Hanan Hassan Fouad

The distribution of hepatitis C virus (HCV) genotypes among Egyptian patients positive for anti-HCV was determined and their influence, when combined with neu-oncoprotein overexpression, on the development of hepatocellular carcinoma (HCC) was examined. The study groups included asymptomatic carriers (ASC) and patients with chronic active hepatitis (CAH) and HCC. HCV genomes were detected in the sera of 27 ASC, 29 CAH and 33 HCC patients known to have HCV infection defined by EIA and recombinant immunoblotting techniques (Inno-LiA) as well as by reverse transcriptase (RT)-PCR. The HCV genotype was determined by a reverse hybridisation technique (Inno-LiPA I and II), whereas neu-overexpression was detected by the Oncogene Science EIA Kit. Eighty-nine patients were eligible for HCV genotyping; 75 patients (84.3%) were infected with a single genotype, including 1a in 11 patients (12.4%), 1b in 2 patients (2.2%) and 2a in 10 patients (11.2%). Genotype 4 (a or c + d) was detected in 51 patients (57.3%) and only one patient had genotype 10a (1.2%). Fourteen patients (15.7%) showed mixed infection; eight of them had 1a + 4 (a or c + d) and four had 2a + 4 (a or c + d); the remaining two cases had 1a + 2a and 1b + 2a. The results revealed an increased incidence of genotype 4 in CAH and HCC patients in comparison with ASC. There was also a significant overexpression of neu-oncoprotein in CAH and HCC patients compared with ASC, which was significantly associated with subtype 4 infection. The results suggest that infection with subtype 1a and 4 HCV may be considered a risk factor for the induction of neu-overexpression and subsequent development of HCC.

The distribution of hepatitis C virus (HCV) genotypes among Egyptian patients positive for anti-HCV was determined and their influence, when combined with neu-oncoprotein overexpression, on the development of hepatocellular carcinoma (HCC) was examined. The study groups included asymptomatic carriers (ASC) and patients with chronic active hepatitis (CAH) and HCC. HCV genomes were detected in the sera of 27 ASC, 29 CAH and 33 HCC patients known to have HCV infection defined by EIA and recombinant immunoblotting techniques (Inno-LiA) as well as by reverse transcriptase (RT)-PCR. The HCV genotype was determined by a reverse hybridisation technique (Inno-LiPA I and II), whereas neu-overexpression was detected by the Oncogene Science EIA Kit. Eighty-nine patients were eligible for HCV genotyping; 75 patients (84.3%) were infected with a single genotype, including 1a in 11 patients (12.4%), 1b in 2 patients (2.2%) and 2a in 10 patients (11.2%). Genotype 4 (a or c + d) was detected in 51 patients (57.3%) and only one patient had genotype 10a (1.2%). Fourteen patients (15.7%) showed mixed infection; eight of them had 1a + 4 (a or c + d) and four had 2a + 4 (a or c + d); the remaining two cases had 1a + 2a and 1b + 2a. The results revealed an increased incidence of genotype 4 in CAH and HCC patients in comparison with ASC. There was also a significant overexpression of neu-oncoprotein in CAH and HCC patients compared with ASC, which was significantly associated with subtype 4 infection. The results suggest that infection with subtype 1a and 4 HCV may be considered a risk factor for the induction of neu-overexpression and subsequent development of HCC.

An association between human papilloma virus (HPV) and bladder cancer has been reported. However, the role of HPV in bilharzial bladder cancer and its prevalence are not yet clarified. We investigated 50 cases for HPV types 16/18 by in situ hybridization (ISH). Also, p53 protein expression by immunohistochemistry was evaluated in 41 of these 50 cases, with correlation of these factors to clinicopathologic parameters and tumor relapse after primary treatment. HPV was detected in 46% of Egyptian bladder carcinomas (23/50 cases). Positivity was 47.8% for squamous cell carcinoma (SCC) and 36.4% for transitional cell carcinoma (TCC). There was a possible viral- bilharzial association as 52.8% of bilharzial cases, while only 12.5% of non bilharzial cases were HPV positive (p<0.05). P53 protein was found in 19/41cases (46.3%). Concordance between HPV and p53 was present in 58.5% of cases. Both factors studied were not related to tumor recurrence after primary treatment. So, HPV may be implicated in the aetiology of bilharzial bladder cancer, however a definite causal relationship remains unsolved. HPV together with p53 alterations might work in synergy to accelerate the carcinogenic process, as there was concordance in the results of both parameters in 24/41 cases (58.5%).

An association between human papilloma virus (HPV) and bladder cancer has been reported. However, the role of HPV in bilharzial bladder cancer and its prevalence are not yet clarified. We investigated 50 cases for HPV types 16/18 by in situ hybridization (ISH). Also, p53 protein expression by immunohistochemistry was evaluated in 41 of these 50 cases, with correlation of these factors to clinicopathologic parameters and tumor relapse after primary treatment. HPV was detected in 46% of Egyptian bladder carcinomas (23/50 cases). Positivity was 47.8% for squamous cell carcinoma (SCC) and 36.4% for transitional cell carcinoma (TCC). There was a possible viral- bilharzial association as 52.8% of bilharzial cases, while only 12.5% of non bilharzial cases were HPV positive (p<0.05). P53 protein was found in 19/41cases (46.3%). Concordance between HPV and p53 was present in 58.5% of cases. Both factors studied were not related to tumor recurrence after primary treatment. So, HPV may be implicated in the aetiology of bilharzial bladder cancer, however a definite causal relationship remains unsolved. HPV together with p53 alterations might work in synergy to accelerate the carcinogenic process, as there was concordance in the results of both parameters in 24/41 cases (58.5%).