Rozprawy doktorskie: „Cancer – Genetic 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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Steggles, Naomi. "Psychological aspects of genetic testing for cancer". Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271020.

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Cheung, Chin-ling, i 張展寧. "Genetic analysis of nasopharyngeal cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B44659866.

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4

Hayat, Roshanai Afsaneh. "Psychological and Behavioral Aspects of Receiving Genetic Counseling for Hereditary Cancer". Doctoral thesis, Uppsala universitet, Vårdvetenskap, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-128870.

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The overall aims of this thesis were to investigate psychological and behavioral effects of receiving cancer genetic counseling for breast, ovarian and colorectal cancer and/or with a family history of these cancer types and to determine whether counselees’ informational needs were met. Study I was performed 3-7 years post-counseling. Participants (n=214) reported a relatively high level of anxiety but a low level of depression compared to cancer patients in general. However, there was no indication that the distress experienced was due to the counseling. Moderate changes in life and family relations, high level of adherence to recommended controls and satisfaction was reported. Study II was a randomized control trial (RCT) intervention study which involved 147 counselees. An increase in the level of knowledge and correct estimation of personal risk was reported in both the intervention and control groups, although this increase declined at later follow-up. Enhanced information led to significantly greater satisfaction with the given information, and the way of informing relatives. Most counselees had shared information with their at-risk relatives. Study III focused on sharing information with at-risk relatives among participants in study II and their relatives (n=81). Counselees were interviewed and answered a questionnaire, whilst their relatives only answered the questionnaire. Counselees reported positive/neutral feelings about communicating genetic information and mostly interpreted their relatives’ reactions as positive/ neutral. Also, approximately 50% of relatives reported positive/neutral reactions and were generally satisfied with the received information. Study IV was conducted in Sweden and Norway based on 235 counselees. Counselees expected counselors to be skillful and thoughtful, take them seriously and provide risk estimations and medical information. Most important issues to counselees were satisfactorily addressed by the counselors. Analyzing importance rankings resulted in five categories of needs: a need for facts, caring communication and medical information, need for understanding and support in sharing genetic information, practical care and medical/practical information. In conclusion, no adverse psychological or behavioral effect on counselees was observed. Apparently, genetic counseling is managed properly and counselors successfully address counselees’ needs. Providing extended information does not seem necessary, however, tailoring information to individual counselees needs may create a more effective counseling.

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5

陳安安 i On-on Annie Chan. "Methylation in colorectal cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B25256312.

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6

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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7

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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8

Wright, C. M. "The prognostic significance of microsatellite instability in sporadic stage C colorectal cancer". Thesis, The University of Sydney, 2008. https://hdl.handle.net/2123/28955.

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Identification and understanding of the molecular events involved in colorectal cancer (CRC) pathogenesis should lead to better comprehension of the disease process, hopefully leading to better prognostic stratification, and as a result more targeted treatment regimens and improved patient outcomes. A sub group of sporadic CRC exhibit microsatellite instability (MSI). MSI is seen when the fidelity of DNA replication is impaired. Cancers may be categorized as MSI-high (MSI-H), MSI-low (MSI-L), or microsatellite stable (MSS), according to the degree of MSI exhibited. This research project was designed to analyse the association between MSI—H and MSI-L, clinicopathological features and survival in an unselected group of patients with sporadic Australian Clinicopathological Stage (ACPS) C / American Joint Committee on Cancer (AJCC) stage III CRC, i.e. patients with lymph node metastases at the time of surgical resection of their cancer. The criteria used to determine MSI, specifically the type and number of microsatellite markers used, were also reviewed. 255 patients who underwent resection for sporadic ACPS stage C CRC were studied; none of these patients received chemotherapy. Archival normal and tumour DNA were extracted and amplified by polymerase chain reaction using a radioactive-labelling technique and a panel of internationally recognised microsatellite markers. MSI-H was defined as instability in 2 40% of 7 markers, MSI-L as instability at > 0% but < 40% of 11 markers, and M88 as no instability. Twenty one MSI-H and 33 MSI-L CRC were identified. Significant results included that MSI-H tumours are more commonly right sided (p < 0.00001); larger (p 5 0.0005); more likely to be high grade (p = 0.049); and, after adjustment for age, sex and other pathology variables, associated with improved survival (p = 0.015). No difference was found between the biological characteristics of MSI-L and MSS CRC. MSI-L CRC showed a trend towards poorer cancer-specific survival than MSS CRC but this difference did not reach statistical significance. Although dependent on the number and type of microsatellites used, similar trends in the results were seen when different criteria were used to determine MSI. This study has contributed to the rapidly expanding literature on CRC carcinogenesis and, at the time completed, was one of the first to show an association between MSI-H and improved survival in clinicopathological stage C CRC patients who had not received chemotherapy. It supports the view that identification of MSI status in patients with sporadic ACPS C / AJCC stage III tumours may help stratify patients according to prognosis and should be considered in therapeutic decision making and future trials of adjuvant therapy. However to accurately determine the clinical usefulness of MSI more precise standardisation of the definition and methodologies used to identify M81 is required.

