Displaying publications 81 - 100 of 501 in total

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  1. Fulltext Germline mutation analysis of MLH1 and MSH2 in Malaysian Lynch syndrome patients
    Zahary MN, Kaur G, Abu Hassan MR, Singh H, Naik VR, Ankathil R
    World J Gastroenterol, 2012 Feb 28;18(8):814-20.
    PMID: 22371642 DOI: 10.3748/wjg.v18.i8.814
    To investigate the protein expression profile of mismatch repair (MMR) genes in suspected cases of Lynch syndrome and to characterize the associated germline mutations.
    Matched MeSH terms: Genetic Predisposition to Disease
  2. Fulltext Lack of association between Gly82Ser, 1704G/T and 2184A/G of RAGE gene polymorphisms and retinopathy susceptibility in Malaysian diabetic patients
    Ng ZX, Kuppusamy UR, Poh R, Tajunisah I, Koay AC, Fong KC, et al.
    Genet. Mol. Res., 2012 Mar 01;11(1):455-61.
    PMID: 22427038 DOI: 10.4238/2012.March.1.2
    Diabetic retinopathy is the most common diabetic eye disease, occurring in about 60% of type 2 diabetic patients. Other than known clinical risk factors, the influence of genes has been suggested as part of the development of diabetic retinopathy. We investigated the association of Gly82Ser, 1704G/T and 2184A/G polymorphisms in the RAGE gene with retinopathy in type 2 diabetic patients in Malaysia. Ninety-eight unrelated retinopathy patients and 185 unrelated healthy controls from all over Malaysia were recruited in this study. The allele and genotype frequencies of the three gene polymorphisms were investigated using PCR-RFLP. The allele frequency of the three polymorphisms did not differ significantly between the control and the retinopathy group (P > 0.05). Analysis of the frequency of GA+AA, GT+TT and AG+GG in the retinopathy group did not reveal significant differences (P > 0.05) compared to the control group. We conclude that RAGE gene Gly82Ser, 1704G/T and 2184A/G polymorphisms are not associated with retinopathy development in the Malaysian population.
    Matched MeSH terms: Genetic Predisposition to Disease
  3. A118G mu opioid receptor polymorphism among drug addicts in Malaysia
    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*
  4. p53 codon 72 polymorphisms and random amplified polymorphic DNA analysis of non-melanoma skin cancer through archival formalin-fixed paraffin-embedded tissue
    Yoke-Kqueen C, Ab Mutalib NS, Sidik SM, Learn-Han L, Geok-Chin T
    Oncol Rep, 2012 Mar;27(3):753-63.
    PMID: 22159872 DOI: 10.3892/or.2011.1581
    Non-melanoma skin cancer (NMSC) is classified among the ten most frequent cancers in Malaysia. A common polymorphism at codon 72 of the p53 tumor suppressor gene and its influence on cancer risk has been studied for different types of cancer with mixed and inconsistent results with limited published data on the Malaysian population so far. In the present study, the frequency of p53 codon 72 polymorphism in 60 patients with NMSC was investigated from archival formalin-fixed paraffin-embedded (FFPE) tissue obtained from Hospital Universiti Kebangsaan Malaysia (HUKM). Additionally, random amplified polymorhic DNA -polymorphic chain reaction (RAPD-PCR) was employed for preliminary biomarker development. NMSC FFPE samples (70%) possess Arg/Arg, 20% with Pro/Pro and 10% with Arg/Pro. In total, there was no significant difference in the p53 codon 72 genotypes between histological types of NMSC, gender, race, tumor location and age group. However, there was an apparent age-associated increase in the Arg/Arg genotype but did not reach statistical significance (P=0.235). NMSC types and demographic characteristics did not influence genotype distribution. On the other hand, BCC and SCC distributions are influenced by age group, race and tumor location.
    Matched MeSH terms: Genetic Predisposition to Disease
  5. Gene, ethnic and gender influences predisposition of adverse drug reactions to artesunate among Malaysians
    Yusof W, Hua GS
    Toxicol. Mech. Methods, 2012 Apr;22(3):184-92.
    PMID: 22003869 DOI: 10.3109/15376516.2011.623331
    Artesunate (AS) and amodiaquine (AQ) are two prodrugs widely used as antimalarial agents and are metabolized by the CYP P450 2A6 (CYP 2A6) and CYP P450 2C8 (CYP 2C8) enzymes, respectively.
