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Search Results: 1 - 10 of 223446 matches for " Ching C. Lau "
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Meta-analysis of multiple microarray datasets reveals a common gene signature of metastasis in solid tumors
Marla H Daves, Susan G Hilsenbeck, Ching C Lau, Tsz-Kwong Man
BMC Medical Genomics , 2011, DOI: 10.1186/1755-8794-4-56
Abstract: We identified 18 publicly available gene expression datasets in the Oncomine database comparing distant metastases to primary tumors in various solid tumors which met our eligibility criteria. We performed a meta-analysis using a modified permutation counting method in order to obtain a common gene signature of metastasis. We then validated this signature in independent datasets using gene set expression comparison analysis with the LS-statistic.A common metastatic signature of 79 genes was identified in the metastatic lesions compared with primaries with a False Discovery Proportion of less than 0.1. Interestingly, all the genes in the signature, except one, were significantly down-regulated, suggesting that overcoming metastatic suppression may be a key feature common to all metastatic tumors. Pathway analysis of the significant genes showed that the genes were involved in known metastasis-associated pathways, such as integrin signaling, calcium signaling, and VEGF signaling. To validate the signature, we used an additional six expression datasets that were not used in the discovery study. Our results showed that the signature was significantly enriched in four validation sets with p-values less than 0.05.We have modified a previously published meta-analysis method and identified a common metastatic signature by comparing primary tumors versus metastases in various tumor types. This approach, as well as the gene signature identified, provides important insights to the common metastatic process and a foundation for future discoveries that could have broad application, such as drug discovery, metastasis prediction, and mechanistic studies.Metastasis, the process involving the spread of cancer, accounts for greater than 90% of cancer deaths [1]. However, therapies to treat those patients with advanced disease are largely ineffective. It is, therefore, imperative that we improve the understanding of the metastatic process and detect patients at risk for developing met
Optimising the Use of TRIzol-extracted Proteins in Surface Enhanced Laser Desorption/ Ionization (SELDI) Analysis
Tsz-Kwong Man, Yiting Li, Tu Dang, Jianhe Shen, Laszlo Perlaky, Ching C Lau
Proteome Science , 2006, DOI: 10.1186/1477-5956-4-3
Abstract: To facilitate the use of TRIzol-extracted proteins, we first compared the ability of four different common solubilizing reagents to solubilize the TRIzol-extracted proteins from an osteosarcoma cell line, U2-OS. Then we analyzed the solubilized proteins by Surface Enhanced Laser Desorption/ Ionization technique (SELDI). The results showed that solubilization of TRIzol-extracted proteins with 9.5 M Urea and 2% CHAPS ([3-[(3-cholamidopropyl)-dimethylammonio]propanesulfonate]) (UREA-CHAPS) was significantly better than the standard 1% SDS in terms of solubilization efficiency and the number of detectable ion peaks. Using three different types of SELDI arrays (CM10, H50, and IMAC-Cu), we demonstrated that peak detection with proteins solubilized by UREA-CHAPS was reproducible (r > 0.9). Further SELDI analysis indicated that the number of ion peaks detected in TRIzol-extracted proteins was comparable to a direct extraction method, suggesting many proteins still remain in the TRIzol protein fraction.Our results suggest that UREA-CHAPS performed very well in solubilizing TRIzol-extracted proteins for SELDI applications. Protein fractions left over after TRIzol RNA extraction could be a valuable but neglected source for proteomic or biochemical analysis when additional samples are not available.TRIzol is a common RNA extraction reagent that has been extensively used in conjunction with microarray analysis and other applications [1-4]. One of the advantages of TRIzol is its capability of extracting RNA, DNA, and proteins from a single sample. However, TRIzol is primarily designed for RNA extraction and the use of TRIzol extracted DNA and proteins for subsequent analysis is still limited. DNA and protein fractions from TRIzol extraction are valuable resources for researchers when the quantity of the starting material is limited, such as small clinical specimens. In addition, if different fractions extracted from the same sample are used for analysis on various high-throughput
CGI: Java Software for Mapping and Visualizing Data from Array-based Comparative Genomic Hybridization and Expression Profiling
Joyce Xiuweu-Xu Gu,Michael Yang Wei,Pulivarthi H. Rao,Ching C. Lau
Gene Regulation and Systems Biology , 2007,
Abstract: With the increasing application of various genomic technologies in biomedical research, there is a need to integrate these data to correlate candidate genes/regions that are identified by different genomic platforms. Although there are tools that can analyze data from individual platforms, essential software for integration of genomic data is still lacking. Here, we present a novel Java-based program called CGI (Cytogenetics-Genomics Integrator) that matches the BAC clones from array-based comparative genomic hybridization (aCGH) to genes from RNA expression profiling datasets. The matching is computed via a fast, backend MySQL database containing UCSC Genome Browser annotations. This program also provides an easy-to-use graphical user interface for visualizing and summarizing the correlation of DNA copy number changes and RNA expression patterns from a set of experiments. In addition, CGI uses a Java applet to display the copy number values of a specifi c BAC clone in aCGH experiments side by side with the expression levels of genes that are mapped back to that BAC clone from the microarray experiments. The CGI program is built on top of extensible, reusable graphic components specifically designed for biologists. It is cross-platform compatible and the source code is freely available under the General Public License.