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9

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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10

Khoo, Ui-soon, i 邱瑋璇. "Genetic susceptibility to gynaecological cancers in the Chinese population". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B25257365.

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11

陳遠光 i Yuen-kwong Chan. "Study on the role of genetic and epigenetic factors in relation to theBRCA genes in epithelial ovarian cancers". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B42576726.

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12

Tong, Tin-wing, i 唐天穎. "Investigation of transcript expression of PRKAR2A, DUSP1, STMN2 and MAPT genes in nasopharyngeal carcinoma, ovarian cancer and benignovarian tumor". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46632700.

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13

Jardim-Perassi, Bruna Victorasso [UNESP]. "Avaliação da angiogênese em resposta ao tratamento com melatonina no câncer de mama: estudo in vitro e in vivo". Universidade Estadual Paulista (UNESP), 2014. http://hdl.handle.net/11449/110553.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
O câncer de mama apresenta altas taxas de incidência e mortalidade, sendo a neoplasia mais comum entre as mulheres. O rápido crescimento do tumor resulta em hipóxia no microambiente tumoral, levando a uma cascata de eventos que induzem a angiogênese e conseqüente progressão do câncer. Assim, a identificação de agentes terapêuticos que possam inibir a angiogênese é essencial para o controle da progressão tumoral. Nesse sentido, tem sido demonstrado que a administração exógena da melatonina, um hormônio naturalmente secretado pela glândula pineal, apresenta diversos efeitos oncostáticos em diferentes tipos de câncer. Assim, o objetivo desse estudo foi avaliar a efetividade do tratamento com melatonina sobre a angiogênese do câncer de mama, em estudos in vitro e in vivo. No estudo in vitro, as linhagens de câncer de mama MCF-7 e MDA-MB-231 foram tratadas com melatonina sob condições de hipóxia mimetizadas pelo Cloreto de Cobalto (CoCl2). A viabilidade celular foi verificada pelo ensaio MTT, a expressão do fator de transcrição induzido por hipóxia (HIF-1α) e do fator de crescimento endotelial vascular (VEGF-A) foi avaliada por PCR em tempo real e imunocitoquímica. Além disso, demais proteínas envolvidas na angiogênese foram avaliadas por Protein Array. No estudo in vivo, as células MDA-MB-231 foram implantadas em camundongos nude atímicos, os quais foram tratados com melatonina (40 mg/kg) por 21 dias. O tumor foi medido semanalmente e a avaliação da angiogênese foi realizada pela técnica de tomografia computadorizada por emissão de fóton único (SPECT), com o radiotraçador Tc- 99m-HYNIC-VEGF-c, agente específico para os receptores de VEGF (VEGFR2/VEGF3). Além disso, as proteínas VEGFR2, VEGFR3, fator de fator de von Willebrand (vWF) e marcador de proliferação celular (Ki-67) foram avaliados no tecido tumoral por imuno-histoquímica, e demais proteínas angiogênicas por Protein Array. O estudo in ...
Breast cancer has high rates of incidence and mortality, and it is the most common cancer among women. The rapid tumor growth results in hypoxia on tumor microenvironment, leading to a cascade of events that induce angiogenesis and subsequent cancer progression. Thus, the identification of therapeutic agents that can inhibit angiogenesis is essential for the control of tumor progression. Exogenous administration of melatonin, a hormone secreted by the pineal gland, has been shown several oncostatics effects on different types of cancers. The aim of this study was to evaluate the effectiveness of melatonin treatment on angiogenesis in breast cancer, in the in vitro and in vivo studies. In the in vitro study, breast cancer cell lines (MCF-7 and MDA-MB-231) were treated with melatonin under cobalt chloride (CoCl2)-induced hypoxic conditions. Cell viability was measured by MTT assay, the expression of hypoxia-inducible factor 1-alpha (HIF-1α) and vascular endothelial growth factor (VEGF-A) was assessed by real-time PCR and immunocytochemistry. Additionally, other proteins involved in angiogenesis were evaluated by the Protein Array. In the in vivo study, the MDA-MB-231 cells were implanted in athymic nude mice, which were treated with melatonin (40 mg/kg) for 21 days. The tumor was measured weekly and evaluation of angiogenesis was performed by single-photon emission computed tomography (SPECT) with Tc-99m-HYNIC-VEGF-c, which is specific for VEGF receptors (VEGFR2/VEGF3). Moreover, VEGFR2, VEGFR3, von Willebrand factor (vWF) and cell proliferation marker (Ki-67) were evaluated in tumor tissue by immunohistochemistry, and other angiogenic proteins by Protein Array. Results from the in vitro study showed that 1 mM of melatonin under hypoxic conditions (200 μM CoCl2) led to decreased cell viability, protein levels of HIF- 1α and gene and protein expression of VEGF-A in both cell lines (p < 0.05). Among other proteins evaluated, melatonin ...

