ArticleProceedings of the National Academy of Sciences of the United States of America2008
Highly parallel identification of essential genes in cancer cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 346 papers, 1 of them a synthesis that pooled it.
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
346 citing papers in PubMed, 1 synthesis or guideline pooled it, 563 citations in OpenAlex.
- Synthetic lethal gene pairs: Experimental approaches and predictive models.Frontiers in genetics · 2022Pooled it
- Evofosfamide for the treatment of human papillomavirus-negative head and neck squamous cell carcinoma.JCI insight · 2018Trial
- A pan-viral map of host dependency factors from multi-omics integration and machine learning across influenza A, SARS-CoV-2, Zika, and dengue viruses.Journal of translational medicine · 2026Article
- Revealing genetic drivers of ovarian cancer and chemoresistance: insights from whole-genome CRISPR-knockout library screens.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Extending gene set variation analysis with a reference dataset to stabilize scores.BMC genomics · 2025Article
- ARID1A mutations protect follicular lymphoma from FAS-dependent immune surveillance by reducing RUNX3/ETS1-driven FAS-expression.Cell death and differentiation · 2025Article
- Combinatorial CRISPR screen revealseLife · 2025Article
- The present and future of the Cancer Dependency Map.Nature reviews. Cancer · 2025Review
- The theory of massively repeated evolution and full identifications of cancer-driving nucleotides (CDNs).eLife · 2024Article
- CRISPR/Cas9 screens identify key host factors that enhance rotavirus reverse genetics efficacy and vaccine production.NPJ vaccines · 2024Article
- Pleiotropy, epistasis and the genetic architecture of quantitative traits.Nature reviews. Genetics · 2024Review
- Unlocking biological mechanisms with integrative functional genomics approaches.Molecules and cells · 2024Review
- Genome-scale CRISPR-Cas9 screening in stem cells: theories, applications and challenges.Stem cell research & therapy · 2024Review
- Framework for in vivo T cell screens.The Journal of experimental medicine · 2024Article
- A genome-wide CRISPR screen identifies BRD4 as a regulator of cardiomyocyte differentiation.Nature cardiovascular research · 2024Article
- Uncovering hidden cancer self-dependencies through analysis of shRNA-level dependency scores.Scientific reports · 2024Article
- Essential transcription factors for induced neuron differentiation.Nature communications · 2023Article
- The effects of ARID1A mutation in gastric cancer and its significance for treatment.Cancer cell international · 2023Review
- Review
- Article
286 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
24 authors at 6 institutions in 1 country.
Funding
Abstract
More complete knowledge of the molecular mechanisms underlying cancer will improve prevention, diagnosis and treatment. Efforts such as The Cancer Genome Atlas are systematically characterizing the structural basis of cancer, by identifying the genomic mutations associated with each cancer type. A powerful complementary approach is to systematically characterize the functional basis of cancer, by identifying the genes essential for growth and related phenotypes in different cancer cells. Such information would be particularly valuable for identifying potential drug targets. Here, we report the development of an efficient, robust approach to perform genome-scale pooled shRNA screens for both positive and negative selection and its application to systematically identify cell essential genes in 12 cancer cell lines. By integrating these functional data with comprehensive genetic analyses of primary human tumors, we identified known and putative oncogenes such as EGFR, KRAS, MYC, BCR-ABL, MYB, CRKL, and CDK4 that are essential for cancer cell proliferation and also altered in human cancers. We further used this approach to identify genes involved in the response of cancer cells to tumoricidal agents and found 4 genes required for the response of CML cells to imatinib treatment: PTPN1, NF1, SMARCB1, and SMARCE1, and 5 regulators of the response to FAS activation, FAS, FADD, CASP8, ARID1A and CBX1. Broad application of this highly parallel genetic screening strategy will not only facilitate the rapid identification of genes that drive the malignant state and its response to therapeutics but will also enable the discovery of genes that participate in any biological process.
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.