A decade of progress in myelodysplastic syndrome with chromosome 5q deletion
Abstract
There are few instances in oncology where reciprocal clinical and laboratory translation studies have accelerated the understanding of disease biology and treatment more so than the decade following the Food and Drug Administration (FDA) approval of lenalidomide (Revlimid TM; Celgene Corporation, Summit, NJ, USA) for the treatment of patients with myelodysplastic syndrome (MDS) and chromosome 5q deletion (del(5q)). Lenalidomide was approved by the FDA in December 2005 on the merits of a multicenter phase 2 study, which demonstrated sustained and prolonged transfusion independence in the majority of participants. Since then, del(5q) MDS has emerged as one of the best characterized bone marrow malignancies and, in particular, has raised our understanding as to how allelic haplodeficiency underlies both its hematological phenotype and the selective sensitivity to lenalidomide by virtue of synthetic lethality. Herein, we review the clinical and biological discoveries that have advanced our understanding of del(5q) MDS and its treatment since its approval by United States and European regulatory agencies.
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Mutations in TP53 lead to resistance to lenalidomide in patients with MDS.
“Accordingly, mutations in TP53 lead to resistance to lenalidomide in patients with MDS97,98 (FIG. 3).”
From Cancer therapies based on targeted protein degradation — lessons learned with lenalidomide (2021) · cites this paper as [97]
Altered regulation of gene expression as a result of IKZF1 degradation might also contribute to responsiveness of myeloid malignancies to lenalidomide.
“Thus, altered regulation of gene expression as a result of IKZF1 degradation might also contribute to responsiveness of myeloid malignancies to lenalidomide97,101.”
From Cancer therapies based on targeted protein degradation — lessons learned with lenalidomide (2021) · cites this paper as [97]
Sequencing of matched clinical specimens has identified RUNX1 mutations associated with lenalidomide resistance.
“sequencing of matched clinical specimens has identified RUNX1 mutations that are associated with lenalidomide resistance97.”
From Cancer therapies based on targeted protein degradation — lessons learned with lenalidomide (2021) · cites this paper as [97]
Lenalidomide-mediated depletion of IKZF1 in del(5q) MDS cells drives RUNX1 upregulation and megakaryocyte differentiation.
“Similarly, lenalidomide-mediated depletion of IKZF1 in del(5q) MDS cells drives RUNX1 upregulation and megakaryocyte differentiation”
From Cancer therapies based on targeted protein degradation — lessons learned with lenalidomide (2021) · cites this paper as [97]
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Current Therapeutic Landscape in Lower Risk Myelodysplastic Syndromes
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- Authors
- List, A., Ebert, B. L., & Fenaux, P.
- Affiliations
- Moffitt Cancer Center (US)
- Dana-Farber Cancer Institute (US)
- Assistance Publique – Hôpitaux de Paris (FR)
- Corresponding author
- Fenaux, Pierre
- Venue
- Leukemia
- Published
- 2018-01-30
- Volume
- 32
- Issue
- 7
- Pages
- 1493-1499
- ISSN
- 0887-6924 (ISSN-L)
- 1476-5551
- OpenAlex
- W2789938738
- Cited by
- 49
- References
- 48
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 6 · 2023: 6 · 2022: 8 · 2021: 9 · 2020: 4 · 2019: 8 · 2018: 5 · 2014: 1
- FWCI
- 1.07
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Leukemia (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL082945)
- National Cancer Institute (P01CA066996)
- Topics
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Degradation and Inhibitors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Keywords
- myelodysplastic syndrome, chromosome 5q deletion, lenalidomide, synthetic lethality, transfusion independence, clinical translation, FDA approval
- MeSH terms
- Drug Development, Lenalidomide, Animals, Chromosome Aberrations, Chromosome Deletion, Chromosomes, Human, Pair 5, Humans, Mutation, Myelodysplastic Syndromes, Prognosis, Leukemia, Myeloid, Acute, Tumor Suppressor Protein p53, Treatment Outcome, Disease Progression, Genetic Heterogeneity, Disease Management, Genetic Predisposition to Disease
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