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14

Jardim-Perassi, Bruna Victorasso. "Avaliação da angiogênese em resposta ao tratamento com melatonina no câncer de mama : estudo in vitro e in vivo /". São José do Rio Preto, 2014. http://hdl.handle.net/11449/110553.

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Orientador: Debora Aparecida Pires de Campos Zuccari
Banca: Ana Elizabete Silva
Banca: Dorotéia Rossi Silva Souza
Banca: Samuel Cos Corral
Banca: Bruno Cogliati
Resumo: O câncer de mama apresenta altas taxas de incidência e mortalidade, sendo a neoplasia mais comum entre as mulheres. O rápido crescimento do tumor resulta em hipóxia no microambiente tumoral, levando a uma cascata de eventos que induzem a angiogênese e conseqüente progressão do câncer. Assim, a identificação de agentes terapêuticos que possam inibir a angiogênese é essencial para o controle da progressão tumoral. Nesse sentido, tem sido demonstrado que a administração exógena da melatonina, um hormônio naturalmente secretado pela glândula pineal, apresenta diversos efeitos oncostáticos em diferentes tipos de câncer. Assim, o objetivo desse estudo foi avaliar a efetividade do tratamento com melatonina sobre a angiogênese do câncer de mama, em estudos in vitro e in vivo. No estudo in vitro, as linhagens de câncer de mama MCF-7 e MDA-MB-231 foram tratadas com melatonina sob condições de hipóxia mimetizadas pelo Cloreto de Cobalto (CoCl2). A viabilidade celular foi verificada pelo ensaio MTT, a expressão do fator de transcrição induzido por hipóxia (HIF-1α) e do fator de crescimento endotelial vascular (VEGF-A) foi avaliada por PCR em tempo real e imunocitoquímica. Além disso, demais proteínas envolvidas na angiogênese foram avaliadas por Protein Array. No estudo in vivo, as células MDA-MB-231 foram implantadas em camundongos nude atímicos, os quais foram tratados com melatonina (40 mg/kg) por 21 dias. O tumor foi medido semanalmente e a avaliação da angiogênese foi realizada pela técnica de tomografia computadorizada por emissão de fóton único (SPECT), com o radiotraçador Tc- 99m-HYNIC-VEGF-c, agente específico para os receptores de VEGF (VEGFR2/VEGF3). Além disso, as proteínas VEGFR2, VEGFR3, fator de fator de von Willebrand (vWF) e marcador de proliferação celular (Ki-67) foram avaliados no tecido tumoral por imuno-histoquímica, e demais proteínas angiogênicas por Protein Array. O estudo in ...
Abstract: Breast cancer has high rates of incidence and mortality, and it is the most common cancer among women. The rapid tumor growth results in hypoxia on tumor microenvironment, leading to a cascade of events that induce angiogenesis and subsequent cancer progression. Thus, the identification of therapeutic agents that can inhibit angiogenesis is essential for the control of tumor progression. Exogenous administration of melatonin, a hormone secreted by the pineal gland, has been shown several oncostatics effects on different types of cancers. The aim of this study was to evaluate the effectiveness of melatonin treatment on angiogenesis in breast cancer, in the in vitro and in vivo studies. In the in vitro study, breast cancer cell lines (MCF-7 and MDA-MB-231) were treated with melatonin under cobalt chloride (CoCl2)-induced hypoxic conditions. Cell viability was measured by MTT assay, the expression of hypoxia-inducible factor 1-alpha (HIF-1α) and vascular endothelial growth factor (VEGF-A) was assessed by real-time PCR and immunocytochemistry. Additionally, other proteins involved in angiogenesis were evaluated by the Protein Array. In the in vivo study, the MDA-MB-231 cells were implanted in athymic nude mice, which were treated with melatonin (40 mg/kg) for 21 days. The tumor was measured weekly and evaluation of angiogenesis was performed by single-photon emission computed tomography (SPECT) with Tc-99m-HYNIC-VEGF-c, which is specific for VEGF receptors (VEGFR2/VEGF3). Moreover, VEGFR2, VEGFR3, von Willebrand factor (vWF) and cell proliferation marker (Ki-67) were evaluated in tumor tissue by immunohistochemistry, and other angiogenic proteins by Protein Array. Results from the in vitro study showed that 1 mM of melatonin under hypoxic conditions (200 μM CoCl2) led to decreased cell viability, protein levels of HIF- 1α and gene and protein expression of VEGF-A in both cell lines (p < 0.05). Among other proteins evaluated, melatonin ...
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15

