Displaying publications 81 - 100 of 503 in total

Abstract:
Sort:
  1. Wyszynski A, Hong CC, Lam K, Michailidou K, Lytle C, Yao S, et al.
    Hum Mol Genet, 2016 Sep 01;25(17):3863-3876.
    PMID: 27402876 DOI: 10.1093/hmg/ddw223
    Breast cancer is the most diagnosed malignancy and the second leading cause of cancer mortality in females. Previous association studies have identified variants on 2q35 associated with the risk of breast cancer. To identify functional susceptibility loci for breast cancer, we interrogated the 2q35 gene desert for chromatin architecture and functional variation correlated with gene expression. We report a novel intergenic breast cancer risk locus containing an enhancer copy number variation (enCNV; deletion) located approximately 400Kb upstream to IGFBP5, which overlaps an intergenic ERα-bound enhancer that loops to the IGFBP5 promoter. The enCNV is correlated with modified ERα binding and monoallelic-repression of IGFBP5 following oestrogen treatment. We investigated the association of enCNV genotype with breast cancer in 1,182 cases and 1,362 controls, and replicate our findings in an independent set of 62,533 cases and 60,966 controls from 41 case control studies and 11 GWAS. We report a dose-dependent inverse association of 2q35 enCNV genotype (percopy OR = 0.68 95%CI 0.55-0.83, P = 0.0002; replication OR = 0.77 95% CI 0.73-0.82, P = 2.1 × 10-19) and identify 13 additional linked variants (r2 > 0.8) in the 20Kb linkage block containing the enCNV (P = 3.2 × 10-15 - 5.6 × 10-17). These associations were independent of previously reported 2q35 variants, rs13387042/rs4442975 and rs16857609, and were stronger for ER-positive than ER-negative disease. Together, these results suggest that 2q35 breast cancer risk loci may be mediating their effect through IGFBP5.
    Matched MeSH terms: Genetic Predisposition to Disease
  2. Nimptsch K, Song M, Aleksandrova K, Katsoulis M, Freisling H, Jenab M, et al.
    Eur J Epidemiol, 2017 May;32(5):419-430.
    PMID: 28550647 DOI: 10.1007/s10654-017-0262-y
    Higher levels of circulating adiponectin have been related to lower risk of colorectal cancer in several prospective cohort studies, but it remains unclear whether this association may be causal. We aimed to improve causal inference in a Mendelian Randomization meta-analysis using nested case-control studies of the European Prospective Investigation into Cancer and Nutrition (EPIC, 623 cases, 623 matched controls), the Health Professionals Follow-up Study (HPFS, 231 cases, 230 controls) and the Nurses' Health Study (NHS, 399 cases, 774 controls) with available data on pre-diagnostic adiponectin concentrations and selected single nucleotide polymorphisms in the ADIPOQ gene. We created an ADIPOQ allele score that explained approximately 3% of the interindividual variation in adiponectin concentrations. The ADIPOQ allele score was not associated with risk of colorectal cancer in logistic regression analyses (pooled OR per score-unit unit 0.97, 95% CI 0.91, 1.04). Genetically determined twofold higher adiponectin was not significantly associated with risk of colorectal cancer using the ADIPOQ allele score as instrumental variable (pooled OR 0.73, 95% CI 0.40, 1.34). In a summary instrumental variable analysis (based on previously published data) with higher statistical power, no association between genetically determined twofold higher adiponectin and risk of colorectal cancer was observed (0.99, 95% CI 0.93, 1.06 in women and 0.94, 95% CI 0.88, 1.01 in men). Thus, our study does not support a causal effect of circulating adiponectin on colorectal cancer risk. Due to the limited genetic determination of adiponectin, larger Mendelian Randomization studies are necessary to clarify whether adiponectin is causally related to lower risk of colorectal cancer.
    Matched MeSH terms: Genetic Predisposition to Disease
  3. Rajasuriar R, Kong YY, Nadarajah R, Abdullah NK, Spelman T, Yuhana MY, et al.
    J Transl Med, 2015;13:30.
    PMID: 25622527 DOI: 10.1186/s12967-015-0391-6
    HIV-infected individuals have an increased risk of cardiovascular disease (CVD). T-allele carriers of the CD14 C-260T single-nucleotide polymorphism (SNP) have reported increased expression of the LPS-binding receptor, CD14 and inflammation in the general population. Our aim was to explore the relationship of this SNP with monocyte/macrophage activation and inflammation and its association with sub-clinical atherosclerosis in HIV-infected individuals.
    Matched MeSH terms: Genetic Predisposition to Disease
  4. Liew SC, Gupta ED
    Eur J Med Genet, 2015 Jan;58(1):1-10.
    PMID: 25449138 DOI: 10.1016/j.ejmg.2014.10.004
