ArticleNature communications2020
Loss of heterozygosity of essential genes represents a widespread class of potential cancer vulnerabilities.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 111 citations in OpenAlex.
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- G-quadruplexes regulate chromatin accessibility and gene expression in Bloom Syndrome.bioRxiv : the preprint server for biology · 2026Article
- Mutation-informed gene pairs to predict melanoma metastasis.Cell communication and signaling : CCS · 2026Article
- DNA Damage and Repair in Thyroid Physiology and Disease.Endocrine reviews · 2026Review
- Modeling and targeting general and chromosome-specific aneuploidy in cancer.Genes & development · 2025Review
- Germline analysis of an international cohort of pediatric diffuse midline glioma patients.Neuro-oncology · 2025Article
- Characterization of a novel comprehensive genomic profiling test with better detection of heterozygous deletions and RNA-based gene fusion analysis.The oncologist · 2025Article
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- Diploidy confers genomic instability inbioRxiv : the preprint server for biology · 2025Article
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- The dynamics of loss of heterozygosity events in genomes.EMBO reports · 2025Review
- Immunogenomic determinants of exceptional response to immune checkpoint inhibition in renal cell carcinoma.Nature cancer · 2025Article
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- A compendium of Amplification-Related Gain Of Sensitivity genes in human cancer.Nature communications · 2025Article
- BRCA1 & BRCA2 methylation as a prognostic and predictive biomarker in cancer: Implementation in liquid biopsy in the era of precision medicine.Clinical epigenetics · 2024Review
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- Pathogenic nsSNPs of protein kinase C-eta with hepatocellular carcinoma susceptibility.Cancer cell international · 2024Article
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10 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Alterations in non-driver genes represent an emerging class of potential therapeutic targets in cancer. Hundreds to thousands of non-driver genes undergo loss of heterozygosity (LOH) events per tumor, generating discrete differences between tumor and normal cells. Here we interrogate LOH of polymorphisms in essential genes as a novel class of therapeutic targets. We hypothesized that monoallelic inactivation of the allele retained in tumors can selectively kill cancer cells but not somatic cells, which retain both alleles. We identified 5664 variants in 1278 essential genes that undergo LOH in cancer and evaluated the potential for each to be targeted using allele-specific gene-editing, RNAi, or small-molecule approaches. We further show that allele-specific inactivation of either of two essential genes (PRIM1 and EXOSC8) reduces growth of cells harboring that allele, while cells harboring the non-targeted allele remain intact. We conclude that LOH of essential genes represents a rich class of non-driver cancer vulnerabilities.
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