Fung, Wai-Ki Vicki, i 馮慧琪. "Epigenetic alterations in gastric cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B45009995.

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16

Lam, Chi-leung David, i 林志良. "Gene expression profiling in non-small cell lung cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B38585777.

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陳潔盈 i Kit-ying Loucia Chan. "Expression analysis of Candidate cancer genes in non-small cell lung cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B45011163.

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Tam, Hok-nang Alex, i 譚學能. "Epigenetic inactivation of protocadherin PCDH10 in esophageal cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B45011011.

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Li, Carmen, i 李嘉敏. "Characterisation of methylator phenotype of colorectal cancer in young patients". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/207182.

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The majority of sporadic colorectal cancer (CRC) cases affects individuals over the age of 50, but about 10% of cases occur in young adults under 50 in Hong Kong. Apart from germline mutation of the DNA mismatch repair genes that predisposes to early-onset CRC with a high-level of microsatellite instability (MSI-H), it is unknown if the mechanisms that give rise to CRC in other young adults differ from those in older individuals. In an effort to understand the genetic and epigenetic basis of early and late-onset CRC outside the Lynch Syndrome setting, we performed a detailed characterization of 36 MSI-H and 198 non-MSI-H tumours from patients of varying ages. This characterization was based primarily on the presence of the CpG island methylator phenotype (CIMP), as measured by the level of DNA methylation; and presence of genetic instability, as measured by DNA copy number aberrations, as well as mutations in BRAF, KRAS, or TP53. Our findings revealed that early (≤50) and late-onset (>50) CRCs have different genetic and epigenetic features. In non-MSI-H cancers, CIMP-H was associated with early-onset, while CIMP-L and KRAS mutation was associated with late-onset. However, in MSI-H tumours, late-onset disease was associated with CIMP-H and BRAF mutation. In addition, promoter methylation of MLH1 in early-onset MSI-H patients had a higher frequency of occurring in the germline that was locus specific, whereas nearly all late-onset MSI-H patients showed somatic regional methylation at the MLH1 locus, as well as regional methylation on other chromosomes. This is the first study to show regional methylation at chromosome 9p21 and 7p14, which encompass the CIMP markers P16 and ELMO1, respectively. We also observed an association between regional methylation and CIMP-H, but in MSI-H cases it was linked with late-onset, whereas in non-MSI-H cases it was irrespective of age. This suggests that mechanisms of methylation seeding and spreading may be different in early and late-onset disease. Moreover, CIMP-H non-MSI-H cases had significantly worse prognosis (p=0.021 for overall survival, p=0.004 for disease-free survival) and poor response to chemotherapy compared to CIMP-L or CIMP-Neg cases. Lastly, a methylation score assigned to non-MSI-H patients based on the degree of methylation of known CIMP markers was a significant prognostic factor of disease-free survival (p=0.004), and patients with a high methylation score showed a poor response to chemotherapy. Thus, our results suggest that different genetic and epigenetic mechanisms may drive tumourigenesis in early and late-onset disease. Although further research will be needed to elucidate the exact nature of these mechanisms, our findings should help to improve current classification of CRC patients with a goal towards personalized treatment.
published_or_final_version
Pathology
Doctoral
Doctor of Philosophy

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20

Mui, Kin-cheong, i 梅堅祥. "Inactivation of DNA match repair proteins in premalignant lesions in Lynch syndrome". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B44659635.

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Tai, Bik-wah Diana, i 戴碧華. "Haplotype analysis of the family with Lynch syndrome". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45153772.

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22

Law, Wai-lok, i 羅韋洛. "NotI microarrays for identification of chromosome 3 methylation signatures in nasopharyngeal carcinoma (NPC) and esophageal squamouscell carcinoma (ESCC)". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45542296.

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Tsang, Chi-kit Percy, i 曾誌傑. "HPV genotyping and integration in cervical cancer and precursor lesions". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45010444.

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Pooley, Karen Anne. "Genetic factors in telomere length". Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609670.