    The Methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism is associated with various diseases (vascular, cancers, neurology, diabetes, psoriasis, etc) with the epidemiology of the polymorphism of the C677T that varies dependent on the geography and ethnicity. The 5,10-Methylenetetrahydrofolate reductase (MTHFR) locus is mapped on chromosome 1 at the end of the short arm (1p36.6). This enzyme is important for the folate metabolism which is an integral process for cell metabolism in the DNA, RNA and protein methylation. The mutation of the MTHFR gene which causes the C677T polymorphism is located at exon 4 which results in the conversion of valine to alanine at codon 222, a common polymorphism that reduces the activity of this enzyme. The homozygous mutated subjects have higher homocysteine levels while the heterozygous mutated subjects have mildly raised homocysteine levels compared with the normal, non-mutated controls. Hyperhomocysteinemia is an emerging risk factor for various cardiovascular diseases and with the increasing significance of this polymorphism in view of the morbidity and mortality impact on the patients, further prevention strategies and nutritional recommendations with the supplementation of vitamin B12 and folic acid which reduces plasma homocysteine level would be necessary as part of future health education. This literature review therefore focuses on the recent evidence-based reports on the associations of the MTHFR C677T polymorphism and the various diseases globally.
    Matched MeSH terms: Genetic Predisposition to Disease
  5. Numata S, Teye K, Krol RP, Karashima T, Fukuda S, Matsuda M, et al.
    J. Dermatol. Sci., 2015 Apr;78(1):82-5.
    PMID: 25766764 DOI: 10.1016/j.jdermsci.2015.02.006
    Matched MeSH terms: Genetic Predisposition to Disease
  6. Chai HC, Chua KH, Lim SK, Phipps ME
    J Immunol Res, 2014;2014:529167.
    PMID: 24741605 DOI: 10.1155/2014/529167
    Polymorphisms in genes involved in toll-like receptor/interferon signalling pathways have been reported previously to be associated with SLE in many populations. This study aimed to investigate the role of seven single nucleotide polymorphisms within TNFAIP3, STAT4, and IRF5, which are involved in upstream and downstream pathways of type I interferon production, in SLE in the South East Asian populations. Genotyping of 360 Malaysian SLE patients and 430 normal healthy individuals revealed that minor alleles of STAT4 rs7574865 and rs10168266 were associated with elevated risk of SLE in the Chinese and Malay patients, respectively (P = 0.028, odds ratio (OR) = 1.42; P = 0.035, OR = 1.80, respectively). Polymorphisms in TNFAIP3 and IRF5 did not show significant associations with SLE in any of the ethnicities. Combined analysis of the Malays, Chinese, and Indians for each SNP indicated that STAT4 rs10168266 was significantly associated with the Malaysian SLE as a whole (P = 0.014; OR = 1.435). The meta-analysis of STAT4 rs10168266, which combined the data of other studies and this study, further confirmed its importance as the risk factor for SLE by having pooled OR of 1.559 and P value of <0.001.
    Study site: University of Malaya Medical Centre (UMMC), Kuala Lumpur, Malaysia
    Matched MeSH terms: Genetic Predisposition to Disease
  7. Xin Y, Hao S, Lu J, Wang Q, Zhang L
    PLoS One, 2014;9(4):e95966.
    PMID: 24763305 DOI: 10.1371/journal.pone.0095966
    To comprehensively evaluate the association of ERCC1 C8092A and ERCC2 Lys751Gln polymorphisms with the risk of glioma.
    Matched MeSH terms: Genetic Predisposition to Disease
  8. Lau TP, Roslani AC, Lian LH, Lee PC, Hilmi I, Goh KL, et al.
    Genet. Mol. Res., 2014;13(3):7079-85.
    PMID: 24682985 DOI: 10.4238/2014.March.19.3
    Colorectal cancer (CRC) is one of the most common types of cancer in both developed and developing countries. This disease is triggered by and progresses via the sequential accumulation of multiple genetic alterations. In addition, the interaction between low-penetrance genes and environmental factors can also increase the risk of developing CRC. Since inflammatory bowel diseases (IBDs) are one of the predisposing factors for CRC, IBD-related genes might, to a certain extent, be associated with cancer initiation. The nucleotide oligomerization domain 2/caspase activating recruitment domain 15 gene (NOD2/CARD15) is the most well-established gene to be associated with increased susceptibility to Crohn's disease. Thus, various studies have been performed to investigate the potential contribution of this gene to CRC risk. In this study, we aimed to determine the frequency of the Arg702Trp, Gly908Arg, 3020insC, Pro268Ser, and JW1 variants of NOD2/CARD15, and to investigate their association with CRC susceptibility. A total of 130 CRC patients and 212 healthy controls were recruited for this study. Subsequently, real-time polymerase chain reaction with TaqMan was performed for the genotyping of these NOD2/ CARD15 variants. None of the NOD2/CARD15 variants was statistically associated to CRC susceptibility in our Malaysian population. Our findings were remarkably similar to those of other Asian cohorts, which indicated that these NOD2/CARD15 variants exhibit genetic heterogeneity between Caucasian and Asian populations.
    Matched MeSH terms: Genetic Predisposition to Disease
  9. Munretnam K, Alex L, Ramzi NH, Chahil JK, Kavitha IS, Hashim NA, et al.
    Mol Biol Rep, 2014;41(4):2501-8.
    PMID: 24443231 DOI: 10.1007/s11033-014-3107-8
