Displaying publications 1 - 20 of 346 in total

  1. Ng SC, Tsoi KK, Kamm MA, Xia B, Wu J, Chan FK, et al.
    Inflamm. Bowel Dis., 2012 Jun;18(6):1164-76.
    PMID: 21887729 DOI: 10.1002/ibd.21845
    BACKGROUND: Inflammatory bowel diseases (IBD) result from an interaction between genetic and environmental factors. Preliminary findings suggest that susceptibility genes differ between IBD patients in Asia and the West. We aimed to evaluate disease-predisposing genes in Asian IBD patients.

    METHODS: A systematic review and meta-analysis were performed of published studies from 1950 to 2010 using keyword searches in MEDLINE, EMBASE, EBM Reviews, and BIOSIS Previews.

    RESULTS: In all, 477 abstracts were identified and data extracted from 93 studies, comprising 17,976 IBD patients and 27,350 age- and sex-matched controls. Major nucleotide oligomerization domain (NOD)-2 variants in Western Crohn's disease (CD) patients were not associated with CD in Han Chinese, Japanese, South Korean, Indian, and Malaysian populations. New NOD2 mutations were, however, associated with CD in Malaysians (JW1), Han Chinese, and Indians (P268S). Autophagy-related protein 16-linked 1 (ATG16L1) was not associated with CD in East Asians (odds ratio [OR] 0.97; 95% confidence interval [CI] 0.84-1.13). Interleukin (IL)-23R was associated with CD in South Koreans (OR 1.8; 95% CI 1.16-2.82) and a single nucleotide polymorphism in IL-23R (Gly149Arg) was protective of CD in Han Chinese (OR 0.3; 95% CI 0.15-0.60). Tumor necrosis factor (TNF) superfamily gene-15 (SF15) polymorphisms were associated with CD (OR 2.68; 95% CI 1.86-3.86), while TNF-308 polymorphisms (OR 1.82; 95% CI 1.15-2.9), cytotoxic T lymphocyte antigen (CTLA)-4 (OR 2.75; 95% CI 1.22-6.22) and MICA allele (OR 2.41; 95% CI 1.89-3.07) were associated with ulcerative colitis in Asians.

    CONCLUSIONS: Genetic mutations of IBD in Asians differ from Caucasians. New mutations and susceptibility genes identified in Asian IBD patients provide an opportunity to explore new disease-associated mechanisms in this population of rising incidence.

    Matched MeSH terms: Genetic Predisposition to Disease*
  2. Naidu R, Har YC, Taib NA
    Onkologie, 2011;34(11):592-7.
    PMID: 22104155 DOI: 10.1159/000334060
    The present study aimed to evaluate the association between the E-Selectin Ser128Arg polymorphism and breast cancer risk and clinicopathological characteristics of the patients.
    Matched MeSH terms: Genetic Predisposition to Disease/genetics*; Genetic Predisposition to Disease/epidemiology*
  3. Barlow-Stewart K, Yeo SS, Meiser B, Goldstein D, Tucker K, Eisenbruch M
    Genet. Med., 2006 Jan;8(1):24-32.
    PMID: 16418596
    In societies such as Australia with a strong multicultural makeup, culturally determined attitudes to genetics, testing, and counseling may be incompatible with current genetics service provision.
    Matched MeSH terms: Genetic Predisposition to Disease/ethnology; Genetic Predisposition to Disease/psychology*
  4. Kabbani T, Abdullah N, Rsheadat Y, Hassan MI
    J Orofac Orthop, 2017 Jan;78(1):62-69.
    PMID: 27896416 DOI: 10.1007/s00056-016-0064-y
    PURPOSE: This research is designed to obtain a better understanding and provide more insight of this phenomenon through evaluating the prevalence of congenital absence of maxillary lateral incisors in a Syrian population.

    METHODS: The method involved clinical examination of 8000 school children with an equal number of males and females (age range 12-15 years) to identify students only affected by bilateral or unilateral congenital absence of maxillary lateral incisors. Agenesis was determined based on radiological evidence.

