CONFERENCE PROGRAM

ICAST 2004 Event Schedule and Location

8:30 - 9:00 Registration (Foyer)

9:00 - 9:15 Opening Remarks by Dr. Brenda Russell (Auditorium Room 134-1)

9:15 - 12:30 Morning Session (Auditorium Room 134-1)
Discussion Leader: Dr. Andrew H.-J. Wang (Academia Sinica, Taiwan, ROC)

9:15 - 9:50 Dr. Andrew H.-J Wang (Academia Sinica, Taiwan, ROC)
Current progress in proteomics and structure biology: In search of disease targets and their functional studies

9:50 - 10:25 Dr. Wen-Hsiung Li (University of Chicago)
Dynamic modeling of cis-regulatory circuits of yeast genes

10:25 - 10:45 Coffee Break

10:45 - 11:20 Dr. Andrzej Joachimiak (Argonne National Laboratory)
Structural Genomics of pathogenic bacteria

11:20 - 11:55 Dr. Robert Goldman (Northwestern University)
Revelation of nuclear lamin functions by human diseases--- from muscular dystrophy to progeria.

11:55 - 12:30 Dr. Judy L. Bolton (University of Illinois at Chicago)
Natural alternatives for traditional estrogen replacement therapy: Mechanistic evaluation

12:30 - 13:45 Lunch Break (Hospital Cafeteria)

13:45 - 17:00 Session A: Molecular Medicine (Auditorium Room 134-2)
Discussion Leader: Dr. William Beck (University of Illinois at Chicago)

13:45 - 14:20 Dr. William Beck (University of Illinois at Chicago)
Protein sumoylation and novel cancer therapeutic targets

14:20 - 14:55 Dr. Han-Xiang Deng (Northwestern University)
Molecular basis of amyotrophic lateral sclerosis

14:55 - 15:30 Dr. Lucio Miele (University of Illinois at Chicago)
Developing a novel target for anti-cancer biopharmaceuticals: Notch signaling in cancer

15:30 - 15:50 Coffee Break

15:50 - 16:25 Dr. Jin-Ding Huang (Cheng-Kung University)
Genetic polymorphism of cytochrome P450

16:25 - 17:00 Dr. Hua-Lin Wu (Cheng-Kung University)
Genetic risk factors of atherothrombotic disease in Taiwan

13:45 - 17:00 Session B: Genomics and Proteomics (Auditorium Room 134-3)
Discussion Leader: Dr. Chung-I Wu (University of Chicago)

13:45 - 14:20 Dr. Chung-I Wu (University of Chicago)
The genetics of racial differentiation---from fly to man

14:20 - 14:55 Dr. Wen-Chang Chang (Cheng-Kung University)
Dephosphorylation of c-Jun C-terminus is involved in phorbol ester-induced interaction between c-Jun and Spl in promotor activation of the human 12(S)-lipoxygenase gene

14:55 - 15:30 Dr. Tatiana Nikolskaya (GeneGo Inc.)
A systems biology platform for visualization and analysis of high-throughput experimental data in the framework of cellular pathways

15:30 - 15:50 Coffee Break

15:50 - 16:25 Dr. Jei-Fu Shaw (Chung-Hsing University)
Plant functional genomics and biotechnology researches in Taiwan.

16:25 - 17:00 Dr. Min-Hao Kuo (Michigan State University)
Protein-protein interactions and post-translational modifications: Lessons from acetylation of histones and tumor suppressor p53

17:00 – 17:20 Closing Remarks by Drs. Chung-I Wu and William Beck (Room 134-1)

17:20 – 18:00 Reception (Foyer)

Current progress in proteomics and structure biology:
In search of disease targets and their functional studies

Andrew H.-J. Wang,

Institute of Biological Chemistry, Academia Sinica

In the post-genomic era, a wealth of genomic information has been accumulated with no ending in sight. How to effectively make use of the available information is a major challenge. Understanding the function of many biological systems requires we go beyond the genomic data. The complex interplays of biological molecules, especially proteins, nucleic acids, carbohydrates, and numerous small molecules demand us to approach the issue with many new technologies. In Taiwan, the government has supported the establishment of a number of critical core facilities, whose management is currently under the joint supervision of Genomic Research Center in Academia Sinica and National Research Program for Genomic Medicine. An important focus of the genomic research is in drug discovery. The process of drug discovery in the post-genomic era has seen a change in the requisite knowledge and technology platforms. This paper describes the progress in our efforts at producing an integrated system starting at gene targeting, proteomic analysis, protein expression and production, crystallographic structural solution, and finally structural-based drug design. Three national core facilities in the Institute of Biological Chemistry have been set up to support this program. Additionally, two new protein crystallography beamlines in NSRRC are under construction and should be ready by the end of 2004. In this new discovery process we also try to employ other technologies such as bioinformatics and antibody to accelerate the efforts. At present, we focus on several enzyme systems which have medical or biotechnology implications. Some specific examples include the high resolution structural analysis of SARS 3CL protease, prenyltransferases and phosphatases.

ACKNOWLEDGEMENTS

This work was supported by National Science Council and Academia Sinica, Taiwan

Dynamic modeling of cis-regulatory circuits of yeast genes

Wen-Hsiung Li

Department of Ecology and Evolution, University of Chicago, USA.

Bor-Sen Chen

Department of Electrical Engineering, National Tsing Hua University, Hsinchu, Taiwan, ROC.

The transcriptional regulation of a eukaryotic gene is typically controlled by multiple transcription factors (TFs) via their interactions with the cis elements (TF binding sites, TFBSs) of the gene. Thus, in order to understand the transcriptional regulation of a gene one must first know what the cis elements of the gene are and how the recognizing TFs interact with the cis elements and among themselves. Such a regulatory program has been termed the cis-regulatory circuit of the gene. Note that in a cis-regulatory circuit we want to know not only the cis elements of the circuit but also the regulatory strength of each recognizing TF and the combinatorial interactions among the TFs. In the post-genomic era there is the ambition to identify and characterize all cis elements and cis-regulatory circuits of a genome. This is an enormous challenge even for the best-studied single-cell model organism Saccharomyces cerevisiae because despite the tremendous effort made in the past only a very limited number of yeast TFBSs are known for sure at the present time. In my talk I shall describe some methods for inferring the cis elements of yeast genes and present a dynamic modeling of cis-regulatory circuits of yeast genes.

Structural Genomics of Pathogenic Bacteria

A. Joachimiak

Bioscience Division, Structural Biology Center and Midwest Center for Structural Genomics, Argonne National Laboratory, 9700 South Cass Avenue, Argonne, IL 60439, USA.

The Midwest Center for Structural Genomics (MCSG) is developing all necessary components of protein structure determination pipeline using x-ray crystallography and synchrotron radiation. The process requires development, optimization, parallelization and integration of a number of experimental and computational processes. The large-scale and cost-effective multi-step manipulations of genetic elements and gene products are made possible with the use of automated methods and robotics. Targets for structural studies are selected from updated databases of genomic sequences with a major focus on pathogenic bacteria. The MCSG pipeline generates well-characterized protein expression systems, produces milligram quantities of proteins and x-ray quality crystals. The cryoprotected crystals are being tested for diffraction using synchrotron beamlines and crystals of x-ray quality are used for structure determination using SAD or MAD approach. Crystals that are not suitable for data collection return for further optimization. Protein structures are determined using semi-automated pipeline. New structures are verified and analyzed using automated computational tools. Majority of steps in the MCSG pipeline are tracked by the databases. The MCSG structure determination pipeline when combined with data collection facilities at third generation synchrotrons, advanced software and computing resources resulted in significant acceleration of protein structure determination and overall reduction of cost. Several recently determined structures of proteins from major human pathogens will be presented.