A systems biology approach reveals common metastatic pathways in osteosarcoma
Ricardo J Flores, Yiting Li, Alexander Yu, Jianhe Shen, Pulivarthi H Rao, Serrine S Lau, Marina Vannucci, Ching C Lau, Tsz-Kwong Man
BMC Systems Biology , 2012, DOI: 10.1186/1752-0509-6-50
Abstract: mRNA expression microarray and N-linked glycoproteomic analyses were performed on two commonly used isogenic pairs of human metastatic OS cell lines, namely HOS/143B and SaOS-2/LM7. Pathway analysis of the differentially regulated genes and glycoproteins separately revealed pathways associated to metastasis including cell cycle regulation, immune response, and epithelial-to-mesenchymal-transition. However, no common significant pathway was found at both genomic and proteomic levels between the two metastatic models, suggesting a very different biological nature of the cell lines. To address this issue, we used a topological significance analysis based on a “shortest-path” algorithm to identify topological nodes, which uncovered additional biological information with respect to the genomic and glycoproteomic profiles but remained hidden from the direct analyses. Pathway analysis of the significant topological nodes revealed a striking concordance between the models and identified significant common pathways, including “Cytoskeleton remodeling/TGF/WNT”, “Cytoskeleton remodeling/Cytoskeleton remodeling”, and “Cell adhesion/Chemokines and adhesion”. Of these, the “Cytoskeleton remodeling/TGF/WNT” was the top ranked common pathway from the topological analysis of the genomic and proteomic profiles in the two metastatic models. The up-regulation of proteins in the “Cytoskeleton remodeling/TGF/WNT” pathway in the SaOS-2/LM7 and HOS/143B models was further validated using an orthogonal Reverse Phase Protein Array platform.In this study, we used a systems biology approach by integrating genomic and proteomic data to identify key and common metastatic mechanisms in OS. The use of the topological analysis revealed hidden biological pathways that are known to play critical roles in metastasis. Wnt signaling has been previously implicated in OS and other tumors, and inhibitors of Wnt signaling pathways are available for clinical testing. Further characterization of this common p
Enriching Stakeholder Theory: Student Identity of Higher Education  [PDF]
Joseph W. C. Lau
American Journal of Industrial and Business Management (AJIBM) , 2014, DOI: 10.4236/ajibm.2014.412082
Abstract: While students commonly assume the identity of being key stakeholders of higher education, the present article explores the possible complications stemmed from such key identity. Stakeholder theory has its strengths attributed by its conceptual breath and versatility; the limits of the theory arise for the same merit. Making reference to the theory with no restrains leads reasonably to the conclusion that the educational institute is unwilling to take measure closely to the long term effect, tangible or intangible, of such approach. Providing multiple perspectives on the identity of students are observed, an enrichment of stakeholder theory catering student identity is necessary.