    RESULTS: The results of this study showed that the prevalence of isolated maxillary lateral incisors agenesis was 1.15%. In the sample studied, 66.3% of the patients were female and 33.7% were male (p 

    Matched MeSH terms: Genetic Predisposition to Disease/genetics; Genetic Predisposition to Disease/epidemiology
  5. Jackson N, Menon BS, Zarina W, Zawawi N, Naing NN
    Ann. Hematol., 1999 May;78(5):233-6.
    PMID: 10391104
    Acute leukemia is more common in males at almost every age, and this fact remains unexplained. A study was carried out in northeast peninsular Malaysia, where the population is predominantly Malay, to examine whether there was a difference in ABO blood group distribution between males and females with acute leukemia (AL). The ABO blood groups of 109 male and 79 female patients with AL (98 ALL, 90 AML) were compared with those of 1019 controls. In the control population, 39.7% were group O. Among males with AL, 39.4% were group O, whereas among females with AL, the proportion was 24.1% (p=0.03). The same trend to a lower proportion of group O among females was seen if the group was divided into adult/pediatric or lymphoblastic/myeloblastic groups, though these differences were not statistically significant. If these findings can be confirmed, they suggest the presence of a "sex-responsive" gene near to the ABO gene locus on chromosome 9, which relatively protects group O women against AL, at least in our population. The existence of such a gene might also partly explain why acute leukemia, and possibly other childhood cancers, are more common in males.
    Matched MeSH terms: Genetic Predisposition to Disease/genetics; Genetic Predisposition to Disease/epidemiology
  6. Lau TP, Lian LH, Cheah PL, Looi LM, Roslani AC, Goh KL, et al.
    Eur. J. Cancer Prev., 2017 11;26(6):506-510.
    PMID: 28059856 DOI: 10.1097/CEJ.0000000000000336
    X-ray repair cross-complementing group 1 (XRCC1) is one of the key components in the base excision repair pathway that repairs erroneous DNA lesions and removes nonbulky base adducts for the maintenance of genome integrity. Studies have revealed that differences in individual DNA repair capacity can impact the interindividual variation in cancer susceptibility, tumour aggressiveness and treatment response. The relationship between XRCC1 and sporadic colorectal cancer (CRC) susceptibility, which is hitherto inconclusive, has been explored in many association studies of different populations. In view of the conflicting findings generated, we aimed to investigate the association between XRCC1 and genetic predisposition to CRC among Malaysians. The present case-control association study was conducted on 130 CRC patients and 212 age-matched healthy controls. The genotyping of XRCC1 Arg194Trp, Arg280His and Arg399Gln single nucleotide polymorphisms was performed with allele-specific real-time PCR approach. This was followed by basic statistical analysis on the single nucleotide polymorphisms and haplotype data obtained. No significant difference in the allele and genotype frequencies was observed between CRC patients and healthy controls (P>0.05). There was also no association observed between XRCC1 haplotypes and CRC (P>0.05). In conclusion, a positive association between XRCC1 gene polymorphisms and CRC risk was not established in our Malaysian population.
    Matched MeSH terms: Genetic Predisposition to Disease/genetics*; Genetic Predisposition to Disease/epidemiology
  7. Apalasamy YD, Mohamed Z
    Hum. Genet., 2015 Apr;134(4):361-74.
    PMID: 25687726 DOI: 10.1007/s00439-015-1533-x
    Obesity is a complex and multifactorial disease that occurs as a result of the interaction between "obesogenic" environmental factors and genetic components. Although the genetic component of obesity is clear from the heritability studies, the genetic basis remains largely elusive. Successes have been achieved in identifying the causal genes for monogenic obesity using animal models and linkage studies, but these approaches are not fruitful for polygenic obesity. The developments of genome-wide association approach have brought breakthrough discovery of genetic variants for polygenic obesity where tens of new susceptibility loci were identified. However, the common SNPs only accounted for a proportion of heritability. The arrival of NGS technologies and completion of 1000 Genomes Project have brought other new methods to dissect the genetic architecture of obesity, for example, the use of exome genotyping arrays and deep sequencing of candidate loci identified from GWAS to study rare variants. In this review, we summarize and discuss the developments of these genetic approaches in human obesity.
    Matched MeSH terms: Genetic Predisposition to Disease
  8. Gunter NV, Yap BJM, Chua CLL, Yap WH
    Front Genet, 2019;10:395.
    PMID: 31130981 DOI: 10.3389/fgene.2019.00395
    Psoriasis is multifactorial disease with complex genetic predisposition. Recent advances in genetics and genomics analyses have provided many insights into the relationship between specific genetic predisposition and the immunopathological mechanisms driving psoriasis manifestation. Novel approaches which utilize array-based genotyping technologies such as genome-wide association studies and bioinformatics tools for transcriptomics analysis have identified single nucleotide polymorphisms, genes and pathways that are associated with psoriasis. The discovery of these psoriasis-associated susceptibility loci, autoimmune targets and altered signaling pathways have provided opportunities to bridge the gap of knowledge from sequence to consequence, allowing new therapeutic strategies for the treatment of psoriasis to be developed. Here, we discuss recent advances in the field by highlighting how immune functions associated with psoriasis susceptibility loci may contribute to disease pathogenesis in different populations. Understanding the genetic variations in psoriasis and how these may influence the immunological pathways to cause disease will contribute to the efforts in developing novel and targeted personalized therapies for psoriasis patients.
    Matched MeSH terms: Genetic Predisposition to Disease
  9. Shalimova A, Fadieienko G, Kolesnikova O, Isayeva A, Zlatkina V, Nemtsova V, et al.
    Curr. Pharm. Des., 2019;25(3):218-227.
    PMID: 30868946 DOI: 10.2174/1381612825666190314124049
    BACKGROUND: Hereditary component plays a significant role in the formation of insulin resistance (IR) - one of the pathogenetic links of arterial hypertension (AH) and type 2 diabetes mellitus (DM2). However, the genetic predisposition to IR can not be realized and does not manifest itself clinically in the absence of appropriate factors of the environment (excessive nutrition, low physical activity, etc.).

