Ravindran Ankathil

Universiti Sains Malaysia

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Azlan Husin

Universiti Sains Malaysia

Ahmad Aizat Abdul Aziz

Hospital Universiti Sains Malaysia

Abdul Aziz Baba

International Medical University

Sarina Sulong

Universiti Sains Malaysia

P Remani

Regional Cancer Center, Thiruvananthapuram

Rosline Hassan

Universiti Sains Malaysia

Marjanu Hikmah Elias

Universiti Sains Islam Malaysia

Nair Mk

University of Florida

Manjusha Nair

Regional Cancer Center, Thiruvananthapuram

T Vijayakumar

SRM Institute of Science and Technology

Cooperative Institutions

Universiti Sains Malaysia

113

Hospital Universiti Sains Malaysia

Regional Cancer Center, Thiruvananthapuram

University of Melbourne

Rambam Health Care Campus

Hospital Sírio-Libanês

Ben-Gurion University of the Negev

Radboud University Nijmegen

Cancer Genetics (United States)

University of Vermont

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Contribution of the MLH1 -93G>A Promoter Polymorphism in Modulating Susceptibility Risk in Malaysian Colorectal Cancer Patients

Asian Pacific Journal of Cancer Prevention (2013)

Mohd Nizam Zahary Ahmad Aizat Abdul Aziz Gurjeet Kaur Muhammad Radzi Abu Hassan Ahmad Shanwani Mohd Sidek

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

Lynch Syndrome

MLH1

Genetic predisposition

Penetrance

10.7314/apjcp.2013.14.2.619

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Citations (8)

A review of AML classification: a single institution experience in a developing country

Journal of Hematopathology (2014)

Hanan Mahmood Wan Zaidah Abdullah Ang Cheng Yong Suhair Ahmed Abu Dzarr Abdullah

Institution

Hematology

10.1007/s12308-014-0198-z

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Citations (8)

Contribution of Genetic Polymorphisms of Inflammation Response Genes on Sporadic Colorectal Cancer Predisposition Risk in Malaysian Patients – A Case Control Study

Asian Pacific Journal of Cancer Prevention (2019)

Ravindran Ankathil Mohd Aminudin Mustapha Ahmad Aizat Abdul Aziz Siti Nurfatimah Mohd Shahpudin Andee Dzulkarnaen Zakaria

AIM: To investigate the frequencies and association of polymorphic genotypes of IL-8 -251 T>A, TNF-α -308G>A, ICAM-1 K469E, ICAM-1 R241G, IL-6 -174 G>C, and PPAR-γ 34 C>G in modulating susceptibility risk inMalaysian colorectal cancer (CRC) patients. Methods: In this case-control study, peripheral blood samples of 560study subjects (280 CRC patients and 280 controls) were collected, DNA extracted and genotyped using PCR-RFLPand Allele Specific PCR. The association between polymorphic genotype and CRC susceptibility risk was determinedusing Logistic Regression analysis deriving Odds ratio (OR) and 95% CI. Results: On comparing the frequencies ofgenotypes of all single nucleotide polymorphisms ( SNPs ) in patients and controls, the homozygous variant genotypesIL-8 -251 AA and TNF-α -308 AA and variant A alleles were significantly higher in CRC patients. Investigation onthe association of the variant alleles and genotypes singly, with susceptibility risk showed the homozygous variant Aalleles and genotypes IL-8 -251 AA and TNF-α -308 AA to be at higher risk for CRC predisposition. Analysis basedon age, gender and smoking habits showed that the polymorphisms IL8 -251 T>A and TNF – α 308 G>A contributeto a significantly higher risk among male and female who are more than 50 years and for smokers in this population.Conclusion: We observed an association between variant allele and genotypes of IL-8-251 T>A and TNF-α-308G>A polymorphisms and CRC susceptibility risk in Malaysian patients. These two SNPs in inflammatory responsegenes which undoubtedly contribute to individual risks to CRC susceptibility may be considered as potential geneticpredisposition factors for CRC in Malaysian population.