Genome-wide array comparative genomic hybridization analysis reveals distinct amplifications in osteosarcoma
Tsz-Kwong Man, Xin-Yan Lu, Kim Jaeweon, Laszlo Perlaky, Charles P Harris, Shishir Shah, Marc Ladanyi, Richard Gorlick, Ching C Lau, Pulivarthi H Rao
BMC Cancer , 2004, DOI: 10.1186/1471-2407-4-45
Abstract: We used a genome-wide screening method – array based comparative genomic hybridization (array-CGH) to identify DNA copy number changes in 48 patients with osteosarcoma. We applied fluorescence in situ hybridization (FISH) to validate some of amplified clones in this study.Clones showing gains (79%) were more frequent than losses (66%). High-level amplifications and homozygous deletions constitute 28.6% and 3.8% of tumor genome respectively. High-level amplifications were present in 238 clones, of which about 37% of them showed recurrent amplification. Most frequently amplified clones were mapped to 1p36.32 (PRDM16), 6p21.1 (CDC5L, HSPCB, NFKBIE), 8q24, 12q14.3 (IFNG), 16p13 (MGRN1), and 17p11.2 (PMP22 MYCD, SOX1,ELAC27). We validated some of the amplified clones by FISH from 6p12-p21, 8q23-q24, and 17p11.2 amplicons. Homozygous deletions were noted for 32 clones and only 7 clones showed in more than one case. These 7 clones were mapped to 1q25.1 (4 cases), 3p14.1 (4 cases), 13q12.2 (2 cases), 4p15.1 (2 cases), 6q12 (2 cases), 6q12 (2 cases) and 6q16.3 (2 cases).This study clearly demonstrates the utility of array CGH in defining high-resolution DNA copy number changes and refining amplifications. The resolution of array CGH technology combined with human genome database suggested the possible target genes present in the gained or lost clones.Osteosarcoma (OS) is a primary malignant tumor of bone arising from primitive bone-forming mesenchymal cells and it accounts for approximately 60% of malignant bone tumors in the first two decades of life [1]. These tumors typically arise in the metaphyseal regions of long bones, with the distal femur, proximal tibia and proximal humerus. A significant number of osteosarcomas are of conventional type which can be subdivided into three major categories based on their predominant differentiation of tumor cells: osteoblastic, chondroblastic, and fibroblastic. Currently, only the histological response (degree of necrosis) to therapy
Information in Repeated Ultimatum Game with Unknown Pie Size
Ching Chyi Lee,William K. Lau
Economics Research International , 2013, DOI: 10.1155/2013/470412
Information in Repeated Ultimatum Game with Unknown Pie Size
Ching Chyi Lee,William K. Lau
Economics Research International , 2013, DOI: 10.1155/2013/470412
Abstract: Within existing literature, it is well known that people’s behavior in ultimatum game experiments cannot be explained by perfect rationality model. There is, however, evidence showing that people are boundedly rational. In this paper, we studied repeated ultimatum game experiments in which the pie size is only known to the proposer (player 1), but the transaction history is made known to both players. We found that subject’s behavior can be very well explained by the history-consistent-rationality model (HCR model) of Lee and Ferguson (2010), which suggests that people’s behavior is affected by what they observed in the past. The HCR model is able to yield point predictions whose errors are on average within 5% of the total pie size. The experimental results provide evidence that subjects' behavior is boundedly rational with respect to the transaction history. 1. Introduction Within the existing ultimatum game literature, it is widely held by economists that game theory fails to predict the subjects' behaviors accurately. Implicit in this evidence are the conjecture of altruistic concerns and the matter of fairness (see, e.g., [1, 2]). While it is commonly known that the decision of accepting or rejecting an offer in ultimatum games depends on respondent's tolerance of unfairness, there have been no prescriptive models in the literature for suggesting the optimal offer that proposer should propose. In this paper, we demonstrate that the history-consistent rationality (hereafter, HCR) model can give point prediction to the proposer's offer in the ultimatum game. This kind of quantitative prediction is different from the past literature which focuses on qualitative prediction. Our research contributions are of twofold. First, our experimental design simulates the real market condition to allow us to better understand how the real economy works. In the existing literatures, scholars have studied ultimatum games with asymmetric information to approximate the real life bargaining situation, as people often do not know how much there is at stake for the other person [3–5]. In our research, we replicate the real market condition by further allowing market information to be available to every subject in the experiment. Consider a person purchasing a house, he would certainly collect market information to bargain for a better deal, because the reservation price of the house owner is usually unknown to the buyer. In each session of our experiments, there are eighteen to twenty pairs of subjects, playing repeated ultimatum games up to twenty periods. The market
