ArticleScience advances2021
Synthetic lethality across normal tissues is strongly associated with cancer risk, onset, and tumor suppressor specificity.
Article in Science advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Synthetic lethality in cancer therapy: Mechanisms, models and clinical translation for overcoming therapeutic resistance.Clinical and translational medicine · 2026Review
- Chromosome 7 Gain Compensates for Chromosome 10 Loss in Glioma.Cancer research · 2024Article
- Deciphering gene expression patterns using large-scale transcriptomic data and its applications.Briefings in bioinformatics · 2024Article
- Cryo-shocked tumor cells deliver CRISPR-Cas9 for lung cancer regression by synthetic lethality.Science advances · 2024Article
- Review
- Genome mining yields putative disease-associated ROMK variants with distinct defects.PLoS genetics · 2023Article
- A landscape of response to drug combinations in non-small cell lung cancer.Nature communications · 2023Article
- Using graph-based model to identify cell specific synthetic lethal effects.Computational and structural biotechnology journal · 2023Article
- Big data in basic and translational cancer research.Nature reviews. Cancer · 2022Review
- Article
- Computational methods, databases and tools for synthetic lethality prediction.Briefings in bioinformatics · 2022Review
- Synthetic lethality-based prediction of anti-SARS-CoV-2 targets.bioRxiv : the preprint server for biology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
Various characteristics of cancers exhibit tissue specificity, including lifetime cancer risk, onset age, and cancer driver genes. Previously, the large variation in cancer risk across human tissues was found to strongly correlate with the number of stem cell divisions and abnormal DNA methylation levels. Here, we study the role of synthetic lethality in cancer risk. Analyzing normal tissue transcriptomics data in the Genotype-Tissue Expression project, we quantify the extent of co-inactivation of cancer synthetic lethal (cSL) gene pairs and find that normal tissues with more down-regulated cSL gene pairs have lower and delayed cancer risk. Consistently, more cSL gene pairs become up-regulated in cells treated by carcinogens and throughout premalignant stages in vivo. We also show that the tissue specificity of numerous tumor suppressor genes is associated with the expression of their cSL partner genes across normal tissues. Overall, our findings support the possible role of synthetic lethality in tumorigenesis.
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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.