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林秉誠 i Bing-shing Lam. "Genetic study of borderline and invasive ovarian cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31970175.

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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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Lau, Tsz-kwan, i 劉子筠. "The expression of RIP140 in breast cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193544.

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Breast cancer is the most common cancer in females worldwide. RIP140 was one of the first proteins recognized as nuclear receptor transcriptional cofactor which interacts with several nuclear receptors. RIP140 plays a central role in metabolic tissues with multifunctional co-regulation. It is an essential protein required for energy homeostasis and mammary gland development. RIP140 has been found to be involved in development of breast cancer in response to estrogen. RIP140 is recruited by estrogen receptors in the presence of estrogen. Increasing levels of estrogen and RIP140 stimulate their transcription and regulate proliferation and differentiation of mammary glands. We hypothesize that RIP140 may be over expressed in breast cancer and may be correlated with clinicopathological features and may thus serve as a possible new prognostic marker in breast cancer. In our study, the correlation between the RIP140 expression and survival was investigated by immunohistochemistry (IHC), and analyzed by Pearson’s chi-square and Kaplan Meier analysis. Cox regression analysis was performed to examine the relationship between clinic-pathological parameters and the survival. Total of one hundred and eighteen breast cancer samples were examined for the RIP140 staining localization in breast cancer cells. Our results showed that the IHC staining of RIP140 was observed in both cytoplasm and nucleus of breast cancer cells. The ER positive staining was significantly correlated with high nuclear expression of RIP140, but not RIP140 cytoplasmic expression. Thus nuclear RIP140 expression was examined for correlation with other clinic-pathological features and patient survival. The correlation between nuclear RIP140 expression and clinic-pathological features by Pearson’s chi-square test showed that high RIP140 nuclear staining score is associated with ER positive status (p-value=0.041) and tumor stage (p-value=0.008). Kaplan Meier test shown that nuclear RIP140 expression is not significant associated with either overall survival or disease-specific survival. However, a trend of high nuclear RIP140 score was observed with poorer overall and disease-specific survival though not statistically significant. To conclude, our results suggest RIP140 is not a useful prognostic marker for breast cancer. Further investigation with larger sample size is necessary to improve the statistical significance of the test.
published_or_final_version
Pathology
Master
Master of Medical Sciences

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28

Wong, Thian-sze Stanley, i 黃天仕. "A study of gene methylation in head and neck cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B31318721.

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Yang, Chongqing, i 楊重慶. "Single nucleotide polymorphism in the coding sequence of follicle stimulating hormone receptor and susceptibility to ovarian andendometrial cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B31456133.

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馮敬業 i King-yip Fung. "Screening of recurrent BRCA gene mutations in Chinese breast and ovarian cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31969720.

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錢文偉 i Man-wai Gary Chien. "Cytogenetic analysis of head and neck cancer by comparative genomic hybridization". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31224209.

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32

Sun, Sophie. "CDKN2Ap16 and familial cancer". Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=24375.

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CDKN2A/p16 is a cell cycle inhibitor which blocks abnormal cell growth and proliferation. The CDKN2A gene is frequently mutated or deleted in a wide variety of tumour types. Germline mutations have also been identified in familial atypical multiple mole melanoma (FAMMM) pedigrees. However, the role of CDKN2A in hereditary cancer is uncertain. To explore the relationship between CDKN2A germline mutations and risk of cancer, 75 families with cancers at multiple sites were analysed for germline mutations in the CDKN2A gene. A Met53Ile mutation was found in a non-FAMMM kindred with multiple cancers, including one case of melanoma. The Met53Ile mutation has been previously reported in three Australian FAMMM kindreds. A known Ala148Thr polymorphism was also detected in 5 individuals. No other families were found to have CDKN2A alterations. There were no reported CDKN2A mutations in families without cases of melanoma. Analysis of microsatellite markers adjacent to CDKN2A on chromosome 9p21 revealed that this family shares a common haplotype with one other family with this mutation, suggesting that Met53Ile is a founder mutation. These results suggest that while CDKN2A mutations are not restricted to FAMMM pedigrees, they are very rare or absent in families with individuals without melanoma.

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Choy, Tsz-hung Joe, i 蔡子雄. "The study of aberrant protein expressions of head and neck cancers andtheir clinicopathological significance". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31224295.

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34

Warusavitarne, Janindra. "Analysis of the factors that influence the biological behaviour and response to chemotherapy in sporadic colorectal carcinomas with microsatellite instability". Thesis, The University of Sydney, 2005. https://hdl.handle.net/2123/27920.

