ArticleBlood advances2024
Monosomy 7/del(7q) cause sensitivity to inhibitors of nicotinamide phosphoribosyltransferase in acute myeloid leukemia.
Article in Blood advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- Article
- NAMPT haploinsufficiency is a therapeutic vulnerability to NAMPT inhibition in -7/-7q MDS.Biomarker research · 2026Article
- [Clinical characteristics and prognostic analysis of pediatric acute myeloid leukemia with -7/7q- abnormalities].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026Article
- From transcriptomic profiling to precision oncology: a bibliometric analysis of RNA sequencing in acute myeloid leukemia.Frontiers in medicine · 2026Article
- Pediatric Acute Megakaryoblastic Leukemia with a GATA2 Mutation and Monosomy 7: A Case Report and Clinical Management Challenges.Reports (MDPI) · 2025Article
- Acquired resistance in cancer: towards targeted therapeutic strategies.Nature reviews. Cancer · 2025Review
- NAMPT haploinsufficiency is a collateral lethal therapeutic vulnerability in high-risk myeloid malignancies withBlood neoplasia · 2025Article
- PRC2-mediated apoptosis evasion is a therapeutic target of MDS/AML harboring inv(3)/t(3;3) and monosomy 7.HemaSphere · 2025Article
- Precision Medicine in Myeloid Neoplasia: Challenges and Opportunities.Journal of personalized medicine · 2025Review
- A line in shifting sand: Can we define and target TP53 mutated MDS?Seminars in hematology · 2024Review
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Authors and funding
9 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
abstractMonosomy 7 and del(7q) (-7/-7q) are frequent chromosomal abnormalities detected in up to 10% of patients with acute myeloid leukemia (AML). Despite unfavorable treatment outcomes, no approved targeted therapies exist for patients with -7/-7q. Therefore, we aimed to identify novel vulnerabilities. Through an analysis of data from ex vivo drug screens of 114 primary AML samples, we discovered that -7/-7q AML cells are highly sensitive to the inhibition of nicotinamide phosphoribosyltransferase (NAMPT). NAMPT is the rate-limiting enzyme in the nicotinamide adenine dinucleotide salvage pathway. Mechanistically, the NAMPT gene is located at 7q22.3, and deletion of 1 copy due to -7/-7q results in NAMPT haploinsufficiency, leading to reduced expression and a therapeutically targetable vulnerability to the inhibition of NAMPT. Our results show that in -7/-7q AML, differentiated CD34+CD38+ myeloblasts are more sensitive to the inhibition of NAMPT than less differentiated CD34+CD38- myeloblasts. Furthermore, the combination of the BCL2 inhibitor venetoclax and the NAMPT inhibitor KPT-9274 resulted in the death of significantly more leukemic blasts in AML samples with -7/-7q than the NAMPT inhibitor alone. In conclusion, our findings demonstrate that AML with -7/-7q is highly sensitive to NAMPT inhibition, suggesting that NAMPT inhibitors have the potential to be an effective targeted therapy for patients with monosomy 7 or del(7q).
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