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Complex synthetic lethality in cancer
The concept of synthetic lethality has been widely applied to identify therapeutic targets in cancer, with varying degrees of success. …
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Gene essentiality in cancer is better predicted by mRNA abundance than by gene regulatory network-inferred activity
Gene regulatory networks (GRNs) are often deregulated in tumor cells, resulting in altered transcriptional programs that facilitate …
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Paralog dispensability shapes homozygous deletion patterns in tumor genomes
Genomic instability is a hallmark of cancer, resulting in tumor genomes having large numbers of genetic aberrations, including …
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Genetic interactions under the microscope
Traditional genetic interaction screens profile phenotypes at aggregate level, missing interactions that may influence the distribution …
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Antibody reliability influences observed mRNA–protein correlations in tumour samples
Reverse phase protein arrays (RPPA) have been used to quantify the abundance of hundreds of proteins across thousands of tumour samples …
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Targeting synthetic lethal paralogs in cancer
Synthetic lethal interactions, where mutation of one gene renders cells sensitive to inhibition of another gene, can be exploited for …
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Experimental reproducibility limits the correlation between mRNA and protein abundances in tumour proteomic profiles
Large-scale studies of human proteomes have revealed only a moderate correlation between mRNA and protein abundances. It is unclear to …
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Comprehensive prediction of robust synthetic lethality between paralog pairs in cancer cell lines
Pairs of paralogs may share common functionality and, hence, display synthetic lethal interactions. As the majority of human genes have …
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Proteomic signatures of radioresistance: Alteration of inflammation, angiogenesis and metabolism-related factors in radioresistant oesophageal adenocarcinoma
The clinical management of locally advanced oesophageal adenocarcinoma (OAC) involves neoadjuvant chemoradiotherapy (CRT), but as …
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Cross-species identification of PIP5K1-, splicing-and ubiquitin-related pathways as potential targets for RB1-deficient cells
The RB1 tumor suppressor is recurrently mutated in a variety of cancers including retinoblastomas, small cell lung cancers, …
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