Heparanase (HPSE) SNPs as A Predictor for Hepatocellular Carcinoma
DOI:
https://doi.org/10.56981/Keywords:
Heparanase, hepatocellular carcinoma, HPSE gene polymorphismAbstract
Introduction: Hepatocellular carcinoma (HCC) is a frequent liver cancer caused by hepatocytes and linked to persistent infections, heavy alcohol intake, and genetic abnormalities. (1) HCC is aggressive and may not show signs until advanced. Surgery, radiation, chemotherapy, and targeted therapies are available depending on cancer stage. Endo-β-D-glycosidase heparanase affects tumour angiogenesis, invasion, and metastasis. (2) Heparanase overexpression in HCC is linked to metastasis and micro-vessel density. Heparanase downregulation reduces HCC cell line invasiveness and metastases. SNPs, the most frequent genetic variation in humans, can affect illness susceptibility and medication response. (3) Metabolic, immunological, and cancer genes have SNPs. Functional studies are needed to identify how SNPs affect gene expression or protein function. Heparanase gene SNPs rs 12331678 and rs 12503843 were linked to HCC in this study. (4) Patients and methods: This study investigated the potential of heparanase (HPSE) single nucleotide polymorphisms (SNPs) as a predictor for hepatocellular carcinoma. It involved 30 cases from various hospitals in Iraq, with 15 cases in a patient group and 15 cases in a control group. The study obtained official approval from the Ethics Committee and collected demographic data, performed clinical examinations, and used laboratory tests to extract and examine genomic DNA. Polymerase chain reaction (PCR) technology was utilised to amplify the DNA samples, and statistical analysis was conducted to establish the significance of the correlation. From July 2019 until September 2020, researchers were actively engaged in this study. Results: The study involved 15 patient and 15 control subjects, with mean ages of 70.2±1.58 and 68.13±1.10, respectively. The patients were 80% male and 20% female, while the control group consisted of 66.7% males and 33.3% females. The study investigated the hematological profile and focal lesions of patients, as well as the correlation between gene polymorphisms and the Child-Pugh score, ALT, and AST levels. The results of the study are presented in various tables and figures, including primer sequences of polymorphisms rs 12331678 and rs 12503843, as well as Pearson correlations between these polymorphisms with ALT, AST, and Child–Pugh scores. Conclusion: In this study of Iraqi patients aged 60 to 80, a statistically significant association between HPSE (rs 12331678 and rs 12503843) and the incidence of HCC was discovered. In this study, we not only discussed the clinical significance of HPSE genetic variation, but also its role as one of the causes of HCC.
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