Sequence Analysis of TP53 Suppressor Gene in Women with Breast Cancer in Mosul City
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TP53 Gene, Sequencing, Exon, Polymorphism and Breast CancerAbstract
Mutations in the TP53 gene, which often result in P53 protein dysfunction, are associated with
more than 75% of malignancies. DNA damage and hypoxia activate TP53, a protein that facilitates DNA
repair and regulates cellular aging and apoptosis. These elements play a vital role in tumor suppression
and also alter cellular responses associated with cell cycle regulation. During September and November
2021, 96 recommendations were issued for female patients aged 35–45 at Mosul's Alternative Nuclear
Medicine and Oncology Hospital. One cohort comprised 25 healthy women, while the other encompassed
71 women diagnosed with breast cancer. This work employed DNA sequencing technology with various
physiological parameters and blood components to detect TP53 polymorphisms at codon 249 in exon 7
and (rs1042522) in exon 4, as well as the nucleotide sequences of the amplified areas. For instance, the
levels of hemoglobin, urea, creatinine, erythrocytes, platelets, and leukocytes. Sequencing study of the
gene's enlarged exons revealed that exons 3, 4, and 6 exhibited varying nucleotide quantities, but exon 5
remained constant. Additionally, a distinctive TP53 genotype with the GeneBank code LC682536.1 was
identified at the NCBI global gene site in Mosul. A novel P53 tumor suppressor protein phenotype was
found in Mosul, with the GenBank accession number BDF83325.1. The research indicated that urea
concentrations in patients were 38.2 mg/dl, and the CA15-3 ratio was 23 U/ml when comparing patients
to healthy controls. The results indicate that, in comparison to healthy controls, breast cancer patients had
significantly lower levels of urea, creatinine, and CA15-3 in their blood plasma. The present investigation
revealed a substantial reduction in the total counts of white blood cells, red blood cells, platelets, and
hemoglobin levels in the blood of breast cancer patients.
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