This work was supported by the by grants from the National Institutes of Health (GM62414) and the U.S. Department of Energy, Office of Biological and Environmental Research, under Contract W-31-109-ENG-38

Revelation of nuclear lamin functions by human diseases
---from muscular dystrophy to progeria.

Robert D. Goldman¹, Dale K. Shumakler¹, Michael R. Erdos², Maria Eriksson³, Anne E. Goldman¹, Leslie B. Gordon⁴, Yosef Gruenbaum⁵, Satya Khuon¹, Melissa Mendez¹, Renee Varga² and Francis S. Collins².

¹ Dept. of Cell & Mol. Biology, Northwestern University

² National Human Genome Research Institute, National Institute of Health

³ Dept. of Medical Nutrition, Karolinska Institute

⁴ Dept. of Anatomy and Cellular Biology, Tufts University

⁵ Dept. of Genetics, Hebrew University.

The nuclear lamins and their associated proteins play essential roles in organizing the nuclear architecture and in regulating many nuclear functions such as DNA replication and transcription. This is highlighted by the recent findings that mutations in lamin A gene are linked to a spectrum of human diseases: Emery-Dreifuss muscular dystrophy (DCM); familial partial lipodystrophy (FPLD); mandibuloacral dysplasia (MAD); dilated cardiomyopathy (DCM); autosomal recessive Charcot-Marie-Tooth disorder type 2 (AR-CMT2); limb girdle muscular dystrophy 1B (LGMD-1B); and Hutchinson-Gilford progeria syndrome (HGPS). In the case of HGPS, this premature aging disorder is caused by a point mutation in the lamin A gene that results in a protein lacking 50 aa near the C terminus (LA50). We have shown by light and electron microscopy that HGPS is associated with significant changes in nuclear shape, including lobulation of the nuclear envelope, thickening of he nuclear lamina, loss of peripheral heterochromatin, and clustering of nuclear pores. These structural defects worsen as HGPS cells age in culture, and their severity correlates with an apparent increase in LA50. Introduction of LA50 into normal cells by transfection or protein injection induces the same changes. We hypothesize that these alterations in nuclear structure are due to a concentration-dependent dominant-negative effect of LA50, leading to the disruption of lamin-related functions ranging from the maintenance of nuclear shape to regulation of gene expression and DNA replication.

Natural alternatives for traditional estrogen replacement therapy: Mechanistic evaluation

Judy L. Bolton

Department of Medicinal Chemistry and Pharmacognosy, University of Illinois at Chicago

There is a clear association between hormone replacement therapy and the development of cancer in breast and endometrial tissues. The results from the Women’s Health Initiative in particular have stimulated women and their doctors to search for natural alternatives to hormone replacement therapy. We have been studying botanicals with estrogenic activity such as hops and red clover. In addition, we have discovered an alternative serotonergic mechanism for the relief of menopausal symptoms which could be important for black cohosh. The hypothesis to be addressed is whether select plant extracts contain potent estrogenic and/or serotonergic compounds useful for the relief of menopausal symptoms as well as other beneficial properties of estrogens such as antioxidant/chemopreventive effects. We have already screened a number of plant extracts and pure compounds for estrogenic effects and investigated their mechanism of action using a variety of in vitro assays including competitive ER binding assays, induction of estrogen sensitive genes, and ERE-luciferase assays. In addition, we have tested several of these extracts for hormonal activity in vivo using the ovariectomized rat model. Our studies are designed to determine which specific botanicals have health benefits for relief of menopausal symptoms and determine their mechanism of action.

Molecular Basis of Amyotrophic Lateral Sclerosis

Han-Xiang Deng, MD., Ph.D.

