Polymorphism Of The Genes In The Complement Pathways And Clinical Data

There is increasing evidence that complement plays a role in the clinical response to rituximab. However, little data is available regarding the polymorphism of genes involved in the complement-mediated pathway.

C1q (complement component 1, subcomponent q), generally associates with C1r and C1s to yield the first component of the complement system. C1q is composed of 18 polypeptide chains including 6 A-chains, 6 B-chains, and 6 C-chains. The A-, B-, and C-chains are arranged in the order A-C-B on chromosome 1. This gene encodes the A-chain polypeptide of C1q, and is located on chromosome 1p36.12.

Racila et al. (72) recently identified a non-coding polymorphism in the C1qA component of complement, which may result in a post-translational splice variant of the C1qA protein. When analyzing the treatment outcome of rituximab monotherapy in 90 FL patients, no difference in response rate was noted according to C1qA gene polymorphism (Table 2). However, a trend of prolonged remission was noted in the group with the AA or AG genotype at the C1qA 276 locus among patients who achieved complete or partial response on rituximab therapy (p = 0.12).

When confined to the group that achieved CR to rituximab monotherapy, patients with the AA or AG genotype at C1qA 276 locus showed a median of 830 days of time to progression (TTP), while those with GG genotype showed 250 days of TTP (p = 0.007). This data suggests that the polymorphism in C1qA may impact on the remission duration of FL patients after rituximab therapy (72). Further study regarding this polymorphism is strongly warranted.

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