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Petaling Jaya, Malaysia

Wan Juhari W.K.,Universiti Sains Malaysia | Md Tamrin N.A.,University Malaysia Sarawak | Mat Daud M.H.R.,University Malaysia Sarawak | Isa H.W.,Universiti Sains Malaysia | And 9 more authors.
HUGO Journal | Year: 2014

Background: The sequencing of two members of the Royal Kelantan Malay family genomes will provide insights on the Kelantan Malay whole genome sequences. The two Kelantan Malay genomes were analyzed for the SNP markers associated with thalassemia and Helicobacter pylori infection. Helicobacter pylori infection was reported to be low prevalence in the north-east as compared to the west coast of the Peninsular Malaysia and beta-thalassemia was known to be one of the most common inherited and genetic disorder in Malaysia.Result: By combining SNP information from literatures, GWAS study and NCBI ClinVar, 18 unique SNPs were selected for further analysis. From these 18 SNPs, 10 SNPs came from previous study of Helicobacter pylori infection among Malay patients, 6 SNPs were from NCBI ClinVar and 2 SNPs from GWAS studies. The analysis reveals that both Royal Kelantan Malay genomes shared all the 10 SNPs identified by Maran (Single Nucleotide Polymorphims (SNPs) genotypic profiling of Malay patients with and without Helicobacter pylori infection in Kelantan, 2011) and one SNP from GWAS study. In addition, the analysis also reveals that both Royal Kelantan Malay genomes shared 3 SNP markers; HBG1 (rs1061234), HBB (rs1609812) and BCL11A (rs766432) where all three markers were associated with beta-thalassemia.Conclusions: Our findings suggest that the Royal Kelantan Malays carry the SNPs which are associated with protection to Helicobacter pylori infection. In addition they also carry SNPs which are associated with beta-thalassemia. These findings are in line with the findings by other researchers who conducted studies on thalassemia and Helicobacter pylori infection in the non-royal Malay population. © 2014, Wan Juhari et al.; licensee Springer.

Vincent-Chong V.K.,University of Malaya | Ismail S.M.,University of Malaya | Rahman Z.A.A.,University of Malaya | Sharifah N.A.,National University of Malaysia | And 9 more authors.
Oral Diseases | Year: 2012

Background: Multistep pathways and mechanisms are involved in the development of oral cancer. Chromosomal alterations are one of such key mechanisms implicated oral carcinogenesis. Therefore, this study aims to determine the genomic copy number alterations (CNAs) in oral squamous cell carcinoma (OSCC) using array comparative genomic hybridization (aCGH) and in addition attempt to correlate CNAs with modified gene expression. Materials and Methods: Genome-wide screening was performed on 15 OSCCs using high-density aCGH. On the basis of pathway analysis, three genes (ISG15, Nestin and WNT11) which mapped to CNA regions were selected for further evaluation of their mRNA expression using quantitative reverse transcriptase PCR (qRT-PCR). Results: Copy number alterations were observed on multiple genomic regions, including amplifications on 1p, 3q, 5p, 6p, 7p, 8q, 9q, 11q, 12q, 16p, 18p and deletions on 3p, 7q, 8p, 11q, 19q and 20q. Among the three selected genes, ISG15 had the highest mRNA expression level with a 22.5-fold increase, followed by Nestin with a 4.5-fold increase and WNT11 with a 2.5-fold increase. Conclusions: This study has identified several major CNAs in oral cancer genomes and indicated that this correlates with over expression of the ISG15, WNT11, and Nestin genes. © 2011 John Wiley & Sons A/S.

Liew J.,University of Malaya | Amir A.,University of Malaya | Chen Y.,University of Malaya | Fong M.Y.,University of Malaya | And 2 more authors.
Clinica Chimica Acta | Year: 2015

Background: Autoantibodies or antibodies against self-antigens are produced either during physiological processes to maintain homeostasis or pathological process such as trauma and infection. Infection with parasites including Plasmodium has been shown to generally induce elevated self-antibody (autoantibody) levels. Plasmodium knowlesi is increasingly recognized as one of the most important emerging human malaria in Southeast Asia that can cause severe infection leading to mortality. Autoimmune-like phenomena have been hypothesized to play a role in the protective immune responses in malaria infection. Methods: We studied the autoantibody profile from serum of eleven patients diagnosed with P. knowlesi. Autoantigen arrays were used to elucidate the autoantibody repertoire of P. knowlesi infected patients. The patented OGT Discovery Array with 1636 correctly folded antigen was employed. Results: Analysis of the patient versus control sera gave us 24 antigens with high reactivity with serum antibodies. Conclusions: Understanding the autoantibody profile of malarious patients infected with P. knowlesi would help to further understand the host-parasite interaction, host immune response and disease pathogenesis. These reactive antigens may serve as potential biomarkers for cases of asymptomatic malaria and mild malaria or predictive markers for severe malaria. © 2015 Elsevier B.V.