Department of Neurology, Northwestern University Feinberg School of Medicine

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder caused by degeneration of motor neurons in brain and spinal cord. About 5-10% of ALS cases is familial (FALS), and the rest are sporadic. We have identified two genes whose mutations lead to ALS. Mutations in Cu/Zn superoxide dismutase (SOD1) are identified in about 20% of the FALS cases, while mutation in ALSIN gene is quite rare. There are more than 90 mutations identified in ALS. These mutations are widely distributed in the entire SOD1 polypeptide. Overexpression of ALS-linked SOD1 mutations lead to ALS phenotype in transgenic mice and SOD1 knockout mice do not develop disease, suggesting the mutant SOD1 displays a toxicity that triggers the motor neuron degeneration. The mechanism by which mutations in SOD1 gene cause ALS is not known. To investigate the molecular basis of motor neuron degeneration in ALS, we developed several transgenic mouse models expressing different parts of SOD1 and ALSIN knockout mouse model. By crossbreed strategy, we found that not only the mutant, but also the wild type SOD1 form aggregates in the motor neurons in ALS mice; overexpressing wild type SOD1 exacerbates the disease. To further define the toxic region of SOD1, we developed a transgenic mouse model expressing a highly unstable, C-terminal truncated SOD1. This mouse model also developed ALS phenotype. Large amount of truncated SOD1 was found in the insoluble aggregates in motor neurons, although little soluble form of this truncated SOD1 was present. Taken together, our results suggested that the aggregation form, rather than soluble form, of mutated SOD1 is the major player in disease process of SOD1-linked ALS; the toxicity leading to motor neuron degeneration is derived from the N-terminal polypeptide; the signaling pathways underlying SOD1- and ALSIN-mediated ALS are independent.

Gentic polymorphism of cytochrome P450.

Jin-ding Huang

Department of Pharmacology, National Cheng Kung University, Tainan, Taiwan.

Drug metabolism enzymes are often not essential enzymes in the body. Variation in those enzymes may have some evolutionary advantages. Genetics in the enzymes is an interesting topic. Single nucleotide polymorphism (SNP) of cytochrome P450s or transporters often result a missense mutation, an early stop codon, or a splicing site shift. It is also frequently that the SNP site results nonsense mutation or a conservative amino acid. Surprisingly, the metabolic activity may not be necessarily altered as predicted. Some unimportant mutations result in clinically important consequence. Some missense mutations end up no activity change. There are several possible reasons. Associating with SNP sites, genes may duplicate or alter the expression of itself or other genes. SNP sites are often linked each other and may also associate with unknown sites. For gene clusters of CYP2C, CYP2D and CYP3A, examples are seen as genes exchange at the genomic DNA or pre-mRNA level. Genetic polymorphism research needs to look beyond a single nucleotide. RNA study and protein modifications are further steps to illustrate the metabolism activity.

Genetic Risk Factors of Atherothrombotic Disease in Taiwan

Yi-Heng Li, Ting-Hsing Chao, Guey-Yueh Shi, and Hua-Lin Wu

Department of Internal Medicine and Department of Biochemistry and Molecular Biology
College of Medicine, National Cheng Kung University, Tainan, Taiwan.

