Liu, Yanan. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2013. / Includes bibliographical references (leaves 87-98). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts also in Chinese.

by Lai Bo San Paul. / "April 1997." / "Revised May 1998." / Thesis (M.D.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (p. 175-228). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstract in Chinese.

肺癌是導致男性死亡的最常見原因以及是排在乳腺癌和結腸癌之後的導致女性死亡的第三大原因。雖然肺癌如此嚴重，但是如今治疗肺癌仍然是一个挑战。現今對肺癌的治療主要集中在化學治療和靶點藥物治療，但是由於這些治療有著很大的副作用和低治愈率，尋找其他的醫學替代方法十分迫切。甘草是其中最常用的中藥，它常常用作食品工業中的甜味劑。以往的研究表明，甘草具有多種的生物活性。但是甘草提取物對於肺癌的治療卻是十分匱乏的。 / 本論文主要目的是評價甘草提取物以及其中的有效成份對非小型肺癌細胞株A549 的影響，以及其作用的機理。我們的數據表明，甘草的乙酸乙酯（EAL）成份比甘草的乙醇提取物有著比較強的抑制癌細胞的作用。另外，對甘草的五個單體進行的測試中發現lico-3 是最具有抑制肺癌作用的。利用高效液相色譜法對甘草活性成份分析表明，lico-3 是EAL中的其中一個單體。 / 乳酸脫氫酶滲漏（LDH）的檢測結果以及异硫氰酸荧光素-碘化丙啶（FITC-PI）雙染的結果表明，EAL 能夠引起肺癌細胞的凋亡現象而非壞死現象。實驗結果表明由EAL引起的A549細胞凋亡是跟Bcl-2家族及Caspase家族有關係，同時EAL還能夠抑制Akt途徑從而導致細胞的死亡。 / 致肺癌細胞死亡的原因進行進一步研究表明，EAL還能夠引起抑制細胞週期的運作，停留在G2/M 時期。這可能是由於EAL引發了p53與p21的上調作用從而抑制了細胞的生長與增殖。 / 實驗結果說明了EAL引起的肺癌細胞株A549的凋亡作用是跟多重細胞通路有關， 同時表明了EAL是具有抗擊肺癌作用的潛能，能夠作為治療肺癌的藥物。 / Lung cancer is the most common cause of cancer death in men and third in women followed by breast cancer and colon cancer, yet treatment of lung cancer remains a challenge. Current treatments including chemotherapy and targeted drug treatment come with side-effects and low successful rate. Alternative medicine for treatment of lung cancer is warranted. Glycyrrhiza uralensis (Gan-Cao), commonly called “licorice, is one of the most commonly used herbs in traditional Chinese medicine (TCM). It is also used as flavoring and sweetening agents in many of food products. Previous studies have indicated that licorice exhibits a variety of biological activities. However, anticancer effects of licorice extract on lung cancer remain unclear. / In this study, we evaluated effects of licorice extract and its chemical components on human lung cancer cell line A549, and studied its mode of action. Our results showed the ethyl acetate fraction of licorice (EAL) was more effective in inhibition of A549 cell growth followed by ETL (IC₅₀: 50μg/mL). Moreover, among the five compounds tested, lico-3 was more potent compound. The HPLC analysis of the active fraction indicated that lico-3 was one of the compounds distributed in the EA fraction. / The results of LDH assay and FITC-PI co-staining method suggested low concentration of EAL can trigger apoptosis but not necrosis. The experimental findings show that EAL induce apoptosis in A549 cell lines involved in Bcl-2 family and caspase cascade. Also, EAL can arrest the Akt survival pathway in A549. Furthermore, the results indicate that EAL triggered G2/M phase arrest. The studies suggest EAL can up-regulate p53 and p21 to promote cell cycle arrest resulting in inhibition of proliferation. / Experimental results indicate that EAL is involved in multiple signal pathways to induce lung cancer cell death. The result suggests EAL is a potential candidate for lung cancer therapy. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Zhou, Yanling. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2012. / Includes bibliographical references (leaves 99-110). / Abstracts in Chinese. / Abstract --- p.III / 論文摘要 --- p.V / Acknowledgement --- p.VII / List of Contents --- p.VIII / List of Figures --- p.X / List of Tables --- p.XI / List of Abbreviations --- p.XII / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Lung cancer --- p.1 / Chapter 1.1.1 --- Overview --- p.1 / Chapter 1.1.2 --- Risk factors --- p.2 / Chapter 1.1.3 --- Types of lung cancer --- p.4 / Chapter 1.1.4 --- Stages and treatment of lung cancer --- p.5 / Chapter 1.1.5 --- Chemotherapy for lung cancer treatment --- p.8 / Chapter 1.2 --- Traditional Chinese Medicines --- p.11 / Chapter 1.2.1 --- Overview --- p.11 / Chapter 1.2.2 --- Licorice --- p.14 / Chapter 1.2.3 --- Chemical study of licorice --- p.16 / Chapter 1.2.4 --- Pharmacological activities of licorice --- p.16 / Chapter 1.3 --- Molecular mechanism of apoptosis --- p.21 / Chapter 1.3.1 --- Overview --- p.21 / Chapter 1.3.2 --- Bcl2 family --- p.21 / Chapter 1.3.3 --- Caspase pathway --- p.23 / Chapter 1.3.4 --- Akt pathway --- p.24 / Chapter 1.3.5 --- p53 protein --- p.26 / Chapter 1.3.6 --- Apoptosis and cancer --- p.27 / Chapter 1.4 --- Cell cycle --- p.29 / Chapter 1.4.1 --- Overview --- p.29 / Chapter 1.4.2 --- Cell cycle and p53 --- p.29 / Chapter 1.4.3 --- Cell cycle and cancer --- p.30 / Chapter 1.5 --- Aims of study --- p.32 / Chapter Chapter 2 --- Materials and Methods --- p.33 / Chapter 2.1 --- Cell culture and treatment --- p.33 / Chapter 2.1.1 --- Cell line --- p.33 / Chapter 2.1.2 --- Chemicals and reagents --- p.34 / Chapter 2.1.3 --- Preparation of solutions --- p.34 / Chapter 2.2 --- Preparation of Licorice sample --- p.35 / Chapter 2.3 --- HPLC analysis --- p.35 / Chapter 2.3.1 --- Chemical and materials --- p.35 / Chapter 2.3.2 --- Instrumentation --- p.36 / Chapter 2.3.3 --- Preparation of Standard solutions --- p.36 / Chapter 2.3.4 --- Preparation of samples --- p.37 / Chapter 2.3.5 --- HPLC conditions --- p.37 / Chapter 2.3.6 --- Method validation --- p.37 / Chapter 2.4 --- Cell viable assay --- p.38 / Chapter 2.4.1 --- Samples preparation --- p.39 / Chapter 2.4.2 --- Procedure --- p.39 / Chapter 2.5 --- LDH assay --- p.40 / Chapter 2.5.1 --- Reagent preparation --- p.40 / Chapter 2.5.2 --- Procedure --- p.41 / Chapter 2.6 --- Annexin V assay --- p.41 / Chapter 2.6.1 --- Reagent --- p.42 / Chapter 2.6.2 --- Procedure --- p.42 / Chapter 2.7 --- Cell cycle study --- p.43 / Chapter 2.7.1 --- Chemicals and reagent --- p.43 / Chapter 2.7.2 --- Procedure --- p.44 / Chapter 2.8 --- Caspase3/7 Assay --- p.44 / Chapter 2.8.1 --- Reagent preparation --- p.45 / Chapter 2.8.2 --- Procedure --- p.46 / Chapter 2.9 --- Western blotting --- p.46 / Chapter 2.9.1 --- Reagent and antibodies --- p.46 / Chapter 2.9.2 --- Procedure --- p.50 / Chapter 2.9.3 --- Determination of protein concentration --- p.51 / Chapter 2.10 --- Data analysis --- p.51 / Chapter Chapter 3 --- Results --- p.52 / Chapter 3.1 --- Chromatographic conditions and HPLC identity conformation --- p.52 / Chapter 3.1.1 --- Linearity, limits of detection and quantification --- p.56 / Chapter 3.1.2 --- Reproducibility --- p.56 / Chapter 3.1.3 --- Analysis of ethyl acetate of licorice (EAL) using the validated method --- p.56 / Chapter 3.2 --- Licorice induces apoptosis in nonsmall cell lung carcinoma --- p.61 / Chapter 3.2.1 --- Cell viability assay --- p.61 / Chapter 3.2.2 --- LDH leakage assay --- p.71 / Chapter 3.2.3 --- Annexin V and PI staining --- p.73 / Chapter 3.3 --- Protein expression in EALinduced apoptotic cells --- p.75 / Chapter 3.3.1 --- Bcl2 family --- p.75 / Chapter 3.3.2 --- Activation of caspases by EAL treatment --- p.77 / Chapter 3.4 --- EAL could block Akt survival pathway --- p.79 / Chapter 3.5 --- EAL induces cell cycle arrest in nonsmall cell lung carcinoma --- p.83 / Chapter Chapter 4 --- Discussion --- p.85 / Chapter 4.1 --- Chemical analysis of licorice --- p.85 / Chapter 4.2 --- Licorice induced apoptosis but not necrosis on lung cancer cell A549 --- p.86 / Chapter 4.2.1 --- Licorice exhibits specific cytotoxicity to different cancer cells in vitro --- p.86 / Chapter 4.2.2 --- EAL induces cell death via apoptosis but not necrosis --- p.87 / Chapter 4.3 --- Growth inhibition by EAL inducing apoptosis --- p.89 / Chapter 4.3.1 --- EAL induces apoptotic cell death through modification of Bcl2 family --- p.89 / Chapter 4.3.2 --- EAL activate the caspase proteins --- p.90 / Chapter 4.4 --- Growth inhibition by EAL inducing survival pathway arrest --- p.92 / Chapter 4.5 --- Growth inhibition by EAL inducing cellcycle arrest --- p.94 / Chapter 4.6 --- General discussion --- p.96 / Reference --- p.99

No description available.

Seeking cancer information is key in coping with the feelings (e.g., fear, uncertainty) and other challenges (e.g., treatment decision-making) confronting individuals diagnosed with cancer. Despite recognition of a variation in why, when, how, and where individuals diagnosed with cancer seek information, few efforts have been made to systematically document patterns in information-seeking. Aim: To explore individuals' patterns of health information-seeking behaviors (HIS B) including the type, amount, and sources ofinforn1ation and the strategies used to process and/or manage cancer information. / La recherche d'information sur Ie cancer est d'une importance determinante pour les personnes atteintes de cette maladie dans Ie contexte OU elles ont gerer des emotions intenses (p. ex. : peur, incertitude) et font face plusieurs defis (p. ex. : processus de decision relatif au traitement). Des variations concernant la recherche d'information par les individus diagnostiques avec un cancer ont ete observees et reconnues notamment en termes des raisons qui motivent la recherche d'information et des moyens utilises pour obtenir l'infomlation desiree. Cependant, a ce jour, peu d'efforts ont ete deployes pour documenter de maniere systematique les differents types de comportements de recherche d'information.

The purpose of this study was to explore the relationship of belief in control and commitment to life to the adult cancer patient's inclination to use unproven cancer therapies. A convenience sample of 40 lung cancer patients completed the Wallston's Multidimensional Health Locus of Control Scale, Crumbaugh's Purpose in Life Scale, Hiratzka's Alternative Therapy Scale, and a patient information sheet. The majority of participants exhibited a strong internal locus of control orientation and a strong commitment to life. Belief in control, commitment to life, and the degree of inclination to use unproven cancer therapies were not significantly associated. However, age was negatively correlated with inclination to use unproven cancer therapies. The majority of participants had heard of five or more unproven cancer remedies, and exhibited a strong inclination to use these unorthodox therapies. The most frequently used unproven therapies were anti-medicines - imagery, faith-healing, megadose vitamins, and taheebo. The rising popularity of these anti-medicines has been reported in the literature. The findings were discussed in relation to theoretical expectations, other research studies, and the methodological problems inherent in the study. Implications of the findings for nursing practice, theory, and education were suggested. Recommendations for further nursing research were made. / Applied Science, Faculty of / Nursing, School of / Graduate

No description available.

