A cross-sectional study of Iraqi patients investigating HPSE SNPs and the incidence of hepatocellular carcinoma

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Suhair Sadai Mahmood
Sabah Ali Jaber Alhelu
Khaleel Ibrahim Ismael
Abbas AbdulWahhab Jumaah
Ban Thabit Saeed
Luai Farhan Zghair
Ali Qais Abdulkafi


Chronic renal failure, Renin , Aspartate Amino Transferase Alanine Amino Transferase , Albumin, Globulin, Calcium , Sodium , Potassium .


In this study, 30 cases from different hospitals in Iraq were included, and they were divided into two groups (a patients group of 15 cases) (a control group of 15 cases). Patient groups were divided according to gender, 12 males (80%) and three females (20%) in the patient’s group while five females (33.3%) and 10 males (6.6%) in the control group. Information related to patients was collected within the study period of 14 months (July 1, 2019 to September 2, 2020). The demographic data of the patients were analyzed using the statistical analysis program IBM SOFT SPSS 22, where the true value and the arithmetic mean of the results were calculated, and the value of the statistical significance to know the type of relationship was also extracted. The results found rs 12503843 with HCV (CC for eight patients were distributed, six HCV positive and two negative patients; CT for five patients were distributed, four patients HCV positive and one negative patient; TT for two patients were distributed with two positive patients). As for the distribution of patients according to the results of the statistical relationship between rs 12331678 with HCV (six cc patients were distributed as five positive HCV and one negative; CA for six patients distributed as two negative HCV and four positive HCV). Finally, we concluded in this study; it was described that heparanase (HPSE) (rs 12331678 and rs 12503843) with the incidence of hepatocellular carcinoma, and a statistically significant relationship was found with a p-value < 0.01. 

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1. Liu YB, Gao SL, Chen XP, et al. Expression and significance of heparanase and nm23-H1 in hepatocellular carcinoma. World J Gastroenterol.
2005; 11: 1378–1381. https://doi.org/10.3748/wjg.v11.i9.1378
2. Ostrovsky O, Shimoni A, Baryakh P, et al. Modification of heparanase gene expression in response to conditioning and LPS treatment: strong correlation to rs4693608 SNP. J Leukoc Biol. 2014; 95: 677–688. https://doi.org/10.1189/jlb.0313147
3. Zhang H, Zhai Y, Hu Z, et al. Genome-wide association study identifies 1p36.22 as a new susceptibility locus for hepatocellular carcinoma in
chronic hepatitis B virus carriers. Nat Genet. 2010; 42: 755–758. https://doi.org/10.1038/ng.638
4. Zhai Y, Qiu W, Dong XJ, et al. Functional polymorphisms in the promoters of MMP-1, MMP2, MMP-3, MMP-9, MMP-12, and MMP-13 are
not associated with hepatocellular carcinoma risk. Gut. 2007; 56: 445–447. https://doi.org/10.1136/gut.2006.112706
5. Yang JM, Wang HJ, Du L, et al. Screening and identification of novel B cell epitopes in human heparanase and their anti-invasion property for
hepatocellular carcinoma. Cancer Immunol Immunother. 2009; 58: 1387–1396. https://doi.org/10.1007/s00262-008-0651-x
6. Ha NB, Ha NB, Ahmed A, et al. Risk factors for hepatocellular carcinoma in patients with chronic liver disease: a case-control study. Cancer Causes Contr. 2012; 23: 455–462. https://doi.org/10.1007/s10552-012-9895-z
7. Zhang Y, Li L, Wang Y, et al. Downregulating the expression of heparanase inhibits the invasion, angiogenesis, and metastasis of human
hepatocellular carcinoma. Biochem Biophys Res Commun. 2007; 358: 124–129. https://doi.org/10.1016/j.bbrc.2007.04.068
8. Xiao Y, Kleeff J, Shi X, et al. Heparanase expression in hepatocellular carcinoma and the cirrhotic liver. Hepatol Res. 2003; 26: 192–198.
9. Weng CJ, Hsieh YH, Tsai CM, et al. Relationship of insulin-like growth factors system gene polymorphisms with the susceptibility and
pathological development of hepatocellular carcinoma. Ann Surg Oncol. 2010; 17(7): 1808–1815. https://doi.org/10.1245/s10434-009-0904-8
10. Ferlay J, Shin HR, Bray F, et al. Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008. Int J Cancer. 2010; 127: 2893–2917.
11. Goldshmidt O, Yeikilis R, Mawasi N, et al. Heparanase expression during normal liver development and following partial hepatectomy. J
Pathol. 2004; 203: 594–602. https://doi.org/10.1002/path.1554
12. Yano Y, Yamashita F, Kuwaki K, et al. Clinical features of hepatitis C virus-related hepatocellular carcinoma and their association with 훼-fetoprotein and protein induced by vitamin K absence or antagonist-II. Liver Int. 2006; 26: 789–795. https://doi.org/10.1111/j.1478-3231.2006.01310.x
13. Chen G, Dang YW, Luo DZ, et al. Expression of heparanase in hepatocellular carcinoma has prognostic significance: a tissue microarray study. Oncol Res. 2008; 17: 183–189. https://doi.org/10.3727/096504008785114138
14. Ralph S, Brenchley PE, Summers A, et al. Heparanase gene haplotype (CGC) is associated with the stage of disease in patients with ovarian
carcinoma. Cancer Sci. 2007; 98: 844–849. https://doi.org/10.1111/j.1349-7006.2007.00461.x
15. Sasisekharan R, Shriver Z, Venkataraman G, et al. Roles of heparan-sulfate glycosaminoglycans in cancer. Nat Rev Cancer. 2002; 2: 521–528.

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