    There is growing global interest to stratify men into different levels of risk to developing prostate cancer, thus it is important to identify common genetic variants that confer the risk. Although many studies have identified more than a dozen common genetic variants which are highly associated with prostate cancer, none have been done in Malaysian population. To determine the association of such variants in Malaysian men with prostate cancer, we evaluated a panel of 768 SNPs found previously associated with various cancers which also included the prostate specific SNPs in a population based case control study (51 case subjects with prostate cancer and 51 control subjects) in Malaysian men of Malay, Chinese and Indian ethnicity. We identified 21 SNPs significantly associated with prostate cancer. Among these, 12 SNPs were strongly associated with increased risk of prostate cancer while remaining nine SNPs were associated with reduced risk. However, data analysis based on ethnic stratification led to only five SNPs in Malays and 3 SNPs in Chinese which remained significant. This could be due to small sample size in each ethnic group. Significant non-genetic risk factors were also identified for their association with prostate cancer. Our study is the first to investigate the involvement of multiple variants towards susceptibility for PC in Malaysian men using genotyping approach. Identified SNPs and non-genetic risk factors have a significant association with prostate cancer.
    Matched MeSH terms: Genetic Predisposition to Disease
  10. Nazree NE, Loke AC, Zainal NZ, Mohamed Z
    Asia Pac Psychiatry, 2015 Mar;7(1):72-7.
    PMID: 24376086 DOI: 10.1111/appy.12118
    Numerous association studies of candidate genes studies with major depressive disorder (MDD) have been conducted for many years; however, the evidence of association between genes and the risk of developing MDD still remains inconclusive. In this study, we aimed to investigate the association between the tryptophan hydroxylase 2 (TPH2) gene and MDD in three ethnic groups (Malay, Chinese and Indian) within the Malaysian population.
    Matched MeSH terms: Genetic Predisposition to Disease
  11. Haerian BS
    Pharmacogenomics, 2013 Dec;14(16):2055-65.
    PMID: 24279859 DOI: 10.2217/pgs.13.217
    A majority of studies have shown a link between the common functional rs6265 polymorphism of the BDNF gene and susceptibility to drug dependence. However, the pattern of results is inconsistent. To precisely evaluate this association, a systematic review and meta-analysis of previous case-control reports was conducted. Data from 20 studies containing 9419 participants (4665 cases and 4754 controls) conducted between 2004 and 2013 restricted to alcohol, nicotine, heroin, substance and methamphetamine dependency were meta-analyzed. Following quality control of the results, a significant association between C allele and methamphetamine dependence remained in south Asian subjects (p = 0.004). Similar results were detected in south Asian subjects for methamphetamine dependence and in Chinese subjects for heroin dependence under an autosomal codominant genotype model (TT vs CC, p = 0.005 and p = 0.0004, respectively). In conclusion, the rs6265 polymorphism may be a risk factor for methamphetamine dependence in south Asian subjects or for heroin dependence in Chinese subjects.
    Matched MeSH terms: Genetic Predisposition to Disease
  12. Subenthiran S, Abdullah NR, Joseph JP, Muniandy PK, Mok BT, Kee CC, et al.
    PLoS One, 2013;8(5):e64827.
    PMID: 23717663 DOI: 10.1371/journal.pone.0064827
    Carbamazepine (CBZ) is used as the first line of treatment of Complex Partial Seizures (CPS) in the Epilepsy Clinic, Neurology Department of Kuala Lumpur Hospital (KLH). More than 30% of the patients remain drug resistant to CBZ mono-therapy. CBZ is transported by the P-glycoprotein (P-gp). The P-gp encoded by the ABCB1 and ABCC2 genes are expressed in drug resistant patients with epilepsy. A few studies have shown significant association between CBZ resistant epilepsy and Linkage Disequilibrium (LD) with adjacent polymorphisms of these genes. Our study is aimed at determining the correlation between patients' response to CBZ mono-therapy to Single Nucleotide Polymorphisms G2677T and C3435T of the ABCB1 gene as well as G1249A and -24C>T of the ABCC2 gene.
    Matched MeSH terms: Genetic Predisposition to Disease
  13. Nizam ZM, Abdul Aziz AA, Kaur G, Abu Hassan MR, Mohd Sidek AS, Yeh LY, et al.
    Asian Pac J Cancer Prev, 2013;14(2):619-24.
    PMID: 23621208
    BACKGROUND: Colorectal cancer (CRC) exists in a more common sporadic form and less common hereditary forms, associated with the Lynch syndrome, familial adenomatous polyposis (FAP) and other rare syndromes. Sporadic CRC is believed to arise as a result of close interaction between environmental factors, including dietary and lifestyle habits, and genetic predisposition factors. In contrast, hereditary forms such as those related to the Lynch syndrome result from inheritance of germline mutations of mismatch repair (MMR) genes. However, in certain cases, the influence of low penetrance alleles in familial colorectal cancer susceptibility is also undeniable.

