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Article

Trisomy 8 clonal expansion during disease progression and azacitidine resistance in VEXAS syndrome: a case report.

Frontiers in immunology - 1 Jan 2026

Sato Keijiro, Zaimoku Yoshitaka, Kano Yui, Kobayashi Miku, Kazama Shintaro, Morikawa Takahiro, Kazumoto Hiroko, Ishii Wataru, Ueki Toshimitsu, Sumi Masahiko, Kobayashi Hikaru, Nannya Yasuhito, Ogawa Seishi, Ichikawa Naoaki

Abstract excerpt

Background: Vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic (VEXAS) syndrome is an adult-onset autoinflammatory disorder driven by clonal hematopoiesis with somatic UBA1 mutations. Azacitidine can reduce the mutant clonal burden and improve inflammatory manifestations. However, the clonal basis of treatment resistance remains poorly understood. Case presentation: A 61-year-old man presented with...

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Share to Azacitidine
Share to Chromosomes, Human, Pair 8

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Myelodysplastic Syndromes

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Source

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Identifiers

PMID: 42358941
DOI: 10.3389/fimmu.2026.1841156
PMCID: PMC13290977

Genes

UBA1

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

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