ArticleCell systems2017
Widespread Post-transcriptional Attenuation of Genomic Copy-Number Variation in Cancer.
Article in Cell systems, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.
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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
76 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.
- Systematic identification of mutations and copy number alterations associated with cancer patient prognosis.eLife · 2018Pooled it
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- The Role of Aurora Kinase A in HBV-Associated Hepatocellular Carcinomas: A Molecular and Immunohistochemical Study.Diagnostics (Basel, Switzerland) · 2026Article
- Divergent proteome tolerance against gain and loss of chromosome arms.Molecular cell · 2025Article
- Proteomic compensation by paralogs preserves protein interaction networks after gene loss in cancer.Molecular systems biology · 2025Article
- Tumor break load quantitates structural variant-associated genomic instability with biological and clinical relevance across cancers.NPJ precision oncology · 2025Article
- Real-time functional proteomics enhances therapeutic targeting in precision oncology molecular tumor boards.NPJ precision oncology · 2025Article
- Dynamics of Single-Cell Protein Covariation during Epithelial-Mesenchymal Transition.Journal of proteome research · 2025Article
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- A compendium of Amplification-Related Gain Of Sensitivity genes in human cancer.Nature communications · 2025Article
- Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Copy-number variations (CNVs) are ubiquitous in cancer and often act as driver events, but the effects of CNVs on the proteome of tumors are poorly understood. Here, we analyze recently published genomics, transcriptomics, and proteomics datasets made available by CPTAC and TCGA consortia on 282 breast, ovarian, and colorectal tumor samples to investigate the impact of CNVs in the proteomes of these cells. We found that CNVs are buffered by post-transcriptional regulation in 23%-33% of proteins that are significantly enriched in protein complex members. Our analyses show that complex subunits are highly co-regulated, and some act as rate-limiting steps of complex assembly, as their depletion induces decreased abundance of other complex members. We identified 48 such rate-limiting interactions and experimentally confirmed our predictions on the interactions of AP3B1 with AP3M1 and GTF2E2 with GTF2E1. This study highlights the importance of post-transcriptional mechanisms in cancer that allow cells to cope with their altered 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.