    OBJECTIVE: The review summarizes the results of studies which describe the contribution of genetic polymorphism to the formation and progression of AH, DM2 and their comorbidity in various populations.

    RESULTS: In many studies, it has been established that genetic polymorphism of candidate genes is influenced by the formation, course and complication of AH and DM2. According to research data, the modulating effect of polymorphism of some genetic markers of AH and DM2 on metabolism and hemodynamics has been established. The results of numerous studies have shown a higher frequency of occurrence of AH and DM2, as well as their more severe course with adverse genetic polymorphisms. At the same time, the role of genetic polymorphism in the formation of AH and DM2 differs in different populations.

    CONCLUSION: Contradictory data on the influence of gene polymorphisms on the formation of AH and DM2 in different populations, as well as a small number of studies on the combined effects of several polymorphisms on the formation of comorbidity, determine the continuation of research in this direction.

    Matched MeSH terms: Genetic Predisposition to Disease
  10. Zain SM, Mohamed Z, Mohamed R
    J. Gastroenterol. Hepatol., 2015 Jan;30(1):21-7.
    PMID: 25167786 DOI: 10.1111/jgh.12714
    BACKGROUND AND AIM: Although studies have suggested that rs780094, a common variant in the glucokinase regulatory (GCKR) gene to be associated with type 2 diabetes, obesity, and their related traits, the genetic basis of the association between GCKR rs780094 and nonalcoholic fatty liver disease (NAFLD) is still being examined. This meta-analysis was performed to evaluate the effect strength caused by GCKR rs780094 on NAFLD.
    METHODS: We searched Medline, PubMed, Scopus, and Embase for relevant articles published up to April 2014. Data were extracted, and summary estimates of the association between GCKR rs780094 and NAFLD were examined. Heterogeneity and publication bias were also examined.
    RESULTS: This meta-analysis incorporated a total of 2091 NAFLD cases and 3003 controls from five studies. Overall, the pooled result indicated that the GCKR rs780094 was significantly associated with increased risk of NAFLD (additive: odds ratio (OR) 1.25, 95% confidence interval (CI) 1.14-1.36, P 
    Matched MeSH terms: Genetic Predisposition to Disease/genetics*
  11. Nurnberger JI, Koller DL, Jung J, Edenberg HJ, Foroud T, Guella I, et al.
    JAMA Psychiatry, 2014 Jun;71(6):657-64.
    PMID: 24718920 DOI: 10.1001/jamapsychiatry.2014.176
    IMPORTANCE: Genome-wide investigations provide systematic information regarding the neurobiology of psychiatric disorders.

    OBJECTIVE: To identify biological pathways that contribute to risk for bipolar disorder (BP) using genes with consistent evidence for association in multiple genome-wide association studies (GWAS).

    DATA SOURCES: Four independent data sets with individual genome-wide data available in July 2011 along with all data sets contributed to the Psychiatric Genomics Consortium Bipolar Group by May 2012. A prior meta-analysis was used as a source for brain gene expression data.

    STUDY SELECTION: The 4 published GWAS were included in the initial sample. All independent BP data sets providing genome-wide data in the Psychiatric Genomics Consortium were included as a replication sample.

    DATA EXTRACTION AND SYNTHESIS: We identified 966 genes that contained 2 or more variants associated with BP at P

    Matched MeSH terms: Genetic Predisposition to Disease/genetics*
  12. Vaithilingam RD, Safii SH, Baharuddin NA, Ng CC, Cheong SC, Bartold PM, et al.
    J. Periodont. Res., 2014 Dec;49(6):683-95.
    PMID: 24528298 DOI: 10.1111/jre.12167
    Studies to elucidate the role of genetics as a risk factor for periodontal disease have gone through various phases. In the majority of cases, the initial 'hypothesis-dependent' candidate-gene polymorphism studies did not report valid genetic risk loci. Following a large-scale replication study, these initially positive results are believed to be caused by type 1 errors. However, susceptibility genes, such as CDKN2BAS (Cyclin Dependend KiNase 2B AntiSense RNA; alias ANRIL [ANtisense Rna In the Ink locus]), glycosyltransferase 6 domain containing 1 (GLT6D1) and cyclooxygenase 2 (COX2), have been reported as conclusive risk loci of periodontitis. The search for genetic risk factors accelerated with the advent of 'hypothesis-free' genome-wide association studies (GWAS). However, despite many different GWAS being performed for almost all human diseases, only three GWAS on periodontitis have been published - one reported genome-wide association of GLT6D1 with aggressive periodontitis (a severe phenotype of periodontitis), whereas the remaining two, which were performed on patients with chronic periodontitis, were not able to find significant associations. This review discusses the problems faced and the lessons learned from the search for genetic risk variants of periodontitis. Current and future strategies for identifying genetic variance in periodontitis, and the importance of planning a well-designed genetic study with large and sufficiently powered case-control samples of severe phenotypes, are also discussed.
    Matched MeSH terms: Genetic Predisposition to Disease/genetics
  13. Loh HC, Tang PY, Tee SF, Chow TJ, Choong CY, Lim SY, et al.
    Psychiatry Res, 2013 Jul 30;208(2):186-8.
    PMID: 23489597 DOI: 10.1016/j.psychres.2013.01.022
    Neuregulin-1 is widely investigated due to its hypothesised association with schizophrenia. Single-nucleotide polymorphisms rs764059, rs2954041 and rs3924999 were investigated (417 patients with schizophrenia and 429 controls). We failed to demonstrate a significant association between rs2954041 and rs3924999 with schizophrenia in the three ethnic groups studied (Malay, Chinese, and Indian), while rs764059 was found to be monomorphic.
    Matched MeSH terms: Genetic Predisposition to Disease/genetics*
  14. Hung KL, Wang JS, Keng WT, Chen HJ, Liang JS, Ngu LH, et al.
    Pediatr. Neurol., 2013 Sep;49(3):185-90.
    PMID: 23835273 DOI: 10.1016/j.pediatrneurol.2013.04.021
    X-linked adrenoleukodystrophy is caused by a defective peroxisomal membrane transporter, ABCD1, responsible for transporting very-long-chain fatty acid substrate into peroxisomes for degradation. The main biochemical defect, which is also one of the major diagnostic hallmarks, of X-linked adrenoleukodystrophy is the accumulation of saturated very-long-chain fatty acids in all tissues and body fluids.
    Matched MeSH terms: Genetic Predisposition to Disease/genetics*
  15. Velapasamy S, Alex L, Chahil JK, Lye SH, Munretnam K, Hashim NA, et al.
    Genet Test Mol Biomarkers, 2013 Jan;17(1):62-8.