In addition, we investigated the cytotoxic effect of a widely used chemotherapeutic agent 5Fu on laryngeal squamous cell cancer cell lines and evaluated the role of p53 in 5Fu treatment. We found that the apoptosis and G1/S cell arrest mediated by 5Fu in laryngeal cancers is p53-independent but p21 WAF1/CIP1-dependent. We further demonstrated the effect of 5Fu on HPV16-associated laryngeal cancer cells. Using cytotoxicity assay and Annexin V staining, we proved that 5Fu induces apoptosis in all of the transfected cells in a dose- and time-dependent manner, suggesting that the process was not prevented by HPV16 E6 or E7. 5Fu induced the accumulation of active pRb and cyclin dependent kinase inhibitor p21WAF1/CIP1 together with an increase in Bak and Bax expression and a decrease in Bcl-2 levels in all the transfected cells. In addition, G1/S phase cell cycle arrest was associated with the antiproliferation activity of 5Fu in all cell lines. Through RT-PCR, 5Fu also presented some effects on the E6 and E7 oncoproteins of HPV16 in transfected UMSCC 12 cells. / Our results suggest that HPV16 E6 and E7 oncoproteins do not prevent 5Fu medicated apoptosis and G1/S cell arrest in laryngeal cancers. The anti-cancer effect of 5Fu is probably decided by the level of p21 WAF1/CIP1 while the sensitivity of laryngeal cancer cells responded to 5Fu treatment is associated with the increase of Bak or/and the decrease in Bcl-2, not with the HPV16 viral proteins and p53 status. 5Fu also presented some effects on the E6 and E7 oncoproteins of HPV16 in laryngeal cancer. However, the anti-viral effect of 5Fu still needs further investigation. / Our study indicated that (1) the evasion of apoptosis mediated by HPV16 E6 and E7 plays a critical role in laryngeal carcinogenesis; (2) HPV16 E6 or E7 plays an important role in regulating the expression of Bak, Bax and Bcl-2; (3) The degradation of Bak by HPV16 E6 is not caused by interacting with the promoter of Bak; (4) The induction of Bcl-2 is mediated through HPV16 E7; (5) HPV16 transfection does not interfere with the apoptosis and cell cycle arrest mediated by 5Fu in human laryngeal squamous cancer cells. / There is a growing body of evidence that human papillomavirus type 16 (HPV16) is involved in the development of human laryngeal cancer, especially in Chinese population. The two oncoproteins, HPV16 E6 and E7 that target host cell tumor suppressor proteins p53 and Rb respectively, may generate antiapoptotic effects and induce cell immortalization. However, the effect of both oncoproteins on apoptosis in laryngeal cancers is not completely clear. In this study, we demonstrated the possible mechanism of high risk HPV16 in laryngeal carcinogenesis and evaluated the effect of 5Fu on HPV16-positive laryngeal cancer cells. / We employed two human laryngeal cancer cell lines---UMSCC12 (with truncated p53) and UMSCC11A (with mutant but functional p53) in this study. These two cell lines were stably transfected with HPV16 E6, E7 or empty vector, pcDNA3.1, which provided a good foundation for further study on the carcinogenic mechanism of HPV16 E6 or E7 in human laryngeal cancers. Through Annexin V staining and protein stability assay, we found that the transfection of HPV16 E6 and E7 induced fewer spontaneous apoptosis in both UMSCC11A and UMSCC12 cells accompanied with enhanced protein stability of Bcl-2 and increased protein degradation of Bak. Similar results were obtained when E6- and E7-transfected cells exposed to apoptosis stimuli---TNF-alpha/CHX. These results indicate that stable transfection of E6 and E7 in human laryngeal cancer cells on one hand shortened the half-life of Bak protein, and on the other hand, enhanced the steady-state levels of Bcl-2 protein. In order to gain insight into the role of Bak and Bcl-2 in regulating apoptosis in HPV-associated laryngeal cancer cells, we performed transient transfection of Bcl-2 into E6- and E7-transfected cells. It is found that HPV16 E7 statistically enhanced the expression of Bcl-2 in laryngeal cancer, indicating that the induction of Bcl-2 require the transfection of HPV16 E7. Furthermore, Luciferase assay was performed to investigate whether the viral proteins E6 and E7 altered the stability of Bak through interaction with the promoter of Bak. Negative results were obtained, suggesting that E6 or E7 do not alter the transcription activity of Bak, indicating the degradation of Bak by E6 or E7 may be mediated through other mechanisms. / Liu Han-ching. / "August 2006." / Advisers: C. A. van Hasselt; George G. Chen. / Source: Dissertation Abstracts International, Volume: 68-03, Section: B, page: 1569. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2006. / Includes bibliographical references (p. 245-274). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts in English and Chinese. / School code: 1307.