Vincent-Chong V.K.,University of Malaya | Karen-Ng L.P.,University of Malaya | Abdul Rahman Z.A.,University of Malaya | Yang Y.-H.,Kaohsiung Medical University | And 8 more authors.
Head and Neck | Year: 2014

The purpose of this study was to investigate the cause of behavioral difference between tongue and cheek squamous cell carcinomas (SCCs) by verifying the copy number alterations (CNAs). Methods. Array comparative genomic hybridization (aCGH) was used to profile unique deletions and amplifications that are involved with tongue and cheek SCC, respectively. This was followed by pathway analysis relating to CNA genes from both sites. Results. The most frequently amplified regions in tongue SCC were 4p16.3, 11q13.4, and 13q34; whereas the most frequently deleted region was 19p12. For cheek SCC, the most frequently amplified region was identified on chromosome 9p24.1-9p23; whereas the most common deleted region was located on chromosome 8p23.1. Further analysis revealed that the most significant unique pathway related to tongue and cheek SCCs was the cytoskeleton remodeling and immune response effect on the macrophage differentiation pathway. Conclusion. This study has showed the different genetic profiles and biological pathways between tongue and cheek SCCs. © 2013 Wiley Periodicals, Inc.

Vincent-Chong V.K.,University of Malaya | Anwar A.,Sengenics Sdn Bhd | Karen-Ng L.P.,University of Malaya | Cheong S.C.,University of Malaya | And 15 more authors.
PLoS ONE | Year: 2013

Despite the advances in diagnosis and treatment of oral squamous cell carcinoma (OSCC), mortality and morbidity rates have not improved over the past decade. A major drawback in diagnosis and treatment of OSCC is the lack of knowledge relating to how genetic instability in oral cancer genomes affects oral carcinogenesis. Hence, the key aim of this study was to identify copy number alterations (CNAs) that may be cancer associated in OSCC using high-resolution array comparative genomic hybridization (aCGH). To our knowledge this is the first study to use ultra-high density aCGH microarrays to profile a large number of OSCC genomes (n = 46). The most frequently amplified CNAs were located on chromosome 11q11(52%), 2p22.3(52%), 1q21.3-q22(54%), 6p21.32(59%), 20p13(61%), 7q34(52% and 72%),8p11.23-p11.22(80%), 8q11.1-q24.4(54%), 9q13-q34.3(54%), 11q23.3-q25(57%); 14q21.3-q31.1(54%); 14q31.3-q32.33(57%), 20p13-p12.3(54%) and 20q11.21-q13.33(52%). The most frequently deleted chromosome region was located on 3q26.1 (54%). In order to verify the CNAs from aCGH using quantitative polymerase chain reaction (qPCR), the three top most amplified regions and their associated genes, namely ADAM5P (8p11.23-p11.22), MGAM (7q34) and SIRPB1 (20p13.1), were selected in this study. The ADAM5P locus was found to be amplified in 39 samples and deleted in one; MGAM (24 amplifications and 3 deletions); and SIRPB1 (12 amplifications, others undetermined). On the basis of putative cancer-related annotations, two genes, namely ADAM metallopeptidase domain 9 (ADAM9) and maltase-glucoamylase alpha-glucosidase (MGAM), that mapped to CNA regions were selected for further evaluation of their mRNA expression using reverse transcriptase qPCR. The over-expression of MGAM was confirmed with a 6.6 fold increase in expression at the mRNA level whereas the fold change in ADAM9 demonstrated a 1.6 fold increase. This study has identified significant regions in the OSCC genome that were amplified and resulted in consequent over-expression of the MGAM and ADAM9 genes that may be utilized as biological markers for OSCC. © 2013 Vincent-Chong et al.

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