    AIM: To investigate the genotype frequencies of MLH1 promoter polymorphism -93G>A and to determine whether it could play any role in modulating familial and sporadic CRC susceptibility risk.

    METHODS: A case-control study comprising of 104 histopathologically confirmed CRC patients as cases (52 sporadic CRC and 52 Lynch syndrome patients) and 104 normal healthy individuals as controls was undertaken. DNA was extracted from peripheral blood and the polymorphism was genotyped employing PCR-RFLP methods. The genotypes were categorized into homozygous wild type, heterozygous and homozygous variants. The risk association between these polymorphisms and CRC susceptibility risk was calculated using binary logistic regression analysis and deriving odds ratios (ORs).

    RESULTS: When risk association was investigated for all CRC patients as a single group, the heterozygous (G/A) genotype showed a significantly higher risk for CRC susceptibility with an OR of 2.273, (95%CI: 1.133-4.558 and p-value=0.021). When analyzed specifically for the 2 types of CRC, the heterozygous (G/A) genotype showed significantly higher risk for sporadic CRC susceptibility with and OR of 3.714, (95%CI: 1.416-9.740 and p-value=0.008). Despite high OR value was observed for Lynch syndrome (OR: 1.600, 95%CI: 0.715-3.581), the risk was not statistically significant (P=0.253).