Nasopharyngeal cancer (NPC) is endemic in Southern China and Hong Kong. It has traditionally been treated by local radiotherapy with great success especially for early stage disease. However the treatment outcome in advanced stage disease is unsatisfactory. / Results from this series of combined clinical, translational and laboratory studies have redefined the role of hypoxia, angiogenesis and metastasis as new therapeutic targets in NPC. Novel biomarkers and new therapeutic approaches were developed based on these targets. / To develop new therapies in NPC, we demonstrated in a randomized controlled phase 2 clinical trial that sequential therapy of neoadjuvant chemotherapy followed by chemoradiotherapy was well tolerated with a manageable toxicity profile that allowed subsequent delivery of full dose chemoradiotherapy. This strategy reduced distant metastasis which translated into improved patient survival. In preclinical studies, the antiangiogenesis agent sunitinib demonstrated potent in vitro and in vivo growth inhibition in NPC. In a phase 2 clinical trial, sunitinib demonstrated modest clinical activity in heavily pretreated NPC patients. However, the unexpected high incidence of severe hemorrhage from upper aero-digestive tract in NPC patients who received prior high dose RT to the region is of concern. We propose to exclude NPC patients with disease recurrence within previous radiation field and/or with vascular invasion from future antiangiogenesis therapy. / To investigate potential new therapeutic targets and biomarkers in NPC, we first confirmed from the Hong Kong NPC study group of 2915 patients' database that distant metastasis was the leading cause of NPC failure after primary radiotherapy. We further showed that hypoxia induced broad changes of both up- and down-regulated gene expressions involved in diverse biological processes in NPC cells. Over-expression of biomarkers of hypoxia and angiogenesis (including HIF-1alpha, CA IX and VEGF) is common in NPC and is associated with poor prognosis. Elevated plasma osteopontin is a biomarker of distant metastasis, and pre-treatment plasma osteopontin level may be a useful biomarker of response to radiotherapy in NPC. / Hui, Pun. / "September 2010." / Adviser: Anthony Chan. / Source: Dissertation Abstracts International, Volume: 73-04, Section: B, page: . / Thesis (M.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 269-293). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.

Pancreatic cancer is one of the most devastating human cancers with the lowest survival rate among 24 commonly diagnosed cancers. It is the seventh and the sixth leading cause of cancer-related deaths in the world and Hong Kong respectively. The current pancreatic cancer treatment options, have limited efficacy and undesirable side effects. Because of the high mortality rate and unsatisfactory treatment outcome, it is necessary to develop new strategies for pancreatic cancer therapy. / In human, an abundant arginine reserve is known to be crucial for tumor cell proliferation. Arginine is a semi-essential amino acid because most of the somatic cells can re-synthesize it from other metabolites like citrulline in urea cycle. However, arginine auxotrophy is observed in certain tumors, such as hepatocarcinoma, melanoma and sarcoma, where restriction or depletion of arginine will lead to tumor death. Further studies have found that deficiency in either