Genetic predisposition

10.31557/apjcp.2019.20.6.1621

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Citations (7)

Next-Generation Sequencing in Cancer

Journal of Maxillofacial and Oral Surgery (2020)

S. Vinod Nair Madhulaxmi Gigi Thomas Ravindran Ankathil

Epigenomics

Massive parallel sequencing

10.1007/s12663-020-01462-4

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Citations (5)

Polymorphism in the tumor necrosis factor alpha promoter region and its influence on colorectal cancer predisposition risk in Malaysian population

Mustapha Mohd Aminudin Mohd Shahpudin Siti Nurfatimah Ahmad Aizat Abdul Aziz Venkata Muralikrishna Bhavaraju Venkatesh R Naik

objective:A case control study was designed to investigate the TNF-a -308 G>A polymorphism allele frequencies and to determine the influence of the polymorphic genotype on sporadic CRC susceptibility risk in Malaysia population. Material and methods: Peripheral blood samples of 164 normal controls and 161 clinically and histopathhologically confirm CRC patients were genotyped for TNF-a -308 G>A polymorphism employing allele specific PCR. The relative associations of various genotypes with CRC susceptibility risk was determined by calculating Odd ratios. Corresponding Chi-square tests on CRC patients and controls were carried out and 95% confidence interval (95% CI) were determined using fisher exact tests. Results: On comparing the frequencies of genotypes of patients and controls, the homozygous variant AA was significabtly higher in CRC patients (p=0.030) compared to controls. On investigating the association of the polymorphic genotypes with CRC susceptibility risk, the homozygous variant TNF-a -308AA showed significantly increased risk with OR 2.5842. Conclusion: Our results suggest that, polymorphic genotype of inflammation response gene TNF-a is significantly associated with CRC susceptibility risk and colud be considered as a high risk variant for CRC predisposition.

Genetic predisposition

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Differential prognostic impact of stratified additional chromosome abnormalities on disease progression among Malaysian chronic myeloid leukemia patients undergoing treatment with imatinib mesylate

Frontiers in Oncology (2022)

Ismail Siti Mariam Ramli Norhidayah Abu Bakar Zulaikha Mohd Yunus Nazihah Rosline Hassan

The emergence of additional chromosome abnormalities (ACAs) in chronic myeloid leukemia (CML) patients during treatment with a tyrosine kinase inhibitor (TKI) regime is generally associated with resistance to treatment and a sign of disease progression to accelerated phase or blast phase. We report the type, frequency, and differential prognostic impact of stratified ACAs with treatment response in 251 Malaysian CML patients undergoing TKI therapy. ACAs were observed in 40 patients (15.9%) of which 7 patients (17.5%) showed ACAs at time of initial diagnosis whereas 33 patients (82.5%) showed ACAs during the course of IM treatment. In order to assess the prognostic significance, we stratified the CML patients with ACAs into four groups, group 1 (+8/+Ph), group 2 (hypodiploidy), group 3 (structural/complex abnormalities); group 4 (high-risk complex abnormalities), and followed up the disease outcome of patients. Group 1 and group 2 relatively showed good prognosis while patients in group 3 and group 4 had progressed or transformed to AP or blast phase with a median survival rate of 12 months after progression. Novel ACAs consisting of rearrangements involving chromosome 11 and chromosome 12 were found to lead to myeloid BP while ACAs involving the deletion of 7q or monosomy 7 led toward a lymphoid blast phase. There was no evidence of group 2 abnormalities (hypodiploidy) contributing to disease progression. Compared to group 1 abnormalities, CML patients with group 3 and group 4 abnormalities showed a higher risk for disease progression. We conclude that the stratification based on individual ACAs has a differential prognostic impact and might be a potential novel risk predictive system to prognosticate and guide the treatment of CML patients at diagnosis and during treatment.

