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Search Results: 1 - 10 of 1967 matches for " Raj Chari "
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Computational Methods for the Analysis of Array Comparative Genomic Hybridization
Raj Chari,William W. Lockwood,Wan L. Lam
Cancer Informatics , 2006,
Abstract: Array comparative genomic hybridization (array CGH) is a technique for assaying the copy number status of cancer genomes. The widespread use of this technology has lead to a rapid accumulation of high throughput data, which in turn has prompted the development of computational strategies for the analysis of array CGH data. Here we explain the principles behind array image processing, data visualization and genomic profile analysis, review currently available software packages, and raise considerations for future software development.
An integrative multi-dimensional genetic and epigenetic strategy to identify aberrant genes and pathways in cancer
Raj Chari, Bradley P Coe, Emily A Vucic, William W Lockwood, Wan L Lam
BMC Systems Biology , 2010, DOI: 10.1186/1752-0509-4-67
Abstract: Here we show how multi-dimensional genomics data analysis would enable the deciphering of mechanisms that disrupt regulatory/signaling cascades and downstream effects. Since not all gene expression changes observed in a tumor are causal to cancer development, we demonstrate an approach based on multiple concerted disruption (MCD) analysis of genes that facilitates the rational deduction of aberrant genes and pathways, which otherwise would be overlooked in single genomic dimension investigations.Notably, this is the first comprehensive study of breast cancer cells by parallel integrative genome wide analyses of DNA copy number, LOH, and DNA methylation status to interpret changes in gene expression pattern. Our findings demonstrate the power of a multi-dimensional approach to elucidate events which would escape conventional single dimensional analysis and as such, reduce the cohort sample size for cancer gene discovery.Genomic analyses have substantially improved our knowledge of cancer. Gene expression profiling, for example, is utilized to delineate subtypes of breast cancer, and has facilitated the derivation of predictive and prognostic signatures [1-5]. However, not all of the gene expression changes observed are causal to cancer development, and global gene expression analysis alone cannot distinguish between causal and reactive changes. Corresponding alteration at the DNA level is regarded as evidence of causality; for example, gene deletion or gene silencing by methylation. Hence, examining genetic and epigenetic events in conjunction with the changes in gene expression pattern should improve the identification of causal changes that lead to disease phenotype.Analysis of gene copy number alone has correlated breast cancer genome features with poor prognosis based on the degree of genomic instability observed [6]. In terms of gene discovery, specific genomic regions containing important loci have been shown to be frequently gained or lost [7-11]. Integrative
Effect of active smoking on the human bronchial epithelium transcriptome
Raj Chari, Kim M Lonergan, Raymond T Ng, Calum MacAulay, Wan L Lam, Stephen Lam
BMC Genomics , 2007, DOI: 10.1186/1471-2164-8-297
Abstract: Twenty-four SAGE profiles of the bronchial epithelium of eight current, twelve former and four never smokers were generated and analyzed. In total, 3,111,471 SAGE tags representing over 110 thousand potentially unique transcripts were generated, comprising the largest human SAGE study to date. We identified 1,733 constitutively expressed genes in current, former and never smoker transcriptomes. We have also identified both reversible and irreversible gene expression changes upon cessation of smoking; reversible changes were frequently associated with either xenobiotic metabolism, nucleotide metabolism or mucus secretion. Increased expression of TFF3, CABYR, and ENTPD8 were found to be reversible upon smoking cessation. Expression of GSK3B, which regulates COX2 expression, was irreversibly decreased. MUC5AC expression was only partially reversed. Validation of select genes was performed using quantitative RT-PCR on a secondary cohort of nine current smokers, seven former smokers and six never smokers.Expression levels of some of the genes related to tobacco smoking return to levels similar to never smokers upon cessation of smoking, while expression of others appears to be permanently altered despite prolonged smoking cessation. These irreversible changes may account for the persistent lung cancer risk despite smoking cessation.Lung cancer has the highest mortality rate among all types of malignancies, accounting for approximately 29% of all cancer-related deaths in the United States [1]. It has been estimated that in 2006 alone, the number of new lung cancer cases will exceed 174,000 and approximately 163,000 people will die of this disease [1]. Tobacco smoking accounts for 85% of the lung cancers. Former heavy smokers remain at an elevated risk for developing lung cancer even years after they stop smoking [2,3]. Fifty percent of newly diagnosed lung cancer patients are former smokers [4]. It is therefore important to understand the effects of tobacco smoking on the
Disruption of the Non-Canonical WNT Pathway in Lung Squamous Cell Carcinoma
Eric H.L. Lee,Raj Chari,Andy Lam,Raymond T. Ng
Clinical Medicine : Oncology , 2008,
Abstract: Disruptions of beta-catenin and the canonical Wnt pathway are well documented in cancer. However, little is known of the non-canonical branch of the Wnt pathway. In this study, we investigate the transcript level patterns of genes in the Wnt pathway in squamous cell lung cancer using reverse-transcriptase (RT)-PCR. It was found that over half of the samples examined exhibited dysregulated gene expression of multiple components of the non-canonical branch of the WNT pathway. In the cases where beta catenin (CTNNB1) was not over-expressed, we identified strong relationships of expression between wingless-type MMTV integration site family member 5A (WNT5A)/frizzled homolog 2 (FZD2), frizzled homolog 3 (FZD3)/dishevelled 2 (DVL2), and low density lipoprotein receptor-related protein 5 (LRP5)/secreted frizzled-related protein 4 (SFRP4). This is one of the first studies to demonstrate expression of genes in the non-canonical pathway in normal lung tissue and its disruption in lung squamous cell carcinoma. These findings suggest that the non-canonical pathway may have a more prominent role in lung cancer than previously reported
Public Databases and Software for the Pathway Analysis of Cancer Genomes
Ivy F.L. Tsui,Raj Chari,Timon P.H. Buys,Wan L. Lam
Cancer Informatics , 2007,
Abstract: The study of pathway disruption is key to understanding cancer biology. Advances in high throughput technologies have led to the rapid accumulation of genomic data. The explosion in available data has generated opportunities for investigation of concerted changes that disrupt biological functions, this in turns created a need for computational tools for pathway analysis. In this review, we discuss approaches to the analysis of genomic data and describe the publicly available resources for studying biological pathways.
