Reference health
Paralog knockout profiling identifies DUSP4 and DUSP6 as a digenic dependence in MAPK pathway-driven cancers
43/43 checkable references clean · checked 2026-07-24
Every reference with a DOI in the deposited reference list resolved to a known work in Crossref or DataCite at the dated check, and none carried a retraction, withdrawal, or removal notice.
4 without a DOI — not checked. A reference deposited without a DOI is never matched by title or guessed at; it stays outside the checked set, and this line discloses that.
The 43 checked references that resolve
resolves10.1016/j.cell.2017.07.005
Project DRIVE: A Compendium of Cancer Dependencies and Synthetic Lethal Relationships Uncovered by Large-Scale, Deep RNAi Screening
resolves10.1038/s41586-019-1103-9
Prioritization of cancer therapeutic targets using CRISPR–Cas9 screens
resolves10.1038/s41586-019-1102-x
WRN helicase is a synthetic lethal target in microsatellite unstable cancers
resolves10.1126/science.aad5944
Disordered methionine metabolism in MTAP/CDKN2A-deleted cancers leads to dependence on PRMT5
resolves10.1016/j.isci.2019.02.006
Werner Syndrome Helicase Is Required for the Survival of Cancer Cells with Microsatellite Instability
resolves10.1126/science.aad5214
<i>MTAP</i>
deletion confers enhanced dependency on the PRMT5 arginine methyltransferase in cancer cells
resolves10.1371/journal.pgen.1008466
Paralog buffering contributes to the variable essentiality of genes in cancer cell lines
resolves10.1158/2159-8290.CD-19-1274
Combined Proteomic and Genetic Interaction Mapping Reveals New RAS Effector Pathways and Susceptibilities
resolves10.1126/science.aaf1420
A global genetic interaction network maps a wiring diagram of cellular function
resolves10.1038/nbt.3834
Synergistic drug combinations for cancer identified in a CRISPR screen for pairwise genetic interactions
resolves10.1126/science.aax4438
Exploring genetic interaction manifolds constructed from rich single-cell phenotypes
resolves10.1038/nmeth.4225
Combinatorial CRISPR–Cas9 screens for de novo mapping of genetic interactions
resolves10.1016/j.molcel.2018.01.017
Combinatorial CRISPR-Cas9 Metabolic Screens Reveal Critical Redox Control Points Dependent on the KEAP1-NRF2 Regulatory Axis
resolves10.1186/s12859-016-1015-8
BAGEL: a computational framework for identifying essential genes from pooled library screens
resolves10.1186/s13059-019-1745-9
GEMINI: a variational Bayesian approach to identify genetic interactions from combinatorial CRISPR screens
resolves10.1038/onc.2013.418
Combined PKC and MEK inhibition in uveal melanoma with GNAQ and GNA11 mutations
resolves10.1038/s41586-019-1660-y
Architecture of autoinhibited and active BRAF–MEK1–14-3-3 complexes
resolves10.1096/fasebj.14.1.6
Dual specificity phosphatases: a gene family for control of MAP kinase function
resolves10.1016/j.semcdb.2016.01.009
The regulation of oncogenic Ras/ERK signalling by dual-specificity mitogen activated protein kinase phosphatases (MKPs)
resolves10.1158/1541-7786.MCR-18-0327
Hyperactivation of MAPK Signaling Is Deleterious to RAS/RAF-mutant Melanoma
resolves10.1016/j.celrep.2016.09.061
Phenotypic Characterization of a Comprehensive Set of MAPK1/ERK2 Missense Mutants
resolves10.1158/0008-5472.CAN-14-2073
ERK Mutations Confer Resistance to Mitogen-Activated Protein Kinase Pathway Inhibitors
resolves10.1073/pnas.0510506103
Structural basis of docking interactions between ERK2 and MAP kinase phosphatase 3
resolves10.4161/cc.9.23.13957
Post-translational regulation of mitogen-activated protein kinase phosphatase-2 (MKP-2) by ERK
resolves10.1038/nature09626
Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation
resolves10.1016/j.ccr.2010.11.023
Acquired Resistance to BRAF Inhibitors Mediated by a RAF Kinase Switch in Melanoma Can Be Overcome by Cotargeting MEK and IGF-1R/PI3K
resolves10.1158/2159-8290.CD-11-0341
EGFR-Mediated Reactivation of MAPK Signaling Contributes to Insensitivity of
<i>BRAF</i>
-Mutant Colorectal Cancers to RAF Inhibition with Vemurafenib
resolves10.1038/nature08833
RAF inhibitors prime wild-type RAF to activate the MAPK pathway and enhance growth
resolves10.1038/nature11814
Modelling vemurafenib resistance in melanoma reveals a strategy to forestall drug resistance
resolves10.1038/nature09627
COT drives resistance to RAF inhibition through MAP kinase pathway reactivation
resolves10.1200/JCO.2010.33.2312
Dissecting Therapeutic Resistance to RAF Inhibition in Melanoma by Tumor Genomic Profiling
resolves10.1038/s41588-018-0155-3
Genome-scale analysis identifies paralog lethality as a vulnerability of chromosome 1p loss in cancer
resolves10.1111/j.2517-6161.1995.tb02031.x
Controlling the False Discovery Rate: A Practical and Powerful Approach to Multiple Testing
resolves10.1038/nbt.3437
Optimized sgRNA design to maximize activity and minimize off-target effects of CRISPR-Cas9
The 4 references without a DOI — listed, not checked
no DOI — not checkedLieb, S. et al. Werner syndrome helicase is a selective vulnerability of microsatellite instability-high tumor cells. eLife 8, e43333 (2019).
no DOI — not checkedFischer, B. et al. A map of directional genetic interactions in a metazoan cell. eLife 4, e05464 (2015).
no DOI — not checkedUnni, A. M., Lockwood, W. W., Zejnullahu, K., Lee-Lin, S.-Q. & Varmus, H. Evidence that synthetic lethality underlies the mutual exclusivity of oncogenic KRAS and EGFR mutations in lung adenocarcinoma. eLife 4, e06907 (2015).
no DOI — not checkedUnni, A. M. et al. Hyperactivation of ERK by multiple mechanisms is toxic to RTK-RAS mutation-driven lung adenocarcinoma cells. eLife 7, e33718 (2018).
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