ArticleCell stem cell2022
Lamin B1 deletion in myeloid neoplasms causes nuclear anomaly and altered hematopoietic stem cell function.
Article in Cell stem cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Lamin B1-dependent regulation of human separase in mitosis.Nucleic acids research · 2026Article
- A generalizable Hi-C foundation model for chromatin architecture, single-cell and multiomics analysis across species.Nature methods · 2026Article
- Lamin B1 safeguards the B cell genome and shapes lymphoma outcome.HemaSphere · 2026Article
- Nuclear Lamins: A Molecular Bridge Coupling Extracellular Mechanical Cues to Intranuclear Signal Transduction and Gene Regulation.International journal of molecular sciences · 2026Review
- Shaping neutrophil morphology and function: the importance of a segmented nucleus.Nature reviews. Immunology · 2026Review
- Dynamic changes in Lamin B1 and heterochromatin coincide with chromatin condensation during human erythropoiesis.Genome biology · 2026Article
- An integrated multi-omics and network analysis of neutrophil differentiation from initial- to late-stage.Genome biology · 2026Article
- Modeling myeloid cell development in health and disease using induced pluripotent stem cells.Frontiers in immunology · 2026Review
- 3D Genome Architecture in Stem Cell Lineage Commitment: from Structural Organization to Precision Regulation.Advanced genetics (Hoboken, N.J.) · 2025Review
- First evidence of coexistence of Pseudo Pelger Huet anomaly and balanced translocation in a two decades retrospectively exposed human subject.Scientific reports · 2025Article
- A SETD2-CDK1-lamin axis maintains nuclear morphology and genome stability.Nature cell biology · 2025Article
- The synergistic effect of c-Myb hyperactivation and Pu.1 deficiency induces Pelger-Huët anomaly and promotes sAML.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Understanding Human Oncogene Function and Cooperativity in Myeloid Malignancy Using iPSCs.Experimental hematology · 2025Review
- Review
- Cancer Stemness Online: A Resource for Investigating Cancer Stemness and Associations with Immune Response.Genomics, proteomics & bioinformatics · 2024Article
- Microarray analysis points to LMNB1 and JUN as potential target genes for predicting metastasis promotion by etoposide in colorectal cancer.Scientific reports · 2024Article
- Chromatin organization in myelodysplastic syndrome.Experimental hematology · 2024Review
- Enhancer-activated RET confers protection against oxidative stress to KMT2A-rearranged acute myeloid leukemia.Cancer science · 2024Article
- Review
- A comprehensive method to study the DNA's association with lamin and chromatin compaction in intact cell nuclei at super resolution.Nanoscale · 2023Article
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
Abnormal nuclear morphology is a hallmark of malignant cells widely used in cancer diagnosis. Pelger-Huët anomaly (PHA) is a common abnormality of neutrophil nuclear morphology of unknown molecular etiology in myeloid neoplasms (MNs). We show that loss of nuclear lamin B1 (LMNB1) encoded on chromosome 5q, which is frequently deleted in MNs, induces defects in nuclear morphology and human hematopoietic stem cell (HSC) function associated with malignancy. LMNB1 deficiency alters genome organization inducing in vitro and in vivo expansion of HSCs, myeloid-biased differentiation with impaired lymphoid commitment, and genome instability due to defective DNA damage repair. Nuclear dysmorphology of neutrophils in patients with MNs is associated with 5q deletions spanning the LMNB1 locus, and lamin B1 loss is both necessary and sufficient to cause PHA in normal and 5q-deleted neutrophils. LMNB1 loss thus causes acquired PHA and links abnormal nuclear morphology with HSCs and progenitor cell fate determination via genome organization.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.