PUBLICATION

Famciclovir leads to failure of hematopoiesis, but may have the benefit of relieving myeloid expansion in MDS-like zebrafish

Authors
Li, J., Meng, P., Zhou, R., Zhang, Y., Lin, Q.
ID
ZDB-PUB-201120-162
Date
2020
Source
Toxicology and applied pharmacology   410: 115334 (Journal)
Registered Authors
Zhang, Yiyue, Zhou, Riyang
Keywords
C-Myb, Famciclovir, Hematotoxicity, MDS, Zebrafish
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Antiviral Agents/pharmacology
  • Antiviral Agents/therapeutic use*
  • Apoptosis/drug effects
  • Apoptosis/physiology
  • Famciclovir/pharmacology
  • Famciclovir/therapeutic use*
  • Hematopoiesis/drug effects*
  • Hematopoiesis/physiology
  • Hematopoietic Stem Cells/drug effects*
  • Hematopoietic Stem Cells/pathology
  • Hematopoietic Stem Cells/physiology
  • Myelodysplastic Syndromes/drug therapy*
  • Myelodysplastic Syndromes/genetics
  • Myelodysplastic Syndromes/pathology
  • Myeloid Cells/drug effects*
  • Myeloid Cells/pathology
  • Zebrafish
PubMed
33207248 Full text @ Tox. App. Pharmacol.
Abstract
Famciclovir (FCV) is an antiviral drug that is often utilized after bone marrow transplantation to prevent viral infection. Yet, its role in hematopoiesis is poorly understood. Here, by utilizing a zebrafish model, we found that FCV exposure led to hematopoietic failure by impairing the proliferation of hematopoietic stem and progenitor cell (HSPC) and inducing HSPC apoptosis. On the other hand, FCV treatment could effectively relieve myeloid malignancies in the c-mybhyper MDS-like fish model, and played a role not only in the embryonic stage but also in adult zebrafish. This study reveals that FCV functions as a double-edged sword, with hematotoxicity at a high level, but that appropriate FCV treatment may be beneficial for the treatment of MDS.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping