ArticleCancer discovery2016
Systematic Functional Interrogation of Rare Cancer Variants Identifies Oncogenic Alleles.
Article in Cancer discovery, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
111 citing papers in PubMed, 183 citations in OpenAlex.
- AKT mutant allele-specific activation dictates pharmacologic sensitivities.Nature communications · 2022Trial
- Principles of ribosome-associated protein quality control during the synthesis of CFTR.The EMBO journal · 2026Article
- An ER stress-responsive RNA rheostat for programmable gene and mRNA therapies.Cell chemical biology · 2026Article
- COSMIC-Linked Ras Mutations at the Interface Between H-Ras and PI3KγBiochemistry · 2026Article
- HIRA-SETDB1-H3K9me3 axis regulates chromatin architecture in leukemia cells.The Journal of biological chemistry · 2026Article
- COSMIC-Linked Ras Mutations at the Interface Between H-Ras and PI3KγbioRxiv : the preprint server for biology · 2026Article
- Excess cysteine drives conjugate formation and impairs proliferation of NRF2-activated cancer cells.Nature metabolism · 2026Article
- A multimodal framework for comprehensive driver variant prediction in cancer.Communications medicine · 2025Article
- Drug resistance and tumor heterogeneity: cells and ensembles.Biophysical reviews · 2025Review
- A Comprehensive Review of Deep Learning Applications with Multi-Omics Data in Cancer Research.Genes · 2025Review
- Clustering of NLRP3 induced by membrane or protein scaffolds promotes inflammasome assembly.Nature communications · 2025Article
- Human Myobundle Platform for Studying the Role of Notch Signaling in Satellite Cell Phenotype and Function.Advanced healthcare materials · 2025Article
- Full-Length Cryptochrome 1 in the Outer Segments of the Retinal Blue Cone Photoreceptors in Humans and Great Apes Suggests a Role Beyond Transcriptional Repression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Protein Phosphatase 1 Regulatory Subunit 3C integrates cholesterol metabolism and isocitrate dehydrogenase in chondrocytes and neoplasia.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- LRP5 promotes adipose progenitor cell fitness and adipocyte insulin sensitivity.Communications medicine · 2025Article
- Article
- Identifying somatic driver mutations in cancer with a language model of the human genome.Computational and structural biotechnology journal · 2025Article
- Article
- Long-term breast cancer response to CDK4/6 inhibition defined by TP53-mediated geroconversion.Cancer cell · 2024Article
51 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
28 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledCancer genome characterization efforts now provide an initial view of the somatic alterations in primary tumors. However, most point mutations occur at low frequency, and the function of these alleles remains undefined. We have developed a scalable systematic approach to interrogate the function of cancer-associated gene variants. We subjected 474 mutant alleles curated from 5,338 tumors to pooled in vivo tumor formation assays and gene expression profiling. We identified 12 transforming alleles, including two in genes (PIK3CB, POT1) that have not been shown to be tumorigenic. One rare KRAS allele, D33E, displayed tumorigenicity and constitutive activation of known RAS effector pathways. By comparing gene expression changes induced upon expression of wild-type and mutant alleles, we inferred the activity of specific alleles. Because alleles found to be mutated only once in 5,338 tumors rendered cells tumorigenic, these observations underscore the value of integrating genomic information with functional studies. SIGNIFICANCE: Experimentally inferring the functional status of cancer-associated mutations facilitates the interpretation of genomic information in cancer. Pooled in vivo screen and gene expression profiling identified functional variants and demonstrated that expression of rare variants induced tumorigenesis. Variant phenotyping through functional studies will facilitate defining key somatic events in cancer. Cancer Discov; 6(7); 714-26. ©2016 AACR.See related commentary by Cho and Collisson, p. 694This article is highlighted in the In This Issue feature, p. 681.
Indexed as
Identifiers
What OpenQuestion holds
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.