In recent years, there is an increase of awareness of genetic risk factors for atherothrombotic disease. Atherothrombosis is a complex process involving lipids, oxidative stress, inflammation, and thrombosis. Single nucleotide polymorphisms of the genes involving these processes are investigated in Taiwan. Hepatic lipase, involving in the metabolism of several lipoproteins, plays an important role in reverse cholesterol transport. Hepatic lipase gene promoter polymorphisms (-514C/T and –250G/A) are significantly associated with lower total cholesterol/HDL-C ratio in Taiwan. However, these single nucleotide polymorphisms are not associated with an increased risk of coronary artery disease in Taiwanese and Koreans. Some genetic variations of cholesteryl ester transfer protein gene and scavenger receptor class B type I gene are reported to be associated with the plasma HDL-C levels in this population. Microsatellite polymorphism in the promoter region of the heme oxygenase-1, an enzyme implicating in the antioxidant defense mechanism, gene is associated with susceptibility to coronary artery disease in type 2 diabetes as well as development of angiographic restenosis after coronary stenting. Recognized as a HDL-associated enzyme protecting lipoproteins from oxidation, the Gln-Arg 191 polymorphism of the human paraoxonase gene is not associated with coronary artery disease in Taiwan; however, this genetic variant is significantly associated with the presence and severity of coronary artery disease in the Western reports. C-31T polymorphism of the interleukin-1 beta gene is a common genetic variation in our population. However, this polymorphism is not significantly associated with the occurrence of acute myocardial infarction. Despite that CD14-260C/T polymorphism is significantly associated with serum titers of Chlamydia pneumoniae, it remains unclear whether this genetic variation significantly increases the risk of myocardial infarction. A significant association between the 5A/6A polymorphism in the promoter region of matrix metalloproteinase-3 gene and young myocardial infarction was observed in Taiwan and Japan. G-33A polymorphism of the thrombomodulin, an intrinsic anticoagulant, is a functional genetic variant that decreases gene transcriptional activity. Its prevalence is low in Caucasian. However, this polymorphism is a common genetic variant in Taiwan, and it may increase the risk of coronary artery disease and myocardial infarction as well as confer worse outcome in young myocardial infarction. Conflicting results regarding the relationship of angiotensin-converting enzyme insertion/deletion polymorphism and endothelial nitric oxide synthase gene polymorphism with the presence of coronary artery disease or myocardial infarction have been reported in the Western population. In Taiwan, the results of studies fail to find any association with atherothrombotic disease. In conclusion, some genetic variations are recognized as important genetic risk factors of atherothrombotic disease in Taiwan. Ethnic background plays an important role in the genesis of discrepancies between the Asian and Western reports.

Dephosphorylation of c-Jun C-terminus is involved in phorbol ester-induced interaction between c-Jun and Sp1 in promoter activation of human 12(S)-lipoxygenase gene.

Ben-Kuen Chen, Chi-Chen Huang, Wei-Chiao Chang and Wen-Chang Chang.

Department of Pharmacology, College of Medicine, National Cheng Kung University
Tainan, Taiwan.

c-Jun/Sp1 interaction is essential for growth factor- and phorbol ester-induced expression of genes, including human 12(S)-lipoxygenase. This study examined the mechanism used to regulate the interaction between c-Jun and Sp1 in the phorbol 12-myristate 13-acetate (PMA)-induced expression of 12(S)-lipoxygenase in human epidermoid carcinoma A431 cells. PMA-induced promoter and enzymatic activities of 12(S)-lipoxygenase were dose-dependently inhibited by a specific calcineurin (PP2B) inhibitor, cyclosporin A. Overexpression of PP2B also enhanced the promoter activity of the 12(S)-lipoxygenase gene in a dose-dependent manner. Moreover, in PMA-treated cells, cyclosporin A inhibited the interaction between c-Jun and Sp1. Overexpression of TAM-67, an N-terminally truncated c-Jun, inhibited the PMA-induced promoter activity of 12(S)-lipoxygenase. TAM-67-M3A, which contains three substitutive alanine at Thr-231, Ser-243, and Ser-249, was about twice as efficacious as TAM-67 in inhibiting the PMA-induced promoter activity of the 12(S)-lipoxygenase gene. GST pull-down assay indicated that, compared to phosphorylated GST-TAM-67 by casein kinase II, GST-TAM-67-M3A bound more efficaciously with Sp1. Taken together, these results indicate that the dephosphorylation of Thr-231, Ser-243, and Ser-249 at the c-Jun C-terminus is essential for the protein-protein interaction between c-Jun and Sp1.

A system biology platform for visualization and analysis of high-throughput experimental data in the framework of cellular pathways

Tatiana Nikolskaya, Ph.D.
CSO & President, GeneGo Inc., 500 Renaissance Drive, St. Joseph, MI 49085, USA

With “reduction to practice” of many genomics technologies, experimental “high-throughput” (HT) data have being quickly accumulated in life science labs, both in academy and industry. The majority of it is not utilized. Statistical analysis of HT data is robust, but the methodology for rational, mechanism-based, systems biology “mining” in its infancy.

Over the last four years, we developed MetaCore™, an expert computational platform designed for the analysis of multiple types of high-throughput data (gene expression on microarrays, SAGE, SNPs and other DNA sequences, proteomics and metabolomic profiles) in the framework of cellular networks. MetaCoreTM integrates a relational database of novel architecture, a comprehensive content of annotated human, mouse and rat metabolic and signaling pathways, reactions, protein interactions, and compounds; and a toolkit for data visualization, mining and network creation. The pathways and their elements are annotated with relevant disease information. MetaCore™ allows concurrent visualization of multiple data types and experiments on pathway maps and networks. MetaCoreTM has multiple applications in drug discovery, such as identification and validation of novel protein drug targets, reconstruction of disease mechanisms, prediction of drug metabolism and toxicity.

I will present the basics of the system and brief on the results of our studies on analysis of glaucoma based on human microarray gene expression; proteomics data for Alzheimer mouse model and drug response in human breast cancer cell lines.

Plant functional genomics and biotechnology research in Taiwan

Jei-Fu Shaw

President, National Chung-Hsing University, Taichung, Taiwan

Institute of botany, Academia Sinica, Taipei, Taiwan

Under the National Agricultural Biotechnology Program, we have established three core projects in the Division of “Useful Plant Genes”.

1. Rice functional genomics and biotechnology. Rice is the most important crop in Taiwan and also one of the most important food crops for the world’s population. Institute of Botany, Academia Sinica represents Taiwan as a member of International Rice Genome Sequencing Project (IRGSP) to Sequence chromosome 5. The whole genome sequence was completed in Dec 2002.We have established a rice functional genomics program to study the function of rice genes for (1) rice genetic engineering to improve quality and yields (2) production of medicinal or industrial products using transgenic rice as a bioreactor. Several examples will be used to highlight the current achievement.

2. Plant senescence-associated genes and postharvest biotechnology: Genes associated with the ripening of papaya , banana and bitter gourd, and the yellowing of broccoli have been studied. Transgenic plant technologies have been successfully used to prolong the shelf life and reduce the postharvest loss of the agricultural produce.

3. Transgenic plants as bioreactors. Transgenic plants as bioreactors have the advantages of low cost, safety, availability in large amount, long term storage and direct processing. Several successful examples will be discussed: (1) Expression of a bacterial amylopullulanase gene in transgenic rice seeds of starch hydrolysis. (2) Production of coat protein of porcine FMD virus and surface antigen (VP1) of Enterovirus in rice and potato.

Deciphering PTM proteomics: using a tethered catalysis/yeast two-hybrid system to identify protein-protein interactions requiring post-translational modifications (PTMs).

Min-Hao Kuo, 401 BCH Building, Department of Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI 48824

Post-translational modifications (PTMs) are critical for the functions of numerous proteins. Significant efforts have been invested in proteomic identification of cellular proteins bearing specific post-translational modifications. Meanwhile, a wealth of evidence has shown that one molecular function of post-translational modifications is to modulate protein-protein interactions. While the global mapping of protein interactions has been accumulating tremendous momentum in different biomedical fields, the effects of post-translational modifications on such interactions remain to be a missing piece of the puzzle. To aide in large-scale screening for protein interactions that are modulated, i.e. enhanced or suppressed, by a selective post-translational modification, we have developed a tethered catalysis/yeast two-hybrid system and shown that this method is able to quickly identify phosphorylation- and acetylation-stimulated protein-protein interactions. In this assay, a constitutive modification of the protein to be screened for interactions is achieved by fusing it to its cognate modifying enzyme, with the physical linkage resulting in highly efficient and constitutive catalysis in vivo. This catalysis maintains substrate modification even in the presence of antagonizing enzyme activities. As a control in the assay, a catalytically inactive mutant of the enzyme is fused to the substrate such that the modification does not occur; this construct enables the rapid identification of modification-independent interactions. Using acetylation of histones and phosphorylation of the carboxyl terminal domain, CTD, of the eukaryotic RNA polymerase II as the testing models, we identified proteins with links to chromatin functions that interact with acetylated histones, and proteins that participate in RNA polymerase II functions and in CTD phosphorylation regulation that interact preferentially with the phosphorylated CTD. Importantly, we also found several SUMO E3 ligases preferentially associate with an acetylated tumor suppressor protein p53. Preliminary results of arginine methylation also indicated the feasibility of this approach. These data strongly support the notions that key protein-protein interactions may be regulated by chemical modifications of one of the two interacting proteins, and that our tethered catalysis/two-hybrid approach likely provides a non-biased tool for constructing a proteomic map involving post-translational modifications.

