Background: Hepatocellular carcinoma (HCC) is considered as the primary malignancy of the liver that usually occurs on top of chronic viral hepatitis. The TP53 (tumor protein 53) is a tumor suppressor gene which is the key in tumor development and progression and the single nucleotide polymorphism (SNP) of the p53 gene codon 72 (p53Arg/Pro) changes the structure of the protein. Objectives: to determine the association of the TP53 Arg72Pro polymorphism with the risk of HCC development in Hepatitis C virus (HCV) infected Egyptian patients. Methodology: This is a case control study conducted in Sohag University Hospital on 100 participants (20 HCC, 20 CHCV, 40 LC and 20 control). TP53 gene polymorphism was identified by Polymerase chain reaction-Restriction fragment length polymorphism (PCR-RFLP), serum level of TP53 was measured by quantitative ELISA. Results: The GG genotype / G allele has the highest frequency in the controls, while the CC genotype/ C allele was more frequently found in the HCC patients. Carriage of TP53 CC genotype and TP53 serum level have a statistical significant association with HCC development. Conclusion: the CC genotype and the Pro (C) allele of TP53, codon 72 are risk factors for HCC in patients infected with HCV and the serum TP53 level is overexpressed in HCC patients.

Apelin is a new multi-functional peptide that has already been linked to blood pressure and cardiac function modulation. It's hypothesized to play a role in hypertension and hypertensive heart diseases development., Nitric oxide (NO) was recognized as an endogenous signaling molecule that modulates vascular compliance and organ perfusion via its powerful vasodilatory effects. Hypertension, atherosclerosis, and chronic renal problems are hypothesized to limit nitric oxide bioavailability, leading to disease progression. Our study aimed to know the role of apelin and nitric oxide in the pathogenesis of essential hypertension and correlate the levels of apelin to nitric oxide in both genders, A total number of 90 participants (70 hypertensive patients and 20 control) were enrolled, and all participants underwent blood pressure, serum apelin and nitric oxide measurement, our results revealed decreased serum apelin levels in essential hypertensive patients, while serum nitric oxide was increased compared to controls with no significant gender difference.

Our review article discusses the relationship between systemic lupus erythematosus and the mannose-binding lectin gene. The complex trait of systemic lupus erythematosus (SLE), which manifests as a variety of clinical phenotypes and the production of several autoantibodies, is SLE. SLE patients experience a wide range of clinical phenotypes, such as skin rash, and neuropsychiatric, and musculoskeletal symptoms, some of which can progress to lupus nephritis. Abnormal complement activation causes inflammation, which damages multiple organs' tissue. About 50% of systemic lupus erythematosus patients, a chronic inflammatory disease, experience kidney damage. Despite effective anti-inflammatory and immunosuppressive therapies, lupus nephritis still results in endstage kidney impairment (ESRD) or chronic kidney disorder (CKD) for an excessive number of patients. It represents a significant risk factor regarding mortality and morbidity in SLE. The family of C-type lectins of collectins includes the mannosebinding lectin (MBL), whose portion in the pre-immune first line of defense seems to involve pattern recognition. MBL can identify carbohydrate modes that abound on the surfaces of numerous pathogenic bacterial, viral, protozoal, and fungal microorganisms. The complement system's lectin pathway is activated when MBL binds to a microorganism. Numerous studies have linked MBL polymorphism, SLE, and lupus nephritis.