Daxx in mitosis and prostate carcinogenesis". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43085337.

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36

Tse, Yuk-ting Edith, i 謝玉婷. "Expression and function of caveolin-1 in hepatocellular carcinoma". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45984554.

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37

Wong, Yuen-sze Sivia, i 王苑斯. "Role of hypoxia-induced upregulation of caveolin-1 in hepatocellular carcinoma". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46944333.

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38

Wang, Jian, i 王健. "Identification and characterization of N-terminal kinase like protein in hepatocellular carcinoma". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47036370.

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39

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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40

Prabhala, Rao H. "Two different molecular pathways of immunomodulation by retinoids and carotenoids". Diss., The University of Arizona, 1989. http://hdl.handle.net/10150/184676.

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Epidemiological studies suggest that both retinoid and carotenoid intakes are inversely correlated with the incidence of human cancers. Animal studies show that both retinoids and carotenoids inhibit tumor cell growth. Both retinoids and carotenoids activate the cytotoxicity function of macrophages in animal experiments. The purpose of this study is to evaluate the molecular mechanism for 13-cis retinoic acid (13-cRA) and beta-carotene (BC) induced immunomodulation which could explain their anti-cancer affects. The effects of 13-cRA and BC were studied on various subpopulations of T-lymphocytes both in vitro and in vivo. For in vitro studies, peripheral blood mononuclear cells (PBMC) were incubated with test compounds at clinically achievable concentrations (10⁻⁸M) for three days. Then the cells were stained with monoclonal antibodies followed by the analysis of flow cytometer. For in vivo studies, PBMC were collected from Barrett's esophagus or oral leukoplakia patients during treatment with 13-cRA (1mg/kg/day) or BC (30 mg/day), respectively. Then the cells were analyzed with monoclonal antibodies and flow cytometry. Both compounds showed the capability of stimulating different subpopulations of T-lymphocytes. 13-cRA predominantly increased the number of T-helper cells, their interleukin 2 (IL-2) receptors and their response to mitogens. Whereas, BC elevated the number of Natural Kill (NK) cells, their IL-2 receptors and their cytotoxicity against K562 target cells. Though these immunomodulatory effects appeared to be unaffected by the presence and cytotoxic functions of macrophages, cytokines seemed to have an important role in the retinoid- and carotenoid-induced immunomodulation. Plasma levels of IL-2 and tumor necrosis factor (TNF) measured by ELISA procedures were increased in patients treated for two months with 13-cRA and BC respectively. Anti-IL-2 and anti-TNF antibodies blocked the retinoic- and carotenoid-induced immunomodulation in in vitro studies. These results indicate that 13-cRA, activating T-helper cells with IL-2 production, and BC, activating NK cells with TNF release, induced immunostimulation which might be able to provide the anti-cancer affects in part seen in epidemiological studies.

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Agenbag, Gloudi. "Molecular genetic analysis of familial breast cancer in South Africa". Thesis, Link to the online version, 2005. http://hdl.handle.net/10019/953.

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Human, Veronique. "Molecular analysis of genes involved in iron overload implicated in oesophageal cancer". Thesis, Link to the online version, 2007. http://hdl.handle.net/10019/391.

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Efstathiou, Jason Alexander. "The role of adhesion molecules in colorectal carcinogenesis". Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670210.

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Wei, Na, i 魏娜. "The function and modulation of programmed cell death 4 (PDCD4) in ovarian cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B45898650.

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Sojic, A. "BIOMEDICAL ONTOLOGIES: EXAMINING ASPECTS OF INTEGRATION ACROSS BREAST CANCER KNOWLEDGE DOMAINS". Doctoral thesis, Università degli Studi di Milano, 2013. http://hdl.handle.net/2434/218887.

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The key ideas developed in this thesis lie at the intersection of epistemology, philosophy of molecular biology, medicine, and computer science. I examine how the epistemic and pragmatic needs of agents distributed across particular scientific disciplines influence the domain-specific reasoning, classification, and representation of breast cancer. The motivation to undertake an interdisciplinary approach, while addressing the problems of knowledge integration, originates in the peculiarity of the integrative endeavour of sciences that is fostered by information technologies and ontology engineering methods. I analyse what knowledge integration in this new field means and how it is possible to integrate diverse knowledge domains, such as clinical and molecular. I examine the extent and character of the integration achieved through the application of biomedical ontologies. While particular disciplines target certain aspects of breast cancer-related phenomena, biomedical ontologies target biomedical knowledge about phenomena that is often captured within diverse classificatory systems and domain-specific representations. In order to integrate dispersed pieces of knowledge, which is distributed across assorted research domains and knowledgebases, ontology engineers need to deal with the heterogeneity of terminological, conceptual, and practical aims that are not always shared among the domains. Accordingly, I analyse the specificities, similarities, and diversities across the clinical and biomedical domain conceptualisations and classifications of breast cancer. Instead of favouring a unifying approach to knowledge integration, my analysis shows that heterogeneous classifications and representations originate from different epistemic and pragmatic needs, each of which brings a fruitful insight into the problem. Thus, while embracing a pluralistic view on the ontologies that are capturing various aspects of knowledge, I argue that the resulting integration should be understood in terms of a coordinated social effort to bring knowledge together as needed and when needed, rather than in terms of a unity that represents domain-specific knowledge in a uniform manner. Furthermore, I characterise biomedical ontologies and knowledgebases as a novel socio-technological medium that allows representational interoperability across the domains. As an example, which also marks my own contribution to the collaborative efforts, I present an ontology for HER2+ breast cancer phenotypes that integrates clinical and molecular knowledge in an explicit way. Through this and a number of other examples, I specify how biomedical ontologies support a mutual enrichment of knowledge across the domains, thereby enabling the application of molecular knowledge into the clinics.

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Chiu, Pui-man, i 趙佩文. "Molecular genetics of cervical cancer: from chromosome number alterations to aberrant gene expressions". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43085544.

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Li, Jin, i 李晋. "Role of AMPK signaling in the anti-cancer effects of silibinin in esophageal squamous cell carcinoma". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46678888.

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Zhao, Wei, i 趙煒. "BRAF mutation and aberrant methylation of gene promoters in the pathogenesis of gastrointestinal tract adenocarcinoma". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B36718464.

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Wang, Hui. "Molecular mechanisms of oridonin-induced cytotoxicity and apoptosis in HepG2 cells". HKBU Institutional Repository, 2010. http://repository.hkbu.edu.hk/etd_ra/1162.

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Fatima, Sarwat. "The role of dickkopfs (DKKs) in hepatocellular carcinoma: with a focus on DKK4". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47029523.

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