ArticleMolecular genetics & genomic medicine2022
Founder genetic variants of ABCC4 and ABCC11 in the Japanese population are not associated with the development of subacute myelo-optico-neuropathy (SMON).
Article in Molecular genetics & genomic medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Prevalence and Study-Level Predictors of Chronic Chemotherapy-Induced Peripheral Neuropathy: A Systematic Review and Meta-Analysis.Journal of pain research · 2026Review
- Clioquinol as a new therapy in epilepsy: From preclinical evidence to a proof-of-concept clinical study.Epilepsia · 2025Article
- Loss-of-function polymorphisms in NQO1 are not associated with the development of subacute myelo-optico-neuropathy.Molecular genetics & genomic medicine · 2024Article
- Founder genetic variants of ABCC4 and ABCC11 in the Japanese population are not associated with the development of subacute myelo-optico-neuropathy (SMON).Molecular genetics & genomic medicine · 2022Article
- NQO1 protects against clioquinol toxicity.Frontiers in pharmacology · 2022Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
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Abstract
backgroundSubacute myelo-optico-neuropathy (SMON) is a severe neurological disorder associated with clioquinol administration, which frequently occurred in Japan during the 1950s and 1960s. The unique genetic background of the Japanese population is considered to be strongly involved in the development of this neurological disease. Recently, genetic variants of ABCC4 (OMIM: 605250) and ABCC11 (OMIM: 607040), which are particularly common in the Japanese population, were suggested as possible genetic susceptibility factors for the development of SMON.
methodsWe analyzed 125 Japanese SMON patients who provided consent for this study. Patient DNA was collected from peripheral blood, and genetic analysis was performed for ABCC4 rs3765534 (c.2268G>A, p.Glu857Lys) and ABCC11 rs17822931 (c.538G>A, p.Gly180Arg) polymorphisms using the Sanger sequencing method and/or TaqMan PCR method. The frequency distribution of each polymorphism was compared with that in healthy Japanese people recorded in two genomic databases (Human Genomic Variation Database and Integrative Japanese Genome Variation Database), and each genotype was compared with the clinical features of patients.
resultsThe frequencies of ABCC4 rs3765334 and ABCC11 rs17822931 polymorphisms in SMON patients and healthy Japanese people were not significantly different in the multifaceted analysis.
conclusionWe conclude that the ABCC4 rs3765334 and ABCC11 rs17822931 polymorphisms are not associated with the development of SMON.
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