Journal
EXPERIMENTAL HEMATOLOGY & ONCOLOGY
Volume 3, Issue -, Pages -Publisher
BMC
DOI: 10.1186/2162-3619-3-13
Keywords
Cohesin; Mutation; RUNX1; Myeloid; Leukemia; Transcription
Categories
Funding
- Royal Society of NZ Marsden Fund [11-UOO-027, 10-UOA-023]
- Leukemia & Blood Cancer NZ (JAH), Gravida Centre for Growth and Development (JAH/JOS)
- Maurice Wilkins Centre for Molecular Biodiscovery (JAH/JOS)
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Recently, whole genome sequencing approaches have pinpointed mutations in genes that were previously not associated with cancer. For Acute Myeloid Leukaemia (AML), and other myeloid disorders, these approaches revealed a high prevalence of mutations in genes encoding the chromosome cohesion complex, cohesin. Cohesin mutations represent a novel genetic pathway for AML, but how AML arises from these mutations is unknown. This review will explore the potential mechanisms by which cohesin mutations contribute to AML and other myeloid malignancies.
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