    Matched MeSH terms: Genetic Predisposition to Disease
  6. Association of hepatocyte nuclear factor 4 alpha polymorphisms with type 2 diabetes with or without metabolic syndrome in Malaysia
    Saif-Ali R, Harun R, Kamaruddin NA, Al-Jassabi S, Ngah WZ
    Biochem Genet, 2012 Apr;50(3-4):298-308.
    PMID: 21983932 DOI: 10.1007/s10528-011-9472-2
    This study investigated the association of hepatocyte nuclear factor 4 (HNF4) alpha single nucleotide polymorphisms (SNPs) with type 2 diabetes with or without metabolic syndrome in Malaysia. Nine HNF4 alpha SNPs were genotyped in 390 type 2 diabetic subjects with metabolic syndrome, 135 type 2 diabetic subjects without metabolic syndrome, and 160 control subjects. The SNPs rs4810424, rs1884613, and rs2144908 were associated with protection against type 2 diabetes without metabolic syndrome (recessive P = 0.018, OR 0.32; P = 0.004, OR 0.25; P = 0.005, OR 0.24, respectively). The 6-SNP haplotype2 CCCGTC containing the risk genotype of these SNPs was associated with higher risk for type 2 diabetes with or without metabolic syndrome (P = 0.002, OR 2.2; P = 0.004, OR 3.1). These data suggest that HNF4 alpha SNPs and haplotypes contributed to increased type 2 diabetes risk in the Malaysian population.
    Matched MeSH terms: Genetic Predisposition to Disease
  7. Fulltext Keloid scarring: understanding the genetic basis, advances, and prospects
    Halim AS, Emami A, Salahshourifar I, Kannan TP
    Arch Plast Surg, 2012 May;39(3):184-9.
    PMID: 22783524 DOI: 10.5999/aps.2012.39.3.184
    Keloid disease is a fibroproliferative dermal tumor with an unknown etiology that occurs after a skin injury in genetically susceptible individuals. Increased familial aggregation, a higher prevalence in certain races, parallelism in identical twins, and alteration in gene expression all favor a remarkable genetic contribution to keloid pathology. It seems that the environment triggers the disease in genetically susceptible individuals. Several genes have been implicated in the etiology of keloid disease, but no single gene mutation has thus far been found to be responsible. Therefore, a combination of methods such as association, gene-gene interaction, epigenetics, linkage, gene expression, and protein analysis should be applied to determine keloid etiology.
    Matched MeSH terms: Genetic Predisposition to Disease
  8. Fulltext A pilot study on cytotoxic T lymphocyte-4 gene polymorphisms in urinary schistosomiasis
    Idris ZM, Yazdanbakhsh M, Adegnika AA, Lell B, Issifou S, Noordin R
    Genet Test Mol Biomarkers, 2012 Jun;16(6):488-92.
    PMID: 22288822 DOI: 10.1089/gtmb.2011.0209
    Urinary schistosomiasis is caused by the digenetic trematode Schistosoma haematobium, characterized by accumulation of eggs in the genitourinary tract. Cytotoxic T-lymphocyte antigen 4 (CTLA-4) can play an important role in parasitic infection due to its major role as a negative regulator of T-cell activation and proliferation. This study was performed in patients with schistosomiasis and healthy controls to analyze the allele and genotype frequencies of four CTLA-4 gene polymorphisms. The CTLA-4 gene was amplified using Taqman real-time polymerase chain reaction, and allele and genotypes of 49 patients with schistosomiasis were analyzed using allelic discrimination analysis followed by subsequent direct sequencing. The results were compared with healthy control subjects. The frequencies of CTLA-4 rs733618 A allele at position -1722 (p=0.001), rs11571316 C allele at position -1577 (p<0.001), and rs231775 A allele at position +49 (p=0.002) in the patient group were significantly higher than the control group. The rs733618 AA genotype (p=0.001), rs11571316 CC genotype (p<0.001), and rs231775 AA genotype (p=0.007) were also significantly overrepresented. Meanwhile, rs733618 AG genotype (p=0.001), rs11571316 CT genotype (p=0.02), and rs231775 GG genotype (p=0.029) were significantly decreased in the patients with schistosomiasis, as compared with the controls. No significant difference was observed in both allele and genotype of rs16841252. The results of this study suggest that the rs733618, rs11571316, and rs231775 polymorphisms in the CTLA-4 gene may influence susceptibility to schistosomiasis infection in the Gabonese children.
    Matched MeSH terms: Genetic Predisposition to Disease*
  9. Genetics of inflammatory bowel disease in Asia: systematic review and meta-analysis
    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*
  10. Fulltext Risk modification of colorectal cancer susceptibility by interleukin-8 -251T>A polymorphism in Malaysians
    Mustapha MA, Shahpudin SN, Aziz AA, Ankathil R
    World J Gastroenterol, 2012 Jun 7;18(21):2668-73.
    PMID: 22690076 DOI: 10.3748/wjg.v18.i21.2668
    To investigate the allele and genotype frequencies and associated risk of interleukin (IL)-8 -251T>A polymorphism on colorectal cancer (CRC) susceptibility risk.
    Matched MeSH terms: Genetic Predisposition to Disease
  11. A novel pathogenic variant of the LDLR gene in the Asian population and its clinical correlation with familial hypercholesterolemia
    Chahil JK, Lye SH, Bagali PG, Alex L
    Mol Biol Rep, 2012 Jul;39(7):7831-8.
    PMID: 22544571 DOI: 10.1007/s11033-012-1626-8
    Familial hypercholesterolemia (FH) is a disease implicated with defects in either, Low density lipoprotein receptor gene (LDLR), Apolipoprotein B-100 gene (APOB), the Proprotein convertase subtilisin/kexin type 9 gene (PCSK9) or other related genes of the lipid metabolism pathway. The general characterization of heterozygous FH is by elevated low-density lipoprotein (LDL) cholesterol and early-onset cardiovascular diseases, while the more severe type, the homozygous FH results in extreme elevated levels of LDL cholesterol and usually death of an affected individual by early twenties. We present here a novel non-synonymous, missense mutation in exon 14 of the LDLR gene in two siblings of the Malay ethnicity discovered during an in-house genetic test. We postulate that their elevated cholesterol is due to this novel mutation and they are positive for homozygous FH. This is the first report of a C711Y mutation in patients with elevated cholesterol in Asia.
    Matched MeSH terms: Genetic Predisposition to Disease*
  12. Fulltext A multi-ethnic study of a PNPLA3 gene variant and its association with disease severity in non-alcoholic fatty liver disease
    Zain SM, Mohamed R, Mahadeva S, Cheah PL, Rampal S, Basu RC, et al.
    Hum Genet, 2012 Jul;131(7):1145-52.
    PMID: 22258181 DOI: 10.1007/s00439-012-1141-y
    The adiponutrin (PNPLA3) rs738409 polymorphism has been found to be associated with susceptibility to non-alcoholic fatty liver disease (NAFLD) in various cohorts. We further investigated the association of this polymorphism with non-alcoholic steatohepatitis (NASH) severity and with histological features of NAFLD. A total of 144 biopsy-proven NAFLD patients and 198 controls were genotyped for PNPLA3 gene polymorphism (rs738409 C>G). The biopsy specimens were histologically graded by a qualified pathologist. We observed an association of G allele with susceptibility to NAFLD in the pooled subjects (OR 2.34, 95% CI 1.69-3.24, p < 0.0001), and following stratification, in each of the three ethnic subgroups, namely Chinese, Indian and Malay (OR 1.94, 95% CI 1.12-3.37, p = 0.018; OR 3.51, 95% CI 1.69-7.26, p = 0.001 and OR 2.05, 95% CI 1.25-3.35, p = 0.005, respectively). The G allele is associated with susceptibility to NASH (OR 2.64, 95% CI 1.85-3.75, p < 0.0001), with NASH severity (OR 1.85, 95% CI 1.05-3.26, p = 0.035) and with presence of fibrosis (OR 1.95, 95% CI 1.17-3.26, p = 0.013) but not with simple steatosis nor with other histological parameters. Although the serum triglyceride level is significantly higher in NAFLD patients compared to controls, the G allele is associated with decreased level of triglycerides (p = 0.029) in the NAFLD patients. Overall, the rs738409 G allele is associated with severity of NASH and occurrence of fibrosis in patients with NAFLD.
    Matched MeSH terms: Genetic Predisposition to Disease
  13. Central and peripheral blood pressure profile of young offspring with hypertensive and normotensive parents
    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*
  14. Association between inflammatory bowel disease gene 5 (IBD5) and interleukin-23 receptor (IL23R) genetic polymorphisms in Malaysian patients with Crohn's disease
    Chua KH, Hilmi I, Lian LH, Patmanathan SN, Hoe SZ, Lee WS, et al.
    J Dig Dis, 2012 Sep;13(9):459-65.
    PMID: 22908971 DOI: 10.1111/j.1751-2980.2012.00617.x
    This study was aimed to investigate the possible association of Crohn's disease (CD) with inflammatory bowel disease gene 5 (IBD5) IGR2198a_1 (rs11739135), IGR2096a_1 (rs12521868) and interleukin-23 receptor (IL23R) genetic variant (rs1004819) in the Malaysian population.
    Matched MeSH terms: Genetic Predisposition to Disease
  15. Association of TGFβ1 and SMAD4 variants in the etiology of keloid scar in the Malay population
    Emami A, Halim AS, Salahshourifar I, Yussof SJ, Khoo TL, Kannan TP
    Arch. Dermatol. Res., 2012 Sep;304(7):541-7.
    PMID: 22805880 DOI: 10.1007/s00403-012-1262-0
    Keloid is a complex condition with environmental and genetic risk-contributing factors. Two candidate genes, TGFβ1 and SMAD4, located in the same signaling pathway are highly expressed in the keloid fibroblast cells. In a case-control design, TGFβ1 haplotypes showed association with the risk of keloid in the present study. The CC haplotype, composed of both c.29C>T and -509T>C variants, was observed more frequently among cases (Corrected p = 0.037, OR = 2.07, 95 % CI = 0.87-4.93), showing a 4.5-fold increased risk for keloid. The AG genotype of the SMAD4 c.5131A>G variant showed a trend of significance (p = 0.0573, OR = 1.75, 95 % CI = 0.99-3.13). Taken together, either of these variants is most probably causative at the expression level or is in linkage disequilibrium with other causative variants in a complex pattern together with the environmental factors that contribute to the condition. To the best of our knowledge, there is only one documented report on a relationship between TGFβ1 and keloid with no association within the Caucasian population, while there have not been any reports for SMAD4. Therefore, the present study is likely the first research showing a significant association between TGFβ1 variants and keloids in the Malay population.
    Matched MeSH terms: Genetic Predisposition to Disease
  16. Identification of a functional variant in SPLUNC1 associated with nasopharyngeal carcinoma susceptibility among Malaysian Chinese
    Yew PY, Mushiroda T, Kiyotani K, Govindasamy GK, Yap LF, Teo SH, et al.
    Mol Carcinog, 2012 Oct;51 Suppl 1:E74-82.
    PMID: 22213098 DOI: 10.1002/mc.21857
    Nasopharyngeal carcinoma (NPC) is a multifactorial and polygenic disease with high incidence in Asian countries. Epstein-Barr virus infection, environmental and genetic factors are believed to be involved in the tumorigenesis of NPC. The association of single nucleotide polymorphisms (SNPs) in LPLUNC1 and SPLUNC1 genes with NPC was investigated by performing a two-stage case control association study in a Malaysian Chinese population. The initial screening consisted of 81 NPC patients and 147 healthy controls while the replication study consisted of 366 NPC patients and 340 healthy controls. The combined analysis showed that a SNP (rs2752903) of SPLUNC1 was significantly associated with the risk of NPC (combined P = 0.00032, odds ratio = 1.62, 95% confidence interval = 1.25-2.11). In the subsequent dense fine mapping of SPLUNC1 locus, 36 SNPs in strong linkage disequilibrium with rs2752903 (r(2) ≥ 0.85) were associated with NPC susceptibility. Screening of these variants by electrophoretic mobility shift and luciferase reporter assays showed that rs1407019 located in intron 3 (r(2)  = 0.994 with rs2752903) caused allelic difference in the binding of specificity protein 1 (Sp1) transcription factor and affected luciferase activity. This SNP may consequently alter the expression of SPLUNC1 in the epithelial cells. In summary, our study suggested that rs1407019 in intronic enhancer of SPLUNC1 is associated with NPC susceptibility in which its A allele confers an increased risk of NPC in the Malaysian Chinese population.
    Matched MeSH terms: Genetic Predisposition to Disease
  17. Fulltext Genome-wide association analyses identify three new susceptibility loci for primary angle closure glaucoma
    Vithana EN, Khor CC, Qiao C, Nongpiur ME, George R, Chen LJ, et al.
    Nat Genet, 2012 Oct;44(10):1142-1146.
