ArticleLaboratory investigation; a journal of technical methods and pathology2021
A MXI1-NUTM1 fusion protein with MYC-like activity suggests a novel oncogenic mechanism in a subset of NUTM1-rearranged tumors.
Article in Laboratory investigation; a journal of technical methods and pathology, 2021. 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, 23 citations in OpenAlex.
- Cross-cohort multi-omics analysis identifies novel clusters driven by epithelial-mesenchymal transition signatures in gastric cancer.Cancer cell international · 2026Article
- Advancing Understanding and Therapeutic Strategies for NUT Sarcomas: Comprehensive Review of the Literature and Two Cases.Journal of immunotherapy and precision oncology · 2025Review
- A novel MXI1-NUTM2B fusion detected in an undifferentiated ovarian cancer.Gynecologic oncology reports · 2025Article
- The expanding universe of NUTM1 fusions in pediatric cancer.Clinical and translational science · 2023Review
- Cancer-Specific Sequences in the Diagnosis and Treatment of NUT Carcinoma.Cancer research and treatment · 2023Article
- Case report: NUT carcinoma with MXI1::NUTM1 fusion characterized by abdominopelvic lesions and ovarian masses in a middle-aged female.Frontiers in oncology · 2022Article
- Review
- NUTM1-rearranged colorectal sarcoma: a clinicopathologically and genetically distinctive malignant neoplasm with a poor prognosis.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021Article
- Diagnosis of NUT Carcinoma Despite False-Negative Next-Generation Sequencing Results: A Case Report and Literature Review.OncoTargets and therapy · 2021Article
- RNA-Binding Proteins CLK1 and POP7 as Biomarkers for Diagnosis and Prognosis of Esophageal Squamous Cell Carcinoma.Frontiers in cell and developmental biology · 2021Article
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Authors and funding
19 authors at 5 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Most NUTM1-rearranged neoplasms (NRNs) have fusions between NUTM1 and BRD (bromodomain-containing) family members and are termed NUT carcinomas (NCs) because they show some squamous differentiation. However, some NRNs are associated with fusions between NUTM1 and members of the MAD (MAX dimerization) gene family of MYC antagonists. Here we describe a small round cell malignancy from the gastro-esophageal junction with a previously unreported fusion between NUTM1 and the MAD family member MXI1. In contrast to NCs, the MXI1-NUTM1 tumor did not show squamous differentiation and did not express MYC, TP63 or SOX2, genes known to be targets of BRD-NUTM1 proteins and critical for NC oncogenesis. Transcriptome analysis showed paradoxical enrichment of MYC target genes in the MXI1-NUTM1 tumor despite the lack of MYC expression. When expressed in vitro MXI1-NUTM1 partially phenocopied MYC, enhancing cell proliferation and cooperating with oncogenic HRAS to produce anchorage-independent cell growth. These data provide evidence that MAD family members, which are normally repressors of MYC activity, can be converted into MYC-like mimics by fusion to NUTM1. The pathological features and novel oncogenic mechanism of the MXI1-NUTM1 tumor show that identification of NUTM1 fusion partners can be important for accurate diagnostic classification of some NRN subtypes, and potentially may guide therapeutic options.
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