MicroRNA Gene Dosage Alterations and Drug Response in Lung Cancer
Katey S. S. Enfield,Greg L. Stewart,Larissa A. Pikor,Carlos E. Alvarez,Stephen Lam,Wan L. Lam,Raj Chari
Journal of Biomedicine and Biotechnology , 2011, DOI: 10.1155/2011/474632
Abstract: Chemotherapy resistance is a key contributor to the dismal prognoses for lung cancer patients. While the majority of studies have focused on sequence mutations and expression changes in protein-coding genes, recent reports have suggested that microRNA (miRNA) expression changes also play an influential role in chemotherapy response. However, the role of genetic alterations at miRNA loci in the context of chemotherapy response has yet to be investigated. In this study, we demonstrate the application of an integrative, multidimensional approach in order to identify miRNAs that are associated with chemotherapeutic resistance and sensitivity utilizing publicly available drug response, miRNA loci copy number, miRNA expression, and mRNA expression data from independent resources. By instigating a logical stepwise strategy, we have identified specific miRNAs that are associated with resistance to several chemotherapeutic agents and provide a proof of principle demonstration of how these various databases may be exploited to derive relevant pharmacogenomic results.
Genomic imbalances in precancerous tissues signal oral cancer risk
Cathie Garnis, Raj Chari, Timon PH Buys, Lewei Zhang, Raymond T Ng, Miriam P Rosin, Wan L Lam
Molecular Cancer , 2009, DOI: 10.1186/1476-4598-8-50
Abstract: At present, risk of progression in oral premalignant lesions (OPLs) is typically determined based on histopathological evaluation of biopsied material. High grade dysplasia (HGD) and carcinoma in situ (CIS) are considered high risk for progression to invasive disease. In contrast, only a small proportion of low grade dysplasias (LGDs) – which represent the majority of diagnosed OPLs – progress to invasive disease [1,2]. Histological features cannot currently be used to delineate "progressing" and "non-progressing" LGDs [3]. Consequently, LGDs that are prime candidates for early intervention are not easily identified. Novel approaches for defining progression likelihood for histopathologically similar LGDs are required.Chromosome instability, particularly loss of chromosome arms 3p and 9p, has previously been associated with an increased probability of progression in oral cancer, demonstrating the potential utility of molecular markers in predicting progression risk [4-7]. Additionally, p53 status has been used to predict progression in Barretts esophagus and other groups have reported genomic instability in tumor-associated dysplastic oral tissue [8-11]. To date, efforts to undertake whole genome analysis of premalignant lesions have been precluded by 1) the rarity of LGD specimens with longitudinal follow-up and clinical outcome details and 2) the lack of robust high resolution genome profiling methodologies that can utilize the limited DNA yield from microdissected formalin-fixed paraffin-embedded lesions. In this study, we compared the genomes of precancerous oral tissues from different disease stages to identify stage-specific DNA alterations. Analysis of this rare sample set not only revealed qualitative and quantitative differences in DNA alterations depending on histopathological stage, but also showed that these features are associated with known clinical outcomes.Genome profiles were generated by tiling-path array CGH for a panel of 86 oral lesions with lon
Ethical challenges facing Zimbabwean media in the context of the Internet
Tendai Chari
Global Media Journal : African Edition , 2011, DOI: 10.5789/3-1-19
Abstract: The Internet has fundamentally transformed the practice of journalism in Africa. It has spawned enormous opportunities and challenges for the African media, and Zimbabwe is no exception. Not only has the concept of news changed but also the manner in which it is gathered and disseminated. Journalists no longer feel compelled to adhere to the ethical cannons of their profession owing to certain qualities of the Internet. This paper investigates ethical challenges faced by the Zimbabwean media as a result of the Internet. In particular the paper discusses ethical challenges in the Zimbabwean media that are either directly or indirectly linked to the Internet. The main argument advanced in this paper is that while the Internet has brought about a number of opportunities for the Zimbabwean media, the same technology has been the root of unethical reporting.
Bilateral dorsal perilunate dislocation of wrist
Chari P
Indian Journal of Orthopaedics , 2010,
Abstract: We present a case of simultaneous dorsal perilunate dislocation of both wrists, without a history of fall on outstretched hands. In contrast, it appeared that the mechanism was reverse. His hands were held in radial deviation with wrists in full palmar flexion. The forearms were in neutral position and elbows in mid-flexion. The wrists were suddenly and forcibly pronated. The radiographs of both wrists showed dorsal perilunate dislocation with avulsion fracture of the tip of ulnar styloid process and avulsion fracture of posterior horn of lunate. Radial translation of the carpal bones was also noted. The mechanism is proposed and discussed.
Susruta and our heritage
Chari P
Indian Journal of Plastic Surgery , 2003,
Abstract:
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