Medulloblastoma outcome is adversely associated with overexpression of EEF1D, RPL30, and RPS20 on the long arm of chromosome 8
Massimiliano De Bortoli, Robert C Castellino, Xin-Yan Lu, Jeffrey Deyo, Lisa Sturla, Adekunle M Adesina, Laszlo Perlaky, Scott L Pomeroy, Ching C Lau, Tsz-Kwong Man, Pulivarthi H Rao, John YH Kim
BMC Cancer , 2006, DOI: 10.1186/1471-2407-6-223
Abstract: We analyzed 71 primary medulloblastomas for chromosomal copy number aberrations (CNAs) using comparative genomic hybridization (CGH). Among 64 tumors that we previously analyzed by gene expression microarrays, 27 were included in our CGH series. We analyzed clinical outcome with respect to CNAs and microarray results. We filtered microarray data using specific CNAs to detect differentially expressed candidate genes associated with survival.The most frequent lesions detected in our series involved chromosome 17; loss of 16q, 10q, or 8p; and gain of 7q or 2p. Recurrent amplifications at 2p23-p24, 2q14, 7q34, and 12p13 were also observed. Gain of 8q is associated with worse overall survival (p = 0.0141), which is not entirely attributable to MYC amplification or overexpression. By applying CGH results to gene expression analysis of medulloblastoma, we identified three 8q-mapped genes that are associated with overall survival in the larger group of 64 patients (p < 0.05): eukaryotic translation elongation factor 1D (EEF1D), ribosomal protein L30 (RPL30), and ribosomal protein S20 (RPS20).The complementary use of CGH and expression profiles can facilitate the identification of clinically significant candidate genes involved in medulloblastoma growth. We demonstrate that gain of 8q and expression levels of three 8q-mapped candidate genes (EEF1D, RPL30, RPS20) are associated with adverse outcome in medulloblastoma.Medulloblastoma is the most common malignant brain tumor of childhood. Treatment with surgery, radiation, and chemotherapy successfully cures many patients, but survivors can suffer significant long-term toxicities affecting their neurocognitive and growth potential. Despite clinical advances, up to 30% of children with medulloblastoma experience tumor progression or recurrence, for which no curative therapy exists [1]. The lack of more effective, less toxic therapies and the inability to stratify patients biologically result from imperfect understanding of the m
First Discovery of Two Polyketide Synthase Genes for Mitorubrinic Acid and Mitorubrinol Yellow Pigment Biosynthesis and Implications in Virulence of Penicillium marneffei
Patrick C. Y. Woo equal contributor ,Ching-Wan Lam equal contributor,Emily W. T. Tam equal contributor,Chris K. F. Leung,Samson S. Y. Wong,Susanna K. P. Lau ,Kwok-Yung Yuen
PLOS Neglected Tropical Diseases , 2012, DOI: 10.1371/journal.pntd.0001871
Abstract: Background The genome of P. marneffei, the most important thermal dimorphic fungus causing respiratory, skin and systemic mycosis in China and Southeast Asia, possesses 23 polyketide synthase (PKS) genes and 2 polyketide synthase nonribosomal peptide synthase hybrid (PKS-NRPS) genes, which is of high diversity compared to other thermal dimorphic pathogenic fungi. We hypothesized that the yellow pigment in the mold form of P. marneffei could also be synthesized by one or more PKS genes. Methodology/Principal Findings All 23 PKS and 2 PKS-NRPS genes of P. marneffei were systematically knocked down. A loss of the yellow pigment was observed in the mold form of the pks11 knockdown, pks12 knockdown and pks11pks12 double knockdown mutants. Sequence analysis showed that PKS11 and PKS12 are fungal non-reducing PKSs. Ultra high performance liquid chromatography-photodiode array detector/electrospray ionization-quadruple time of flight-mass spectrometry (MS) and MS/MS analysis of the culture filtrates of wild type P. marneffei and the pks11 knockdown, pks12 knockdown and pks11pks12 double knockdown mutants showed that the yellow pigment is composed of mitorubrinic acid and mitorubrinol. The survival of mice challenged with the pks11 knockdown, pks12 knockdown and pks11pks12 double knockdown mutants was significantly better than those challenged with wild type P. marneffei (P<0.05). There was also statistically significant decrease in survival of pks11 knockdown, pks12 knockdown and pks11pks12 double knockdown mutants compared to wild type P. marneffei in both J774 and THP1 macrophages (P<0.05). Conclusions/Significance The yellow pigment of the mold form of P. marneffei is composed of mitorubrinol and mitorubrinic acid. This represents the first discovery of PKS genes responsible for mitorubrinol and mitorubrinic acid biosynthesis. pks12 and pks11 are probably responsible for sequential use in the biosynthesis of mitorubrinol and mitorubrinic acid. Mitorubrinol and mitorubrinic acid are virulence factors of P. marneffei by improving its intracellular survival in macrophages.
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