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High frequency microsatellite instability (MSI—H) is an alternate pathway of colorectal carcinogenesis and is present in approximately 15% of all sporadic colorectal cancers. These tumours are predominantly located in the right colon, occur mainly in the elderly and have a better prognosis than microsatellite stable (MSS) CRCs. In addition they are usually of mucinous type histology, tend to be locally invasive, metastasise less and are of larger size than MSS CRCs. The mismatch repair (MMR) genes hMLHl is most commonly mutated or methylated in sporadic colorectal cancers with MSI-H. Several other gene mutations occur as a result of the defective mismatch repair genes and mutations in a 10 x A repeat region of the TGFBRII gene occurs in approximately 90% of MSI-H CRCs. TGFB is an important tumour suppressor and TGFB signalling is impaired in the absence of TGFBRH. Several studies have shown that restoring TGFB signalling in MSI-H CRC results in reduced tumorigenicity suggesting that the lack of TGFB signalling may be responsible for the increased tumorigenicity seen in these CRCs. In breast and pancreatic cancer TGFB signalling has been associated with an increased metastatic rate and it is postulated that the lack of TGFB signalling in MSI-H CRC is associated with the reduced metastatic rate seen in these tumours when compared with MSS CRCS.

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35

Chiu, Yuk-tim, i 趙玉甜. "Sirtuin 6 expression in breast cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48541254.

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Sirtuins (Silent Information Regulator Two (SIR2) protein) are NAD-dependent protein deacetylases, originally discovered in yeast. Sirtuins play a critical role in the regulation of different cellular processes involving aging, chromatin silencing and cellular differentiation. SIRT6 is a member of Sirtuins and plays a role in regulation of DNA repair and suppression of genomic instability. Many studies have shown SIRT6 to be associated with diseases of aging, including cancer. The finding by our collaborator that SIRT6 expression was found in chemotherapy-resistant breast cancer cell lines stimulated this study which aims to explore the role of SIRT6 expression as a prognostic marker in breast cancer. One hundred and eighteen breast cancer samples in tissue microarray blocks were examined for SIRT6 expression by immunohistochemistry. As SIRT6 expression is predominantly located in the nucleus but with a small fraction in cytoplasm, the calculation of nuclear or cytoplasmic localization scores were divided by total localization scores to increase accuracy. The nuclear localization scores represent the SIRT6 expression in breast cancer. Statistical analysis was performed using SPSS software. SIRT6 overexpression in the nucleus was significantly associated with poorer overall survivals (p=0.018) while low cytoplasmic expression of SIRT6 was also associated with poorer overall survivals (p=0.014). There was no relationship between SIRT6 expression and disease-specific survivals. By multivariate analysis, SIRT6 expression was an independent predicator of poorer overall survivals. These results suggest that SIRT6 overexpression induces apoptosis in cancer cells through deacetylation of transcription factor p65. SIRT6 interacts with and deacetylates p65 to activate nuclear factor kappa B gene linked to cancer. Also high levels of SIRT6 were associated with resistance to paclitaxel and epirubicin inMCF-7 breast cancer cell lines. This provides evidence that Sirt6 is an important prognostic marker and therapeutic target for breast cancer.
published_or_final_version
Pathology
Master
Master of Medical Sciences

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36

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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37

Lo, Yee-nga, i 盧懿雅. "Effect of t(11;14)(p13;q32) translocation on the expression of PDHX, the telomeric gene on chromosome 11p13, in mature B-cell malignancies". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46632505.

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38

陳俊良 i Tsun-leung Chan. "Genomic instability and DNA mismatch repair gene mutations in colorectal cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31238221.

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39

鄧國全 i Kwok-tsuen Dang. "Methylation status of endometrial cancer related genes". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31970497.

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40

Tan, Wooi-keng, i 陳慧卿. "Expression patterns of housekeeping genes in cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B29892892.

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41

Wong, Yim-han, i 黃艷嫺. "Expression of sirtuin 1 in breast cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193549.