    CONCLUSION: Our results suggest an influence of MLH1 promoter polymorphism -93G>A in modulating susceptibility risk in Malaysian CRC patients, especially those with sporadic disease.

    Matched MeSH terms: Genetic Predisposition to Disease
  14. 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
  15. 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
  16. Chang CC, Too CL, Murad S, Hussein SH
    Int J Dermatol, 2011 Feb;50(2):221-4.
    PMID: 21244392 DOI: 10.1111/j.1365-4632.2010.04745.x
    BACKGROUND: Carbamazepine (CBZ), a frequently used anticonvulsant drug, is one of the most common causes of life-threatening cutaneous adverse drug reactions such as toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome (SJS). Recent studies have revealed a strong association between HLA-B*1502 and CBZ-induced TEN/SJS in the Taiwan Han Chinese population.
    OBJECTIVES: This study is aimed to investigate the association between human leucocyte antigens (HLA) and CBZ-induced TEN/SJS in the multi-ethnic Malaysian population.
    METHODS: A sample of 21 unrelated patients with CBZ-induced TEN/SJS and 300 race-matched, healthy controls were genotyped for HLA-A, -B and -DR using polymerase chain reaction (PCR). Allele frequencies were compared.
    RESULTS: HLA-B*1502 was present in 75.0% (12/16) of Malay patients with CBZ-induced TEN/SJS but in only 15.7% (47/300) of normal controls (odds ratio 16.15, 95% confidence interval 4.57-62.4; corrected P-value  = 7.87 × 10(-6) ), which suggests a strong association between HLA and CBZ-induced TEN/SJS. Additionally, HLA-B*1502 was found in all three Chinese and two Indian patients. Existing data show that frequencies of the HLA-B*1502 allele are generally much higher in Asian populations than in White European populations, which explains the higher incidences of SJS and TEN in Asian countries.
    CONCLUSIONS: HLA-B*1502 is strongly associated with CBZ-induced TEN/SJS in the Malay population in Malaysia, as has been seen in Han Chinese in Taiwan. This indicates that the genetic association apparent in the incidence of CBZ-induced TEN/SJS is linked with the presence of HLA-B*1502, irrespective of racial origin. Screening of patients for this genetic marker can help to prevent the occurrence of TEN/SJS.
    Matched MeSH terms: Genetic Predisposition to Disease
  17. Hamid S, Yang YH, Peng KN, Ismail SM, Zain RB, Lim KP, et al.
    Oral Oncol, 2009 Jun;45(6):496-500.
    PMID: 18804411 DOI: 10.1016/j.oraloncology.2008.06.003
    The MDM2 SNP309 has been associated with increased expression of the protein which could suppress p53 function, and has been shown to modulate risk to cancer. We have previously shown that overexpression of MDM2 is a common event in oral cancers. In the present study, we determined the association between the MDM2 SNP309 polymorphism and oral cancer in 207 oral cancer patients and 116 normal subjects. We genotyped the MDM2 SNP309 by PCR-RFLP. Logistic regression was adapted to calculate odds ratios for MDM2 SNP309 polymorphism from univariate and multivariable adjusted models. Our results suggest that MDM2 SNP309 does not confer increased risk to oral cancer (OR=1.55, 95% CI=0.77-3.11). However, the GG/TG genotype was associated with later disease onset in women above 55 years of age. Collectively, our data suggests that MDM2 SNP309 may modulate the risk to oral cancer and is a modifier of the age at oral cancer onset in women above the age of 55 years.
    Matched MeSH terms: Genetic Predisposition to Disease
  18. Subahir MN, Shah SA, Zainuddin ZM
    Asian Pac J Cancer Prev, 2009;10(6):1015-20.
    PMID: 20192575
    INTRODUCTION: In Malaysia, prostate cancer is ranked 6th among male cancer and expected to increase in the future. Several factors have shown to be related to prostate cancer such as sociodemographic, lifestyle, diet, occupational exposure, medical and health status. This is the first time a similar study was conducted in Malaysia to recognize the risk factors for prostate cancer patients who came for treatment at University Kebangsaan Malaysia Medical Centre (UKMMC).

