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Mannan‐Binding Lectin (MBL) and MBL‐Associated Serine Protease 2 (MASP‐2) Genotypes in Colorectal Cancer
Author(s) -
Ytting H.,
Christensen I. J.,
Steffensen R.,
Alsner J.,
Thiel S.,
Jensenius J. C.,
Hansen U.,
Nielsen H. J.
Publication year - 2011
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2010.02480.x
Subject(s) - mannan binding lectin , genotype , single nucleotide polymorphism , lectin pathway , ficolin , immunology , biology , medicine , complement system , lectin , genetics , gene , alternative complement pathway , antibody
Mannan‐binding lectin (MBL) and MBL‐associated serine protease 2 (MASP‐2) are key factors of the lectin pathway of complement activation. Polymorphisms of the MBL2 and MASP‐2 genes affect serum levels of MBL and MASP‐2. In patients with colorectal cancer (CRC), the MBL and MASP‐2 serum levels are increased and high MASP‐2 levels are associated with recurrence and poor survival, whereas low MBL levels predict post‐operative pneumonia. It is not known whether these associations are genetically based. In this study, the MBL and MASP‐2 genotypes are investigated in 593 patients with CRC and 348 healthy controls. The potential association between genetic profile and infections, recurrence and survival is evaluated. Four single‐nucleotide polymorphisms (SNPs) of MBL2 were analysed using TaqMan assays, with characterization of MBL2 wildtype A, variants B, C and D and alleles H/L, Y/X and P/Q. The SNP D120G for MASP‐2 was determined. Serum levels of MBL and MASP‐2 were measured. The MBL2 and MASP‐2 genotype distribution was similar among patients with CRC and healthy controls and MBL2 genotype significantly associated with MBL concentration in serum ( P < 0.0001). No significant association between MBL2/MASP‐2 genotype and post‐operative infectious complications ( P = 0.33 and 0.22), recurrent cancer or survival ( P = 0.74 and P = 0.61 respectively) was found. Thus, the increased serum levels of MBL and MASP‐2 found in patients with CRC are not explained for by genetic profiles. In contrast to what has been demonstrated for serum levels of MBL and MASP‐2, the genotypes do not predict disease course of the CRC patients.