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Genetic Variants in C5 and Poor Response to Eculizumab

by Wano, Yuji , Inazawa, Johji , Ohyashiki, Kazuma , Lazarowski, Alberto , Masuko, Masayoshi , Johnson, Krista , Nishimura, Jun-ichi , Hase, Masakazu , Li, Lan , Tamburini, Paul , Kanakura, Yuzuru , Matsumoto, Takuro , Shichishima, Tsutomu , Kinoshita, Taroh , Takahashi, Toru , Shibayama, Hirohiko , Yamamoto, Masaki , Noji, Hideyoshi , Ando, Kiyoshi , Brodsky, Andres L , Eto, Tetsuya , Hayashi, Shin , Kitamura, Kunio

in Antibodies, Monoclonal, Humanized - pharmacokinetics / Antibodies, Monoclonal, Humanized - therapeutic use / Asian Continental Ancestry Group / Biological and medical sciences / Complement C5 - genetics / Complement component C5 / Drug Resistance - genetics / General aspects / Genetic diversity / Hemoglobin / Hemoglobinuria, Paroxysmal - drug therapy / Hemoglobinuria, Paroxysmal - ethnology / Hemoglobinuria, Paroxysmal - genetics / Hemolysis / Humans / Immunomodulators / Japan / Medical research / Medical sciences / Monoclonal antibodies / Mortality / Mutation / Mutation, Missense / Paroxysmal nocturnal hemoglobinuria / Pharmaceuticals / Pharmacology. Drug treatments / Sequence Analysis, DNA / Thrombosis

2014

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2014

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2014

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Journal Article

Genetic Variants in C5 and Poor Response to Eculizumab

Wano, Yuji,

Inazawa, Johji,

Ohyashiki, Kazuma,

Lazarowski, Alberto,

Masuko, Masayoshi,

Johnson, Krista,

Nishimura, Jun-ichi,

Hase, Masakazu,

Li, Lan,

Tamburini, Paul,

Kanakura, Yuzuru,

Matsumoto, Takuro,

Shichishima, Tsutomu,

Kinoshita, Taroh,

Takahashi, Toru,

Shibayama, Hirohiko,

Yamamoto, Masaki,

Noji, Hideyoshi,

Ando, Kiyoshi,

Brodsky, Andres L,

Eto, Tetsuya,

Hayashi, Shin,

Kitamura, Kunio

2014

Overview

Patients with paroxysmal nocturnal hemoglobinuria who had a poor response to eculizumab therapy were found to have a genetic polymorphism in C5 that prevents binding by the antibody. Paroxysmal nocturnal hemoglobinuria (PNH) arises as a consequence of clonal expansion of hematopoietic stem cells that have acquired a somatic mutation in the gene encoding phosphatidylinositol glycan anchor biosynthesis class A ( PIGA ). 1 – 3 The resulting hematopoietic cells are deficient in glycosylphosphatidylinositol-anchored proteins, including the complement regulatory proteins CD55 and CD59; this accounts for the intravascular hemolysis that is the primary clinical manifestation of PNH. 4 – 6 PNH frequently develops in association with disorders involving bone marrow failure, particularly aplastic anemia. Thrombosis is a major cause of PNH-associated morbidity and mortality, particularly among white patients. 7 – 9 Eculizumab (Soliris, Alexion Pharmaceuticals) . . .

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Publisher

Massachusetts Medical Society

Subject

Antibodies, Monoclonal, Humanized - pharmacokinetics

/ Antibodies, Monoclonal, Humanized - therapeutic use

/ Asian Continental Ancestry Group

/ Biological and medical sciences

/ Complement C5 - genetics

/ Complement component C5

/ Drug Resistance - genetics