argininosuccinate synthetase 1 (ASS1) or ornithine transcarbamylase (OTC) expression contributes to arginine auxotrophy in these tumors. These findings implicated the potential of using arginine deprivation as a novel pancreatic cancer treatment strategy. / PEG-BCT-100 is a pegylated recombinant human arginase that metabolizes arginine into urea and ornithine. This study examined the preclinical anti-tumor efficacy of PEG-BCT-100 and the underlying mechanism in pancreatic cancer. Six pancreatic cancer cell lines AsPC-1, BxPC-3, CFPAC-1, Capan-2, MIA PaCa-2 and Panc10.05 were used as in vitro cell model. Cell growth was either completely stopped or dramatically reduced in arginine-free medium, suggesting pancreatic cancer cells were arginine auxotrophic. The protein and mRNA expression levels of the ASS1, OTC and argininosuccinate lyase (ASL), which are enzymes involved in arginine, were studied. The results showed that ASL was highly expressed in all cell lines, suggesting it is not an essential regulator in arginine auxotrophy in pancreatic cancer. On the other hand, ASS1 was only detected in BxPC-3 and CFPAC-1, while OTC was undetectable in all cell lines in both mRNA and protein levels. The effect of PEG-BCT-100 was illustrated via cell cycle progression, cell proliferation and viability. Single drug effect combining PEG-BCT-100 with other anti-tumor drugs, such as 5-FU and gemcitabine, was further explored. Synergistic effect of PEG-BCT-100 and gemcitabine under combination of PEG-BCT-100 and gemcitabine was observed in CFPAC-1 and MIA PaCa-2. Overexpression of OTC and ASS1 decreased the sensitivity of towards PEG-BCT-100 significantly. Taken together, OTC deficiency is a potential indicative marker for the sensitivity of arginine depletion treatment in pancreatic cancer. / 胰腺癌是最具毀滅性的人類癌症之一，在二十四種常見的癌症中，它有着最低的存活率。儘管不在發病率最高的十種癌症中，胰腺癌仍舊是世界第七大致死癌症，以及香港第六大致死癌症。手術治療，放射治療，以及化學藥物治療是現今常用的胰腺癌治療手段，但是這些療法不是限制繁多，就是收效甚微，並常常伴有強烈的副作用。由於胰腺癌具有很高的致死率以及缺乏有效的治療方法，所以新的治療策略亟待開發。 / 於人類而言，精氨酸是一種半必需氨基酸，因爲它可以通過尿素循環中的其他代謝產物，如鳥氨酸以及瓜氨酸，重新合成。然而，精氨酸缺陷出現在多種腫瘤中，像肝癌，黑色素瘤，以及血癌。限制或者減少精氨酸的供應會導致這些腫瘤死亡。除此之外，腫瘤細胞的快速生長也依賴於充足的精氨酸。進一步的研究表明，在這些腫瘤中，精氨琥珀酸合成酶1（ASS1）或者鳥氨酸氨甲醯基轉移酶（OTC）的任意一個缺乏都會導致精氨酸缺陷。本文將探討將剝奪精氨酸作爲一種新策略來治療胰腺癌的可行性。 / PEG-BCT-100又名金氨素，是一種聚乙二醇化重組人精氨酸酶，它可以催化精氨酸分解爲尿素和鳥氨酸。我們研究了PEG-BCT-100在胰腺癌細胞中的抗癌效果以及探討了與其相關的作用機理。在我們的研究中，AsPC-1, BxPC-3, CFPAC-1, Capan-2, MIA PaCa-2以及Panc10.05這六個細胞株用作體外的細胞模型。爲了評估PEG-BCT-100治療胰腺癌的可行性，我們首先調查了精氨酸對胰腺癌細胞的重要性。通過將這些胰腺癌細胞培養在有精氨酸供應和沒有精氨酸供應的完全培養基中，我們發現剝奪精氨酸能完全停止或者極大地減少了胰腺癌細胞的生長。這說明了這些胰腺癌細胞也都是精氨酸營養缺陷型的細胞。通過蛋白印跡和實時定量聚合酶鏈式反應實驗，我們進一步研究了精氨酸代謝相關基因在這些胰腺癌細胞中的表達水平。結果表明，精氨琥珀酸裂解酶（ASL）在全部的六條細胞系中都有被檢測到。ASS1只出現在BxPC-3和CFPAC-1中。然而在全部的細胞中，無論是蛋白質水平還是mRNA水平，OTC都沒有被檢測到。緊接着，我們研究了PEG-BCT-100在胰腺癌細胞活力，細胞增殖，細胞週期以及細胞凋亡等方面的影響。結果表明，PEG-BCT-100可以從多個方面抑制胰腺癌細胞。我們還嘗試探索了PEG-BCT-100與其他胰腺癌治療藥物在胰腺癌細胞中的聯合使用效果。然後發現PEG-BCT-100與吉西他滨（gemcitabine）聯合使用具有協同效果。最後，我們構建了四種不同表達類型的MIA PaCa-2細胞模型：（ASS1-/OTC-）, (ASS1-/OTC+), (ASS1+/OTC-)以及(ASS1+/OTC+)。接着我們測試了PEG-BCT-100在這些細胞模型中的效果。結果表明，同時在MIA PaCa-2細胞中表達ASS1和OTC可以明顯地提高其對PEG-BCT-100的抗性，單表達其中一個基因對PEG-BCT-100的抗性也有些許提高，但效果不如雙表達明顯。 / 總而言之，對於胰腺癌細胞而言，精氨酸是必不可少的。PEG-BCT-100有很明顯的胰腺癌效果。在胰腺癌中，OTC的表達情況可以作爲預估PEG-BCT-100治療效果的重要生物標誌。 / Deng, Haohao. / Thesis M.Phil. Chinese University of Hong Kong 2015. / Includes bibliographical references (leaves 111-117). / Abstracts also in Chinese. / Title from PDF title page (viewed on 14, October, 2016). / Deng, Haohao. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only.