Chronology of ICAST Conferences

Conference Name	CAPAMA President	Conference Location	Conference Co-Chair	Program Co-Chair	Major Co-Sponsor
CAPAMA 85	Ben C. Liu	UlC Chicago, IL	Carl K. Chang	Kwang-Ya Fang Chung-Yi Wang	UIC
CAPAMA 86	Webster Kiang	NIU Dekalb, IL	Yen-Chou Chou	T. S. Jiang	NIU
ICAT 87	Wai-Kai Chen	Ramada Hotel Rosemont, IL	Tse L. Wang	Chi-Haur Wu Yih-Wu Han	MACSTA
ICAST 88	C. Peter Chiang	IIT Chicago, IL	An-Chi Liu	Alan M. Lin K. Vincent Liu	IIT
MACAST 89	Chung-Yi Wang	UIC Chicago, IL	James C. Lin	Jyh-Yee Lan	AMOCO
MACAST 90	Tse L. Wang	Holiday Inn Evanston, IL	I-Hung Li	Wei-Chung Lin Chen-Shiou Jan	NWU
ICAST 91	K. Vincent Liu	Argonne Lab Argonne, IL	James C. Lin	Yun-Lai Chan Phil Gustafson	Argonne
ICAST 92	James C. Lin	Argonne Lab Argonne, IL	Carl Hsu	Erie Suen	Argonne
ICAST 93	Jesse Wang	Motorola Schaumburg, IL	Carl K. Chang	Weider Yu Hung-Yu Yang	Motorola
ICAST 94	Carl K. Chang	AT&T Naperville, IL	Hermann Tai	Robert Carlson Tse L. Wang	AT&T
ICAST 95	Jinn H. Wang	UC Chicago, IL	Shem-Mong Chou Ralph Nicholas	Yun-Lai Chan Alice Chang	UC Chiao Tung U.
ICAST 96	Yun-Lai Chan	UIC Chicago, IL	Wei-Pang Chin R. John Solaro	Win L. Chiou Weider Yu	UIC
ICAST 97	Barbara Liu	Motorola Schaumburg, IL	Pao-Sheng Chang Terry Heng	Chengwen Liu Dave Morgan	Motorola DePaul U.
ICAST 98	Weider Yu	Lucent Naperville, IL	Chung Lee	Lawrence Henchen	Lucent NWU
ICAST 99	Shem-Mong Chou	Argonne Lab Argonne, IL	Bang-Jean Hsieh Norman Peterson	Shih-Chang Chao Shi-Shang Jang	Argonne NTHU
ICAST 2000	Bang-Jean Hsieh	Fermi Lab Batavia, IL	Di-Jen Leu G. P. Yeh	Shih-Chang Chao Mao-Tung Cheng	Fermi Depaul U. Lucent Tech. Motorola
ICAST 2001	Di-Jen Lu	IIT Chicago, IL	Morris Chang	Ching-Rong Chou Viginia Shen	IIT
ICAST 2002	Shuh-Haw Sheen	Chicago State U. Chicago, IL	Robert Chierico Johng-Chern Chern	Paosheng Chang Shih-Chang Chao	Chicago State University
ICAST 2004	Chwan-Shyang Jih	UIC Chicago, IL	Brenda Russell Wen-Hsiung Li	William Beck Ying-Hao Chou	UIC