ArticleNature biotechnology2016
Characterizing genomic alterations in cancer by complementary functional associations.
Article in Nature biotechnology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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.
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Who cites it
62 citing papers in PubMed.
- Stress adaptation pathways and HA-CD44 signaling maintain the survival of pancreatic cancer cells with centrosome amplification.Cell communication and signaling : CCS · 2026Article
- Article
- Synthetic lethality in cancer drug discovery: challenges and opportunities.Nature reviews. Drug discovery · 2026Review
- Integrated computational and experimental approach to identify Nrf2-regulated molecular targets in cerebral ischemia.Pharmacological reports : PR · 2025Article
- Androgen receptor-mediated regulation of BRCA1 modulates the antioxidant defense in prostate cancer.The Journal of pathology · 2025Article
- Self-amplifying NRF2-EZH2 epigenetic loop converts KRAS-initiated progenitors to invasive pancreatic cancer.Nature cancer · 2025Article
- NRF2 supports non-small cell lung cancer growth independently of CBP/p300-enhanced glutathione synthesis.EMBO reports · 2025Article
- YAP-driven malignant reprogramming of oral epithelial stem cells at single cell resolution.Nature communications · 2025Article
- Evolutionary dependency of cancer mutations in gene pairs inferred by nonsynonymous-synonymous mutation ratios.Genome medicine · 2024Article
- Building a translational cancer dependency map for The Cancer Genome Atlas.Nature cancer · 2024Article
- MicroRNA-367-3p directly targets RAB23 and inhibits proliferation, migration and invasion of bladder cancer cells and increases cisplatin sensitivity.Journal of cancer research and clinical oncology · 2023Article
- Deciphering the Functional Roles of Individual Cancer Alleles Across Comprehensive Cancer Genomic Studies.bioRxiv : the preprint server for biology · 2023Article
- YAP-Driven Malignant Reprogramming of Epithelial Stem Cells at Single Cell Resolution.Research square · 2023Article
- Exploring cell competition for the prevention and therapy of esophageal squamous cell carcinoma.Biochemical pharmacology · 2023Review
- Predicting gene knockout effects from expression data.BMC medical genomics · 2023Article
- Differential regulation of TNFα and IL-6 expression contributes to immune evasion in prostate cancer.Journal of translational medicine · 2022Article
- Identification of a Molecularly-Defined Subset of Breast and Ovarian Cancer Models that Respond to WEE1 or ATR Inhibition, Overcoming PARP Inhibitor Resistance.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Glutathione peroxidase 2 is a metabolic driver of the tumor immune microenvironment and immune checkpoint inhibitor response.Journal for immunotherapy of cancer · 2022Article
- The β-TrCP-Mediated Pathway Cooperates with the Keap1-Mediated Pathway in Nrf2 DegradationMolecular and cellular biology · 2022Article
- CHMP2A regulates tumor sensitivity to natural killer cell-mediated cytotoxicity.Nature communications · 2022Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
35 authors.
Funding
Abstract
Systematic efforts to sequence the cancer genome have identified large numbers of mutations and copy number alterations in human cancers. However, elucidating the functional consequences of these variants, and their interactions to drive or maintain oncogenic states, remains a challenge in cancer research. We developed REVEALER, a computational method that identifies combinations of mutually exclusive genomic alterations correlated with functional phenotypes, such as the activation or gene dependency of oncogenic pathways or sensitivity to a drug treatment. We used REVEALER to uncover complementary genomic alterations associated with the transcriptional activation of β-catenin and NRF2, MEK-inhibitor sensitivity, and KRAS dependency. REVEALER successfully identified both known and new associations, demonstrating the power of combining functional profiles with extensive characterization of genomic alterations in cancer 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.