ArticleOncogene1999
A role for PML and the nuclear body in genomic stability.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
95 citing papers in PubMed, 231 citations in OpenAlex.
- Trial
- Distinct ATRX functions cooperate with 9-1-1 and CST complexes to safeguard replication and telomere integrity.Nature structural & molecular biology · 2026Article
- Mitotic BLM functions are required to maintain genomic stability.Nucleic acids research · 2026Article
- TRIM24 directs replicative stress responses to maintain ALT telomeres via chromatin signaling.Molecular cell · 2025Article
- Liquid-liquid phase separation of membrane-less condensates: from biogenesis to function.Frontiers in cell and developmental biology · 2025Review
- Function of PML-RARA in Acute Promyelocytic Leukemia.Advances in experimental medicine and biology · 2024Review
- Structural Basis of PML-RARA Oncoprotein Targeting by Arsenic Unravels a Cysteine Rheostat Controlling PML Body Assembly and Function.Cancer discovery · 2023Article
- Single-Cell, High-Content Microscopy Analysis of BK Polyomavirus Infection.Microbiology spectrum · 2023Article
- Alterations induced by the PML-RARα oncogene revealed by image cross correlation spectroscopy.Biophysical journal · 2022Article
- Review
- Vpu modulates DNA repair to suppress innate sensing and hyper-integration of HIV-1.Nature microbiology · 2020Article
- PML Regulates the Epidermal Differentiation Complex and Skin Morphogenesis during Mouse Embryogenesis.Genes · 2020Article
- PML2-mediated thread-like nuclear bodies mark late senescence in Hutchinson-Gilford progeria syndrome.Aging cell · 2020Article
- Telomere length heterogeneity in ALT cells is maintained by PML-dependent localization of the BTR complex to telomeres.Genes & development · 2020Article
- Who's In and Who's Out-Compositional Control of Biomolecular Condensates.Journal of molecular biology · 2018Review
- Pml nuclear body disruption cooperates in APL pathogenesis and impairs DNA damage repair pathways in mice.Blood · 2018Article
- Multimodal Light Microscopy Approaches to Reveal Structural and Functional Properties of Promyelocytic Leukemia Nuclear Bodies.Frontiers in oncology · 2018Review
- Around and beyond 53BP1 Nuclear Bodies.International journal of molecular sciences · 2017Review
- PML is a ROS sensor activating p53 upon oxidative stress.The Journal of experimental medicine · 2017Article
- Host cell restriction factors that limit transcription and replication of human papillomavirus.Virus research · 2017Review
35 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The PML gene of acute promyelocytic leukemia (APL) encodes a cell-growth and tumor suppressor. PML localizes to discrete nuclear bodies (NBs) that are disrupted in APL cells. The Bloom syndrome gene BLM encodes a RecQ DNA helicase, whose absence from the cell results in genomic instability epitomized by high levels of sister-chromatid exchange (SCE) and cancer predisposition. We show here that BLM co-localizes with PML to the NB. In cells from persons with Bloom syndrome the localization of PML is unperturbed, whereas in APL cells carrying the PML-RARalpha oncoprotein, both PML and BLM are delocalized from the NB into microspeckled nuclear regions. Treatment with retinoic acid (RA) induces the relocalization of both proteins to the NB. In primary PML-/- cells, BLM fails to accumulate in the NB. Strikingly, in PML-/- cells the frequency of SCEs is increased relative to PML+/+ cells. These data demonstrate that BLM is a constituent of the NB and that PML is required for its accumulation in these nuclear domains and for the normal function of BLM. Thus, our findings suggest a role for BLM in APL pathogenesis and implicate the PML NB in the maintenance of genomic stability.
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What OpenQuestion holds
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.