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Genetic and Functional Evidence of Complement Dysregulation in Multiple Myeloma Patients with Carfilzomib-Induced Thrombotic Microangiopathy Compared to Controls.

Eugenia GkaliagkousiDimitra DalampiraFoteini TheodorakakouChristine-Ivy LiacosNikolaos KanelliasEvangelos Eleutherakis-PapaiakovouEvangelos TerposMaria GavriatopoulouEvgenia VerrouTheodora TriantafyllouAggeliki SevastoudiEvaggelia-Evdoxia KoravouTasoula TouloumenidouChristos VarelasApostolia PapalexandriIoanna SakellariMeletios- Athanasios DimopoulosEfstathios KastritisEirini Katodritou
Published in: Journal of clinical medicine (2022)
We confirmed the previous findings that implicated complement-related genes in the pathogenesis of carfilzomib-induced TMA. Most importantly, by incorporating a control group of non-TMA MM patients treated with carfilzomib-based regimens and functional complement assays, we enhanced the credibility of our findings.
Keyphrases
  • multiple myeloma
  • high glucose
  • diabetic rats
  • drug induced
  • oxidative stress
  • endothelial cells
  • genome wide
  • stress induced
  • single cell