ReviewNature reviews. Cancer2019
Targeting chromatin complexes in fusion protein-driven malignancies.
Review in Nature reviews. Cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.
- The Significance of theFrontiers in oncology · 2020Pooled it
- Pediatric sarcomas: challenges and opportunities.Genes & development · 2026Review
- Nanoscale Analysis beyond Imaging by Atomic Force Microscopy: Molecular Perspectives on Oncology and Neurodegeneration.Small science · 2025Review
- Phase-separating fusion proteins drive cancer by upsetting transcription regulation.Genome biology · 2025Article
- RNA-mediated condensation of TFE3 oncofusions facilitates transcriptional hub formation to promote translocation renal cell carcinoma.Nature communications · 2025Article
- FET fusion oncoproteins enrich SWI/SNF complex subtypes and interaction partners.Cellular & molecular biology letters · 2025Article
- Tumor-Immune Interactions in Pediatric Oral Rhabdomyosarcoma: A Narrative Review on Immuno-Oncology and Emerging Therapies.Children (Basel, Switzerland) · 2025Review
- Identification of malignant cells in single-cell transcriptomics data.Communications biology · 2025Review
- KAT6A chimeras form a self-reinforcing epigenetic module with NURF and MLL/COMPASS to sustain AML.Genome biology · 2025Article
- CRISPR screening reveals that RNA helicase DDX41 triggers ribosome biogenesis and cancer progression through R-loop-mediated RPL/RPS transcription.Nature communications · 2025Article
- Subversion of mRNA degradation pathways by EWSR1::FLI1 represents a therapeutic vulnerability in Ewing sarcoma.Nature communications · 2025Article
- Article
- Phase Separation in Chromatin Organization and Human Diseases.International journal of molecular sciences · 2025Review
- Transcription regulation by biomolecular condensates.Nature reviews. Molecular cell biology · 2025Review
- Biomolecular condensation of human IDRs initiates endogenous transcription via intrachromosomal looping or high-density promoter localization.Nucleic acids research · 2025Article
- Short circuit: Transcription factor addiction as a growing vulnerability in cancer.Current opinion in structural biology · 2024Review
- Unraveling molecular similarities between colorectal polyps and colorectal cancer: a systems biology approach.Intestinal research · 2024Article
- Targeting the epigenome to reinvigorate T cells for cancer immunotherapy.Military Medical Research · 2023Review
- Immunoproteasome function maintains oncogenic gene expression in KMT2A-complex driven leukemia.Molecular cancer · 2023Article
- The oncogenic fusion protein TAZ::CAMTA1 promotes genomic instability and senescence through hypertranscription.Communications biology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Recurrent chromosomal rearrangements leading to the generation of oncogenic fusion proteins are a common feature of many cancers. These aberrations are particularly prevalent in sarcomas and haematopoietic malignancies and frequently involve genes required for chromatin regulation and transcriptional control. In many cases, these fusion proteins are thought to be the primary driver of cancer development, altering chromatin dynamics to initiate oncogenic gene expression programmes. In recent years, mechanistic insights into the underlying molecular functions of a number of these oncogenic fusion proteins have been discovered. These insights have allowed the design of mechanistically anchored therapeutic approaches promising substantial treatment advances. In this Review, we discuss how our understanding of fusion protein function is informing therapeutic innovations and illuminating mechanisms of chromatin and transcriptional regulation in cancer and normal cells.
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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.