| Autor: |
Li, Jianping, Kulis, Marta, Riva, Alberto, Casellas Román, Heidi, Dupere-Richer, Daphne, Clerio, Monica, Trejo, Melanie L., Menes, Michael, Lamberto, Anthony Joseph, Sobh, Amin, Kaestner, Charlotte Leonie, Bennett, Richard Lynn, Martin Subero, Iñaki I., Licht, Jonathan D. |
| Zdroj: |
Blood; November 2023, Vol. 142 Issue: 1, Number 1 Supplement 1 p2771-2771, 1p |
| Abstrakt: |
Background:NSD2/MMSET/WHSC1, a histone lysine methyltransferase (HMT), is an oncoprotein first characterized by its overexpression in multiple myeloma (MM). NSD2mutations within the catalytic SET domain are frequently identified in lymphoid malignancies including acute lymphoblastic leukemia (ALL), chronic lymphocytic leukemia (CLL), and mantle cell lymphoma (MCL). We previously demonstrated that NSD2p.E1099K mutation caused an imbalance of H3K36me2/H3K27me3 and drove glucocorticoid resistance in pediatric ALL. In MCL, NSD2mutations, especially p.E1099K and p.T1150A, are found in 10-15% of cases of MCL and are enriched in MCL patients who relapse from targeted therapies such as ibrutinib, an inhibitor of B cell signaling. However, the activity of NSD2mutations in MCL remains unexplored. We hypothesize that NSD2mutations contribute to disease progression and therapy resistance due to aberrant chromatin modification. |
| Databáze: |
Supplemental Index |
| Externí odkaz: |
|