    PMID: 22922875 DOI: 10.1038/ng.2390
    Primary angle closure glaucoma (PACG) is a major cause of blindness worldwide. We conducted a genome-wide association study including 1,854 PACG cases and 9,608 controls across 5 sample collections in Asia. Replication experiments were conducted in 1,917 PACG cases and 8,943 controls collected from a further 6 sample collections. We report significant associations at three new loci: rs11024102 in PLEKHA7 (per-allele odds ratio (OR)=1.22; P=5.33×10(-12)), rs3753841 in COL11A1 (per-allele OR=1.20; P=9.22×10(-10)) and rs1015213 located between PCMTD1 and ST18 on chromosome 8q (per-allele OR=1.50; P=3.29×10(-9)). Our findings, accumulated across these independent worldwide collections, suggest possible mechanisms explaining the pathogenesis of PACG.
    Matched MeSH terms: Genetic Predisposition to Disease*
  18. Complement components 2 and 7 (C2 and C7) gene polymorphisms are not major risk factors for SLE susceptibility in the Malaysian population
    Lian LH, Ching AS, Chong ZY, Chua KH
    Rheumatol Int, 2012 Nov;32(11):3665-8.
    PMID: 21881993 DOI: 10.1007/s00296-011-2070-0
    There have been numerous studies linking complement components and the pathogenesis of systemic lupus erythematosus (SLE). This is due to their numerous roles in modulating immune responses in the human body. This study examined the association of C2 and C7 genetic polymorphisms with the susceptibility to SLE based on two separate cohorts of patient and control samples from Malaysia. The 28-bp deletion in the C2 exon-intron junction and single nucleotide polymorphism in the 3'untranslated region in the C7 genes were detected based on direct polymerase chain reaction (PCR) and PCR-restriction fragment length polymorphism, respectively. A total of 150 patient and 150 healthy control samples were screened, but there was no association detected between either genes. All individuals presented with null deletion in C2 genes, while the C allele and CC genotypes were most commonly scored. These overall results suggest a lack of strong association with the C2 and C7 gene polymorphisms to the susceptibility of SLE in the Malaysian population.
    Matched MeSH terms: Genetic Predisposition to Disease*
  19. Genetic association of SNPs in the FTO gene and predisposition to obesity in Malaysian Malays
    Apalasamy YD, Ming MF, Rampal S, Bulgiba A, Mohamed Z
    Braz. J. Med. Biol. Res., 2012 Dec;45(12):1119-26.
    PMID: 22911346
    The common variants in the fat mass- and obesity-associated (FTO) gene have been previously found to be associated with obesity in various adult populations. The objective of the present study was to investigate whether the single nucleotide polymorphisms (SNPs) and linkage disequilibrium (LD) blocks in various regions of the FTO gene are associated with predisposition to obesity in Malaysian Malays. Thirty-one FTO SNPs were genotyped in 587 (158 obese and 429 non-obese) Malaysian Malay subjects. Obesity traits and lipid profiles were measured and single-marker association testing, LD testing, and haplotype association analysis were performed. LD analysis of the FTO SNPs revealed the presence of 57 regions with complete LD (D' = 1.0). In addition, we detected the association of rs17817288 with low-density lipoprotein cholesterol. The FTO gene may therefore be involved in lipid metabolism in Malaysian Malays. Two haplotype blocks were present in this region of the FTO gene, but no particular haplotype was found to be significantly associated with an increased risk of obesity in Malaysian Malays.
    Matched MeSH terms: Genetic Predisposition to Disease/genetics*
  20. Fulltext BDNF and DARPP-32 genes are not risk factors for schizophrenia in the Malay population
    Loh HC, Tang PY, Tee SF, Chow TJ, Cheah YC, Singh SS
    Genet. Mol. Res., 2012;11(1):725-30.
    PMID: 22576830 DOI: 10.4238/2012.March.22.2
    A number of studies have pointed to the association of BDNF (brain-derived neurotrophic factor) and DARPP-32 (dopamine- and cAMP-regulated phosphoprotein, 32 kDa) with schizophrenia. The purpose of this study was to determine whether these two genes are involved in the pathogenesis of schizophrenia in the Malay population. Two single nucleotide polymorphisms Val66Met of BDNF, -2036C>G and g.1238delG of DARPP-32 were genotyped in the Malay population in 200 patients with schizophrenia and 256 healthy controls. Analysis of allele and genotype frequencies in these two groups revealed no significant association of BDNF or DARPP-32 polymorphisms with schizophrenia in Malays. This is the first such association study in the Malay population.
    Matched MeSH terms: Genetic Predisposition to Disease
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