ArticleCell reports2021
Copy number aberrations drive kinase rewiring, leading to genetic vulnerabilities in cancer.
Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- A pan-cancer analysis of the oncogenic role of KDELR2 in human cancers.Discover oncology · 2025Article
- CNRein: an evolution-aware deep reinforcement learning algorithm for single-cell DNA copy number calling.Genome biology · 2025Article
- ARHGEF17/TEM4 regulates the cell cycle through control of G1 progression.The Journal of cell biology · 2025Article
- Insights into the Clinical, Biological and Therapeutic Impact of Copy Number Alteration in Cancer.International journal of molecular sciences · 2024Review
- The Reign of Follistatin in Tumors and Their Microenvironment: Implications for Drug Resistance.Biology · 2024Review
- CNAViz: An interactive webtool for user-guided segmentation of tumor DNA sequencing data.PLoS computational biology · 2022Article
- Molecular Subtyping of Cancer Based on Robust Graph Neural Network and Multi-Omics Data Integration.Frontiers in genetics · 2022Article
- A commercial ARHGEF17/TEM4 antibody cross-reacts with Nuclear Mitotic Apparatus protein 1 (NuMA).PloS one · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Somatic DNA copy number variations (CNVs) are prevalent in cancer and can drive cancer progression, albeit with often uncharacterized roles in altering cell signaling states. Here, we integrate genomic and proteomic data for 5,598 tumor samples to identify CNVs leading to aberrant signal transduction. The resulting associations recapitulate known kinase-substrate relationships, and further network analysis prioritizes likely causal genes. Of the 303 significant associations we identify from the pan-tumor analysis, 43% are replicated in cancer cell lines, including 44 robust gene-phosphosite associations identified across multiple tumor types. Several predicted regulators of hippo signaling are experimentally validated. Using RNAi, CRISPR, and drug screening data, we find evidence of kinase addiction in cancer cell lines, identifying inhibitors for targeting of kinase-dependent cell lines. We propose copy number status of genes as a useful predictor of differential impact of kinase inhibition, a strategy that may be of use in the future for anticancer therapies.
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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.