TY - JOUR
T1 - MBL2 and MASP2 gene polymorphisms in patients with hepatocellular carcinoma
AU - Segat, L.
AU - Fabris, A.
AU - Padovan, L.
AU - Milanese, M.
AU - Pirulli, D.
AU - Lupo, F.
AU - Salizzoni, M.
AU - Amoroso, A.
AU - Crovella, S.
PY - 2008/5
Y1 - 2008/5
N2 - The pathogenesis of hepatocellular carcinoma (HCC) is not fully understood, but the majority of patients with HCC are associated with hepatitis B virus (HBV) or hepatitis C virus (HCV) infection. Mannan-binding lectin (MBL) is a collectin that can act directly as opsonine or activate MBL-associated serine proteases (MASPs) thus initiating the antibody-independent pathway of the complement system. In our study, we analysed two MBL2 and MASP2 functional polymorphisms (MBL2 allele A/0 and MASP2 D120G) as well as MASP2 polymorphism (Y371D) responsible for an amino acidic change in the protein in 215 HCC patients (HBV-infected, HCV-infected, HBV/HCV co-infected and patients with HCC with no viral infection) and 164 healthy controls to give new insights regarding the role of these two molecules in HCC and viral infection pathogenesis. No significant association was found between MBL2 or MASP2 alleles or genotypes, neither comparing the total patients with HCC and healthy controls nor between the different groups of HCC subjects divided for type of viral infection. Also, dividing the total HCC patients group into low MBL producer (A0 and 00 genotypes) and normal producer (AA genotype) and comparing MASP2 polymorphisms in these two groups, no significant differences were found. Our data do not seem to suggest a role for MBL2 and MASP2 polymorphisms in HCC susceptibility either for HBV-HCV infection-dependent HCC or for HCC raised as a consequence of exposure to different risk factors.
AB - The pathogenesis of hepatocellular carcinoma (HCC) is not fully understood, but the majority of patients with HCC are associated with hepatitis B virus (HBV) or hepatitis C virus (HCV) infection. Mannan-binding lectin (MBL) is a collectin that can act directly as opsonine or activate MBL-associated serine proteases (MASPs) thus initiating the antibody-independent pathway of the complement system. In our study, we analysed two MBL2 and MASP2 functional polymorphisms (MBL2 allele A/0 and MASP2 D120G) as well as MASP2 polymorphism (Y371D) responsible for an amino acidic change in the protein in 215 HCC patients (HBV-infected, HCV-infected, HBV/HCV co-infected and patients with HCC with no viral infection) and 164 healthy controls to give new insights regarding the role of these two molecules in HCC and viral infection pathogenesis. No significant association was found between MBL2 or MASP2 alleles or genotypes, neither comparing the total patients with HCC and healthy controls nor between the different groups of HCC subjects divided for type of viral infection. Also, dividing the total HCC patients group into low MBL producer (A0 and 00 genotypes) and normal producer (AA genotype) and comparing MASP2 polymorphisms in these two groups, no significant differences were found. Our data do not seem to suggest a role for MBL2 and MASP2 polymorphisms in HCC susceptibility either for HBV-HCV infection-dependent HCC or for HCC raised as a consequence of exposure to different risk factors.
KW - HBV
KW - HCV
KW - Hepatocellular carcinoma
KW - MASP2
KW - MBL2
KW - Polymorphisms
UR - http://www.scopus.com/inward/record.url?scp=41549102898&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=41549102898&partnerID=8YFLogxK
U2 - 10.1111/j.1365-2893.2008.00965.x
DO - 10.1111/j.1365-2893.2008.00965.x
M3 - Article
C2 - 18221301
AN - SCOPUS:41549102898
SN - 1352-0504
VL - 15
SP - 387
EP - 391
JO - Journal of Viral Hepatitis
JF - Journal of Viral Hepatitis
IS - 5
ER -