ArticleNature genetics2020
Discovery of regulatory noncoding variants in individual cancer genomes by using cis-X.
Article in Nature genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 68 citations in OpenAlex.
- Reactivation of a TAL1 progenitor cell enhancer region by non-coding somatic variants in T-lineage acute lymphoblastic leukemia.bioRxiv : the preprint server for biology · 2026Article
- Mechanisms of enhancer-driven oncogene activation.International journal of cancer · 2026Review
- Article
- Towards methylation-based redefinition of TAL1 positive T-cell acute lymphoblastic leukaemia (T-ALL).Leukemia · 2025Article
- The Noncoding Mutational Landscape of Pancreatic Cancer Reveals Recurrent Somatic Mutations in Enhancer Regions.Cancer research communications · 2025Article
- Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q.Blood cancer discovery · 2025Article
- Allelic expression patterns of imprinted and non-imprinted genes in cancer cell lines from multiple histologies.Clinical epigenetics · 2025Article
- An Overview of Analytical Approaches to Cancer Proteogenomics.Methods in molecular biology (Clifton, N.J.) · 2025Review
- Origins and impact of extrachromosomal DNA.Nature · 2024Article
- HYENA detects oncogenes activated by distal enhancers in cancer.Nucleic acids research · 2024Article
- Oncogenic Enhancers in Leukemia.Blood cancer discovery · 2024Review
- Article
- Developmental origins shape the paediatric cancer genome.Nature reviews. Cancer · 2024Review
- HYENA detects oncogenes activated by distal enhancers in cancer.bioRxiv : the preprint server for biology · 2024Article
- Genetic and epigenetic features of bilateral Wilms tumor predisposition in patients from the Children's Oncology Group AREN18B5-Q.Nature communications · 2023Article
- Chromatin accessibility landscape of relapsed pediatric B-lineage acute lymphoblastic leukemia.Nature communications · 2023Article
- Transcriptome sequencing identifies novel EVX fusions involved in transcriptional activation of HOX family genes in pediatric immature T-cell acute lymphoblastic leukemia: two cases reports and a literature review.International journal of hematology · 2023Review
- Allele-specific RNAGenome research · 2023Article
- Functional analysis of structural variants in single cells using Strand-seq.Nature biotechnology · 2023Article
- TAL1 activation in T-cell acute lymphoblastic leukemia: a novel oncogenic 3' neo-enhancer.Haematologica · 2023Article
Corrections and comments
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Authors and funding
22 authors at 4 institutions in 2 countries.
Funding
Abstract
We developed cis-X, a computational method for discovering regulatory noncoding variants in cancer by integrating whole-genome and transcriptome sequencing data from a single cancer sample. cis-X first finds aberrantly cis-activated genes that exhibit allele-specific expression accompanied by an elevated outlier expression. It then searches for causal noncoding variants that may introduce aberrant transcription factor binding motifs or enhancer hijacking by structural variations. Analysis of 13 T-lineage acute lymphoblastic leukemias identified a recurrent intronic variant predicted to cis-activate the TAL1 oncogene, a finding validated in vivo by chromatin immunoprecipitation sequencing of a patient-derived xenograft. Candidate oncogenes include the prolactin receptor PRLR activated by a focal deletion that removes a CTCF-insulated neighborhood boundary. cis-X may be applied to pediatric and adult solid tumors that are aneuploid and heterogeneous. In contrast to existing approaches, which require large sample cohorts, cis-X enables the discovery of regulatory noncoding variants in individual cancer genomes.
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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.