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DNA INSTABILITY ASSOCIATED WITH FOLATE DEfiCIENCY Salih, Alyaa Abdulhadi
Journal of Medical Genetics and Clinical Biology Vol. 1 No. 9 (2024): Journal of Medical Genetics and Clinical Biology
Publisher : PT ANTIS INTERNATIONAL PUBLISHER

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.61796/jmgcb.v1i9.918

Abstract

Folate, also referred to as Vitamin B9, is a type of vitamin that dissolves in water and plays a central role in preserving the integrity of DNA molecules and gene expression through the construction of DNA and methylation. Folate cannot be synthesised in vivo and must be obtained from the diet, particularly fruits and green leafy vegetables. deficiency of folate increases the risk of DNA stability due to uracil misincorporation into the DNA backbone and chromosome breaks, it can lead to the accumulation of deoxyuridine monophosphate (dUMP) which impairs the pathway of dTMP synthesis. in addition, it reduces the availability of methyl donors which causes impaired methylation patterns. Finally, it can generate oxidative stress leading to mtDNA damage and eventually to genomic instability. Different studies and measurement methods have produced varying evidence on the connection between folate and DNA stability, So we encourage to increase in folic acid intake for at-risk groups, but more rigorous human studies are needed before scientifically based public health recommendations about dietary requirements can be made.
DNA INSTABILITY ASSOCIATED WITH FOLATE DEfiCIENCY Salih, Alyaa Abdulhadi
Journal of Medical Genetics and Clinical Biology Vol. 1 No. 9 (2024): Journal of Medical Genetics and Clinical Biology
Publisher : PT. Antis International Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.61796/jmgcb.v1i9.918

Abstract

Folate, also referred to as Vitamin B9, is a type of vitamin that dissolves in water and plays a central role in preserving the integrity of DNA molecules and gene expression through the construction of DNA and methylation. Folate cannot be synthesised in vivo and must be obtained from the diet, particularly fruits and green leafy vegetables. deficiency of folate increases the risk of DNA stability due to uracil misincorporation into the DNA backbone and chromosome breaks, it can lead to the accumulation of deoxyuridine monophosphate (dUMP) which impairs the pathway of dTMP synthesis. in addition, it reduces the availability of methyl donors which causes impaired methylation patterns. Finally, it can generate oxidative stress leading to mtDNA damage and eventually to genomic instability. Different studies and measurement methods have produced varying evidence on the connection between folate and DNA stability, So we encourage to increase in folic acid intake for at-risk groups, but more rigorous human studies are needed before scientifically based public health recommendations about dietary requirements can be made.
EPIGENETIC REGULATION OF ESTROGEN GENE EXPRESSION IN OVARY CANCER IN HUMAN Salih, Alyaa Abdulhadi
Journal of Medical Genetics and Clinical Biology Vol. 1 No. 12 (2024): Journal of Medical Genetics and Clinical Biology
Publisher : PT. Antis International Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.61796/jmgcb.v1i12.1051

Abstract

Objective: This study examines how epigenetic mechanisms control the expression of the estrogen receptor (ER) gene in ovarian cancer, concentrating on DNA methylation, histone modifications, and non-coding RNAs in Iraqi population samples. Method: Bisulfite sequencing was used to measure the DNA methylation levels of the ER gene in tissue samples from ovarian cancer patients and healthy controls, and chromatin immunoprecipitation (ChIP) tests were used to examine histone alterations. Using RNA sequencing, important non-coding RNAs affecting ER pathways were found. The epigenetic variations between malignant and healthy tissues were assessed using comparative analysis. Results: The results showed that the ER gene was significantly more methylated in cancer tissues (67%) than in healthy samples (21%), which resulted in decreased cellular estrogen responses and increased proliferation. Oncogenes were activated by elevated histone H3K9 acetylation levels (1.7 AU vs. 0.8 AU), but tumor suppressor genes were inhibited by elevated H3K27 methylation (2.1 AU). These modifications draw attention to important epigenetic modifications that aid in the development of ovarian cancer. Novelty: By identifying region-specific epigenetic markers in ovarian cancer, this work highlights the significance of population-targeted research in enhancing cancer outcomes and provides insights into tailored therapy approaches.