    METHODS: Prostate cancer cases diagnosed between 2003 and 2008 which met with the inclusion criteria were included in the study. One hundred and twelfth (112) pairs of cases and controls matched by age and ethnicity were analysed. McNemar Odds Ratios (OR(M)) were calculated using McNemar Calculator software for univariate analysis while conditional logistic regression was used for multivariate analysis, both using SPSS version 12.0.

    RESULTS: Most of the prostate cancer patients (68.8%) that came for treatment in UKMMC were above 70 years old. The majority were Chinese (50.0%) followed by Malay (46.4%) and Indian (3.6%). Multivariate analysis showed cases were more likely to have a first-degree relative with a history of cancer (OR= 3.77, 95% CI= 1.19-11.85), to have been exposed to pesticides (OR= 5.57, 95% CI= 1.75-17.78) and consumed more meat (OR= 12.23, 95% CI= 3.89-39.01). Significantly reduced risks of prostate cancer were noted among those consuming more vegetables (OR= 0.12, 95% CI= 0.02-0.84), more tomatoes (OR= 0.35, 95% CI= 0.13-0.93) and those who had frequent sexual intercourse (OR= 0.44, 95% CI= 0.19-0.96).

    CONCLUSION: Some lifestyle and occupation factors are strong predictors of the occurrence of prostate cancer among patients in UKMMC. More importantly, with the identification of the potentially modifiable risk factors, proper public health intervention can be improved.

    Matched MeSH terms: Genetic Predisposition to Disease
  19. Al-Naggar RA, Isa ZM, Shah SA, Nor MI, Chen R, Ismail F, et al.
    Asian Pac J Cancer Prev, 2009;10(6):1075-8.
    PMID: 20192587
    Survival after diagnosis of cancer is one of the major outcome measurements and a key criterion for assessing quality of cancer control related to both the preventive and the therapeutic level. The purpose of this study was to determine the 8-year survival time in Malaysia based on socio-demographic and clinical characteristics. A retrospective study of 472 Malaysian women with breast cancer from the Medical Record Department at University Kebangsaan Malaysia Medical Centre (UKMMC) was therefore performed with survival analysis carried out using the Kaplan-Meier with log-rank test for univariate analysis and Cox-regression for multivariate analysis. Women who had cancer or family history of cancer had a longer 8-year survival time (p = 0.008) compared with others who did not have such a history. Tamoxifen use, positive oestrogen receptor status, and race were prognostic indicators for 8-year survival time (p = 0.036, p = 0.018, p = 0.053, respectively) in univariate analysis. Multivariate analysis showed that being Malays and having no family history of cancer were independent prognostic factors for shorter survival time (p = 0.008, p = 0.012, respectively). In conclusion, being Chinese and having a family history of cancer are predictors of longer survival among the Malaysian breast cancer women.
    Matched MeSH terms: Genetic Predisposition to Disease
  20. Chong YM, Tan JA, Zubaidah Z, Rahimah A, Kuldip K, George E
    Med J Malaysia, 2006 Jun;61(2):217-20.
    PMID: 16898315
    Thalassaemia is an inherited blood disorder and is a significant public health problem in Malaysia, with many not knowing they carry the gene for thalassaemia. The two major forms are alpha and beta thalassaemia. An individual can co-inherit both the alpha and beta thalassaemia genes. This study determined the frequency of concurrent carriers of alpha thalassaemia in 231 beta thalassaemia carriers. Gap-PCR was done on extracted DNA of the beta thalassaemia samples to check for alpha thalassaemia 1 molecular defect. Eight (3.5%) samples were found to have concurrently inherited the alpha thalassaemia 1 (- -SEA) deletion. The significant carrier rate for alpha thalassaemia 1 indicates the need for the implementation of DNA analysis to complement thalassaemia screening in high risk populations.
    Matched MeSH terms: Genetic Predisposition to Disease
Filters
Contact Us

Please provide feedback to Administrator (afdal@afpm.org.my)

External Links