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Breast cancer is the most frequent malignancy in women. Recent studies have proposed that sirtuin 1 (SIRT1) may play a certain role in the tumorgenesis and disease progression of cancer. Therefore, in this study, we demonstrate the localization of SIRT1 in the breast cancer cells by immunohistochemistry method and try to correlate the expression level of SIRT1 with various clinical-pathological parameters as well as the survival time of breast cancer patients. One hundred and eighteen breast cancer cases, arrayed as dual‐cores, were studied in the tissue microarray blocks for their SIRT1 nuclear and cytoplasmic stain. The expression of SIRT1 is found in over 95% of the tumor samples. Although the active functioning site of SIRT1 is known to be mainly the nucleus, both nuclear and cytoplasmic localization score are assessed separately for SIRT1 expression for more accurate statistically analysis. By bi‐variate Pearson correlation analysis, high nuclear localization of SIRT1 is significantly correlated with low tumor grade (p=0.006) and ER (p=0.001) and PR positive status (p=0.044). Moreover, the cytoplasmic localization score of SIRT1 shows positive correlation with tumor grade (p=0.010). The relationship of SIRT1 expression and survival time of breast cancer patient was studied by Kaplan‐Meier analysis. Despite a marginal fail in obtaining a statistically significant result, the trend in survival curve clearly indicated that nuclear localization of SIRT1 is associated with a poorer overall survival (p=0.052). Although the pathway of how SIRT1 affects the survival of breast cancer patient is still unknown, many studies suggested that it is largely due to the deacetylated inactivation of p53 tumor suppressor protein by SIRT1. In conclusion, we propose that nuclear localization of SIRT1 can be a potential prognostic factor of breast cancer patients.
published_or_final_version
Pathology
Master
Master of Medical Sciences

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42

Tang, Kei-shuen, i 鄧紀旋. "Role of BRCA1 in stress-induced autophagy in breast and ovarian cancercells". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B45847204.

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43

Cheng, Wan-biu, i 鄭雲標. "Genetic analysis on the EPHB2 gene in breast cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45009946.

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44

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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45

Flach, Susanne. "Structural variation of the genome in breast cancer". Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648565.

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46

Hu, Xiaotong, i 胡曉彤. "Novel IGH translocations in gastric non-Hodgkin's B-cell lymphoma". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B38688098.

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47

Lesniak, Karen. "Psychological and Sociodemographic Predictors of Psychological Distress in BRCA1 and BRCA2 Genetic Testing Participants within a Community Based Genetic Screening Program". Thesis, University of North Texas, 2000. https://digital.library.unt.edu/ark:/67531/metadc2565/.

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Mutations in BRCA1 and BRCA2, the first two breast cancer susceptibility genes identified, carry as much as an 85% lifetime risk of developing breast, ovarian or other cancers. Genetic testing for mutations in these two genes has recently become commercially available. There have been varying amounts of psychological distress noted among women with a family history of breast cancer. Distress has been observed to impact psychological functioning, activities of daily living, and the practice of breast cancer surveillance behaviors. Within the genetic screening process, psychological distress has been shown to impact the decision to undergo genetic screening, the comprehension and retention of risk assessment information, as well as affecting the subject following the receipt of the genetic test results. Little work has been done to examine predictors of distress within at risk subjects. This study examines psychological distress among 52 community women presenting for BRCA1 and BRCA2 genetic mutation testing. Predictors of distress included family cancer history, education, age, Ashkenazi ethnicity, and Internality and Powerful Others Health Locus of Control. Vulnerable sub-groups of patients include younger women, women with higher levels of education and women of Ashkenazi ethnicity.

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48

Warneford, Sally. "Genetic and biological studies in a Li-Fraumeni syndrome family". Thesis, The University of Sydney, 1993. https://hdl.handle.net/2123/26604.