    PMID: 23113749 DOI: 10.1089/gtmb.2012.0223
    The identification of high-risk individuals can help to improve early cancer detection and patient survival. Risk assessment, however, can only be accomplished if the risk factors are known. To date, the genetic risk factors for ovarian cancer, other than mutations in the BRCA1/2 genes, have never been systematically explored in Malaysia. The present study aims to identify from a panel of cancer-associated single-nucleotide polymorphisms (SNPs), those associated with ovarian cancer risk in Malaysia.
    Matched MeSH terms: Genetic Predisposition to Disease*
  16. Haerian BS, Baum L
    Seizure, 2013 Jan;22(1):53-8.
    PMID: 23140995 DOI: 10.1016/j.seizure.2012.10.007
    PURPOSE: The gamma-aminobutyric acid A receptor, gamma 2 (GABRG2) gene encodes the GABRγ2 protein, which has been implicated in susceptibility to epilepsy. Several studies have examined a possible link between the exonic GABRG2 rs211037 locus and susceptibility to febrile seizure (FS) and idiopathic generalized epilepsy (IGE), however results have been inconclusive. We therefore performed a systematic review and meta-analysis to examine whether this polymorphism is associated with FS or IGE.
    METHODS: Eight studies comprising 1871 epilepsy patients and 1387 controls, which evaluated association of the GABRG2 rs211037 polymorphism with susceptibility to epilepsy, were included in this meta-analysis. Meta-analysis was carried out separately for FS and IGE.
    RESULTS: Meta-analysis showed a significant association between this polymorphism and susceptibility to FS in a codominant (TT vs. CC, OR 0.47, 95% CI 0.30-0.73, p=0.0008 and TT vs. CT, OR 0.59, 95% CI 0.42-0.83, p=0.003) and dominant (OR 0.54, 95% CI 0.39-0.75, p=0.0002) genetic models, influenced by two studies with small sample size. Neither allele nor genotype association was observed with IGE.
    CONCLUSION: This study showed significant association of GABRG2 rs211037 with susceptibility to FS, caused by two studies with small sample sizes, however the possibility of false positive results due to the effect of significant studies for FS cannot be excluded. Future studies with larger sample sizes of these patients are suggested to verify the results.
    Matched MeSH terms: Genetic Predisposition to Disease*
  17. Nagaya D, Ramanathan S, Ravichandran M, Navaratnam V
    J. Integr. Neurosci., 2012 Mar;11(1):117-22.
    PMID: 22744787
    Drug addiction is an important social problem in many countries. Genetic and environmental factors contribute to the predisposition of drug addiction. Genetic variations at the μ opioid receptor (OPRM1) gene locus have been associated with opiate addiction. The present study aims to delineate the frequency of A118G allele of OPRM1 among Malaysian subjects. The frequency of A allele and G allele were 51% and 49%, respectively for addicts and about 73% and 27% respectively for healthy volunteers. The frequency of G allele was 1.77-fold higher in addicts by odds ratio calculation at 95% Cl, which indicate the G allele to be strongly associated with addiction X(2) = 15.31,P < 0.0001; odds ratio 2.51; 95% Cl (1.575-3.994), compared to healthy volunteers. A significant association was observed between A118G polymorphism in μ opioid receptor gene and drug addiction.
