ArticleNature2012
Passenger deletions generate therapeutic vulnerabilities in cancer.
Article in Nature, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 232 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
232 citing papers in PubMed, 353 citations in OpenAlex.
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- TNG961 Is a Selective Oral HBS1L Molecular Glue Degrader for the Treatment of FOCAD-Deleted Cancers.Cancer discovery · 2026Article
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- Targeting enolase isoenzyme 2 enables precision glycolysis inhibition in VHL-mutant renal cell carcinoma.Cell death & disease · 2026Article
- Context-dependent synthetic lethality - an emerging precision therapeutic approach.Nature reviews. Cancer · 2026Review
- 1p/19q codeletion induces targetable and imageable vulnerabilities in glucose metabolism in oligodendrogliomas.Neuro-oncology · 2026Article
- IGF2BP3 promotes glycolysis of osteosarcoma stem cells by reading RNA m⁶A to stabilize ENO1 and promote malignant biological behavior of osteosarcoma.Cell biology and toxicology · 2026Article
- Enolase 1: A paradigm of metabolic enzyme moonlighting in tumorigenesis (Review).International journal of oncology · 2026Review
- An integrated network toxicology and multi-omics study identifies ENO1 as a candidate mediator in benzo[a]pyrene-related gastric cancer progression.Frontiers in pharmacology · 2026Article
- Passenger co-deletion confounds glutaminolysis signatures anchored on PTEN loss: A cautionary case for location-aware signature design.PloS one · 2026Article
- Collateral lethality of NAD kinase in 1p36 deleted tumors drives vulnerability to NAD kinase 2 depletion.BBA advances · 2026Article
- Synthetic lethality in cancer drug discovery: challenges and opportunities.Nature reviews. Drug discovery · 2026Review
- Collateral metabolic vulnerabilities unveiled by loss of isozyme diversity in breast cancer.Genome medicine · 2025Article
- Epigenetic targeting of PGBD5-dependent DNA damage in SMARCB1-deficient sarcomas.The Journal of clinical investigation · 2025Article
- Modeling and targeting general and chromosome-specific aneuploidy in cancer.Genes & development · 2025Review
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- The Landscape of Cancer Metabolism as a Therapeutic Target.Pathology international · 2025Review
- Cytidine diphosphate diacylglycerol synthase 2 is a synthetic lethal target in mesenchymal-like cancers.Nature genetics · 2025Article
- Incomplete paralog compensation generates selective dependency on TRA2A in cancer.PLoS genetics · 2025Article
- Warburg effect and lactylation in cancer: mechanisms for chemoresistance.Molecular medicine (Cambridge, Mass.) · 2025Review
172 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Commented on by
- Erratum issued
Authors and funding
22 authors at 3 institutions in 1 country.
Funding
Abstract
Inactivation of tumour-suppressor genes by homozygous deletion is a prototypic event in the cancer genome, yet such deletions often encompass neighbouring genes. We propose that homozygous deletions in such passenger genes can expose cancer-specific therapeutic vulnerabilities when the collaterally deleted gene is a member of a functionally redundant family of genes carrying out an essential function. The glycolytic gene enolase 1 (ENO1) in the 1p36 locus is deleted in glioblastoma (GBM), which is tolerated by the expression of ENO2. Here we show that short-hairpin-RNA-mediated silencing of ENO2 selectively inhibits growth, survival and the tumorigenic potential of ENO1-deleted GBM cells, and that the enolase inhibitor phosphonoacetohydroxamate is selectively toxic to ENO1-deleted GBM cells relative to ENO1-intact GBM cells or normal astrocytes. The principle of collateral vulnerability should be applicable to other passenger-deleted genes encoding functionally redundant essential activities and provide an effective treatment strategy for cancers containing such genomic events.
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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.