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This thesis presents various clinical, genetic and biological aspects of a cancer-prone family. Two probands were studied at the initiation of the study: a 36-year-old female with infiltrating ductal breast carcinoma and a recent history of adrenocortical carcinoma (ACC), and her 21/2-year-old son, also with ACC. The occurrence of the latter, an extremely rare tumour, in two members of the one family prompted speculation that these two individuals may belong to a Li-Fraumeni cancer syndrome (LFS) family. ACC is a hallmark tumour of this particular cancer family syndrome, which also includes tumours affecting such diverse tissues as breast, soft-tissue, bone, brain and haematopoietic cells. A pedigree spanning ﬁve generations was compiled using family recollections and medical records of cancer. A comparison of the pedigree for this family with the clinical requirements for LFS and a genetic analysis confirming that the cancer predisposition was inherited in an autosomal dominant fashion showed that this was indeed an LFS cancer family. Because the predisposing lesion for LFS had not yet been discovered at the initiation of this study. examination of the cancer inheritance in this family was of interest. In order to provide material for long-term studies and to enable a preliminary characterisation of tumourigenesis in the probands, attempts were made to grow tumour and constitutional cells from both probands in culture. The primary breast carcinoma grew for a brief period only, before stromal ﬁbroblast-like cells took over the culture. A bony metastasis of the same tumour, however, was found to grow as non—adherent multicellular spheroids which persisted longer in culture, probably indicative of the progressive changes that occurred in vivo. The stromal ﬁbroblasts were found to be normal and thence served as a constitutional control for the breast carcinoma. The boy's adrenocortical carcinoma recurred twice before his death at age 6 years and it was from the first and second recurrences of his tumour that cells were cultured. The cells which grew were heterogeneous in morphology and were not immortalised. There were also morphological and immunocytochemical differences between the cell strains derived from the first and second relapses. These differences were thought to indicate both the heterogeneous nature of the adrenocortical carcinoma and to represent progressive changes in tumourigenesis. Normal abdominal skin ﬁbroblasts were cultured as constitutional controls. In order to investigate the predisposing lesion for the cancer predisposition, the p53 tumour suppressor gene was selected as a candidate, based on its frequent involvement in sporadic tumours of the same type as those found in LFS patients and also the ﬁnding that transgenic mice expressing a mutant p53 allele showed a higher frequency of malignancy than normal controls. The involvement of the p53 gene was examined by Northern and Southern blot analysis, 81 nuclease mapping, and genomic DNA and cDNA PCR/sequencing. An additional larger transcript was found in both tumour and constitutional RNA from the probands, and in constitutional RNA from some obligate carriers, that was not present in controls and unaffected individuals. This was thought to be indicative of an underlying germline alteration to the p53 gene in those individuals with the larger transcript. The size discrepancy in the transcripts was not caused by a genomic rearrangement but was found to be due to the retention of all or most of intron 4 in the mature mRNA because of a germline point mutation in the intron 4 5' splice donor site (at the last base o fexon 4) of one p53 allele. The frequent occurrence of stop codons in intron 4 ensured that if a protein could be produced from the larger transcript. it would be truncated and the p53 immunoprecipitations gave some evidence for the existence of a truncated protein product. Interestingly. the mutation, a G to A transition, appeared to produce only a partial disruption to splicing in Northern and cDNA PCR/sequencing analysis, with a proportion of the transcripts produced from the mutant allele being normally spliced. The mutation was in the last base of exon 4 which is also the last base of codon 125. Because of coding degeneracy, it was found that these normally-spliced mutant transcripts would not result in an amino acid substitution when translated implying that this mutation, rather than abolishing the functionality of the mutant allele could result in a reduction in p53 levels. Thus the mutation is unusual in that it is potentially weaker in its effect than most other sporadic and germ-line p53 mutations. This is the first report of a germ-line splicing mutation in the p53 gene and appears to be the most 5' of the LFS germ-line mutations reported. The secondary events in tumourigenesis in both of the probands. in particular the fate of the remaining p53 allele, were investigated. Evidence from Northern and PCR/sequence analysis suggested that the second p53 allele had been lost during development of both the breast carcinoma and the ACC in the probands, with retention of the mutant allele. Both tumours showed extensive karyotypic abnormalities including aneuploidy, with translocations, deletions and both consistent and random chromosome losses. Some of the consistent chromosomal losses were thought to be linked to the loss of tumour suppressor genes involved in the tumoun'genic process. Other genetic events included the over-expression of the dominantly-acting nuclear oncogene c-myc in the breast carcinoma, which is linked to a highly proliferative tumour and a poor prognosis, and the over-expression of Rb in the ACC. The over-expression of Rb was carried through to over-production of an apparently wild-type pr, probably due to disruption of the Rb functional pathway. The over-expression of Rb was an unusual ﬁnding as this gene is normally mutated or lost in tumours. This gene over-expression and protein overproduction in the ACC could also have been inﬂuenced by the lack of sufﬁcient functional p53, which would normally down-regulate the expression of Rb. In contrast to the reports of others, the constitutional ﬁbroblasts of both probands did not show an increased rate of spontaneous immortalisation nor did they show karyotypic abnormalities, perhaps because of the weak nature of the germ-line mutation uncovered in this family. Thus, in this project a cancer-prone family was identified, and constitutional and tumour cells from two probands were cultured for analysis. A putative predisposing lesion for the cancer-predisposition in an LFS cancer family was discovered in the p53 gene. The mutation was novel in both its location (in exon 4 rather than the hotspot for LFS mutations, exon 7) and type (a splicing mutation rather than the more common missense mutation). The tumourigenic process in the two probands was investigated and some of the secondary genetic events in the tumours of the probands were uncovered, including the loss of the remaining allele of the p53 gene, overexpression of C-myc and Rb. Please note that the literature reviewed in this thesis is current up to February 1993.

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Fan, Wai-leong, i 樊偉亮. "Study of gene expression on ovarian cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B44659039.

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50

Yang, Haiyan. "Mutagenesis and antimutagenesis in Big Blue lacI transgenic rats". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ62534.pdf.

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