Imatinib Mesylate

10.3389/fonc.2022.720845

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Citations (4)

P1-042: A Multigenic Approach to Predict Risk and Survival among Indian Lung Cancer Patients

Journal of Thoracic Oncology (2007)

Leelakumari Sreeja Jayaprakash Madhavan Ravindran Ankathil

XRCC1

GSTP1

10.1097/01.jto.0000283656.97993.43

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Citations (1)

Complex Chromosomal Rearrangement der(5)ins(5;3)(q31;q25q29), t(3;12)(q24;p12.2) In A Dysmorphic Child, - A Case Report

Journal of Biomedical and Clinical Sciences (JBCS) (2018)

Aziati Azwari Annuar Nik Mohd Zulfikri Mat Zin Siti Mariam Ismail Nurul Alia Mohd Nawi Nazihah Mohd Yunus

Complex chromosome rearrangements (CCRs) are structural aberrations or rearrangements involving three or more cytogenetics breakpoints on two or more chromosomes [1]. Balanced and unbalanced are known to have significant risk of mental retardation and phenotypic anomalies. CCRs are also associated with infertility in males and recurrent abortion in females. Here we report one case of apparently balanced CCR involving three chromosomes 3, 5 and 12 in a child with abnormal features. G banding and FISH were performed to clarify the nature of this complex abnormality. The proband was a 3 years old Malay girl, referred for cytogenetic analysis due to abnormal features. She was very short at 5 th centile, has triangular facies, strabismus, short neck and had significant delay in speech. Blood investigations including full blood count, serum amino acid, renal, liver and thyroid function tests were normal. There was no history of mental retardation, congenital malformation, or recurrent miscarriages in either family. Peripheral blood lymphocytes of the proband was cultured and chromosome preparations were made as per standard procedures. Karyotype analysis was carried out based on ISCN (2016). Fluorescence in situ hybridisation (FISH) technique was carried out using Whole Chromosome Painting Probes (WCP) for chromosome 3, 5 and 12 as per standard procedures. Cytogenetic analysis on 32 GTG banded metaphases at the resolution level of 400-550 bphs showed 46,XX,der(5)ins(5;3)(q31;q25q29),t(3;12)(q24;p12.2) complex karyotype pattern (Figure 1). This abnormal karyotype showed derivative chromosome 5 resulting from an insertion of a segment 3q25q29 from the long arm of chromosome 3 into the long arm of chromosome 5 at band 5q31. The segment is replaced by translocation of a segment 12p12.2 from the short arm of chromosome 12 to the chromosome 3 at band 3q24. This three way translocations has been confirmed by FISH using WCP for chromosome 3, 5 and 12 (Figure 2). CCRs are very rare events in the human population that can be inherited or de novo and can be balanced or imbalanced. Balanced CCRs can lead to an unbalanced condition of gametes during meiosis. Most de novo CCRs originate from spermatogenesis and cause mental retardation in high incidence, whereas most familial CCRs are of maternal origin and usually have three to four breakpoints [2]. This proband had CCRs with 4 chromosomal breakpoints and involved three chromosomes. The abnormal features in this present case might be attributable to gene disruption, cryptic imbalances and/or from position effects of genes. Recently, FISH with specific DNA probes for whole chromosomes or for indicated specific chromosomal segments, has significantly improved the characterization of CCRs [3]. Although FISH contributes in elucidating the complexity of CCR, painting FISH is limited in detecting submicroscopic deletions or identifying changes due to gene position effect. There are several mechanisms that leads to chromosomal rearrangements. A simultaneous double stranded DNA breaks were induced by unknown stimulus including free radiation or ionizing radiation, followed by joining of the break fragments in the wrong place due to microhomology shared by these regions [1]. The origin of the complex translocation in the present case, whether inherited or de novo, could not be established due to lack of consent of parents for the cytogenetic examination.

Proband

Chromosomal rearrangement

Breakpoint

Derivative chromosome

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Increased Levels of Mutagen-Induced Chromosome Breakage in Down Syndrome Children with Malignancy

Cancer Genetics and Cytogenetics (1997)

Ravindran Ankathil P. Kusumakumary Manjusha Nair

Trisomy

Nijmegen breakage syndrome