    Matched MeSH terms: Genetic Predisposition to Disease/genetics*
  18. Othman AS, Othman NI, Rosman A, Nudin SS, Rahman AR
    J. Hypertens., 2012 Aug;30(8):1552-5.
    PMID: 22635140 DOI: 10.1097/HJH.0b013e328355207b
    OBJECTIVES: In this cross-sectional study we compared the central aortic systolic pressure (CASP), peripheral brachial systolic pressure (PSP), peripheral brachial diastolic pressure (PDP) and augmentation index (AIx) between normotensive offspring of nonhypertensive parents (ONT) and normotensive offspring with at least one hypertensive parent (OHT).
    METHODOLOGY: A total of 100 healthy ONT (mean age 20.95 ± 2.06) and 100 healthy OHT (mean age 20.89 ± 2.12) individuals were recruited. Parental history of hypertension was determined by detailed history taking. CASP, PSP, PDP and AIx were measured using the BPro device. All blood pressure (BP) measurements were calibrated using oscillometric BP readings.
    RESULTS: The OHT group had higher PSP (117.57 ± 10.06 versus 114.52 ± 8.94, P < 0.05), PDP (72.39 ± 7.28 versus 70.39 ± 6.50, P < 0.05) and CASP (103.72 ± 8.95 versus 101.37 ± 7.74, P < 0.05) compared to the ONT group. There was no significant difference in AIx in the ONT group (57.97 ± 11.02 versus 58.08 ± 12.16, P = 0.95) in comparison to the OHT group. However, following adjustments for certain cardiovascular risk factors, only PSP (117.33 versus 114.76, P < 0.05) remained significantly higher in the OHT group compared to the ONT group. Analysis of adjusted data within sex showed that CASP was higher in the female OHT group compared to the female ONT group, whereas PDP were higher in the male OHT group compared to the male ONT group.
    CONCLUSION: Alterations in PSP, PDP and CASP are already present in early life in normotensive offspring of hypertensive parents, with possible differences in mechanism between different sexes.
    Study site: Clinical Research Laboratory in Cyberjaya University College of Medical Sciences, Selangor, Malaysia
    Matched MeSH terms: Genetic Predisposition to Disease*
  19. Khor CC, Do T, Jia H, Nakano M, George R, Abu-Amero K, et al.
    Nat. Genet., 2016 May;48(5):556-62.
    PMID: 27064256 DOI: 10.1038/ng.3540
    Primary angle closure glaucoma (PACG) is a major cause of blindness worldwide. We conducted a genome-wide association study (GWAS) followed by replication in a combined total of 10,503 PACG cases and 29,567 controls drawn from 24 countries across Asia, Australia, Europe, North America, and South America. We observed significant evidence of disease association at five new genetic loci upon meta-analysis of all patient collections. These loci are at EPDR1 rs3816415 (odds ratio (OR) = 1.24, P = 5.94 × 10(-15)), CHAT rs1258267 (OR = 1.22, P = 2.85 × 10(-16)), GLIS3 rs736893 (OR = 1.18, P = 1.43 × 10(-14)), FERMT2 rs7494379 (OR = 1.14, P = 3.43 × 10(-11)), and DPM2-FAM102A rs3739821 (OR = 1.15, P = 8.32 × 10(-12)). We also confirmed significant association at three previously described loci (P < 5 × 10(-8) for each sentinel SNP at PLEKHA7, COL11A1, and PCMTD1-ST18), providing new insights into the biology of PACG.
    Matched MeSH terms: Genetic Predisposition to Disease*
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