Nature Search

Inducible CRISPR–Cas9 screening platform to interrogate non-proliferative cellular states

Here, the authors provide a platform for inducible CRISPR–Cas9 screening to interrogate non-proliferative cellular states.

Gabriele Casagrande Raffi
Hendrik J. Kuiken
Liqin Wang
Protocols08 Oct 2025
Nature Protocols

P: 1-31
cFLIP suppression and DR5 activation sensitize senescent cancer cells to senolysis

Bernards and colleagues identify cFLIP as a common dependency of cancer cells by conferring protection from senolytic-induced cell death. They nominate combination of DR5 activation and cFLIP suppression for enhanced killing of senescent cancer cells.

Liqin Wang
Haojie Jin
René Bernards
Research22 Nov 2022
Nature Cancer

Volume: 3, P: 1284-1299
Inhibition of telomerase limits the growth of human cancer cells

William C. Hahn
Sheila A. Stewart
Robert A. Weinberg
Research01 Oct 1999
Nature Medicine

Volume: 5, P: 1164-1170
An shRNA barcode screen provides insight into cancer cell vulnerability to MDM2 inhibitors

Thijn R Brummelkamp
Armida W M Fabius
Roderick L Beijersbergen
Research13 Feb 2006
Nature Chemical Biology

Volume: 2, P: 202-206
CRISPR knockout screening outperforms shRNA and CRISPRi in identifying essential genes

CRISPR knockout screens outperform shRNA and CRISPR-interference screens in a side-by-side comparison.

Bastiaan Evers
Katarzyna Jastrzebski
Rene Bernards
Research25 Apr 2016
Nature Biotechnology

Volume: 34, P: 631-633
A large-scale RNAi screen in human cells identifies new components of the p53 pathway

Katrien Berns
E. Marielle Hijmans
René Bernards
Research25 Mar 2004
Nature

Volume: 428, P: 431-437
Creation of human tumour cells with defined genetic elements

William C. Hahn
Christopher M. Counter
Robert A. Weinberg
Research29 Jul 1999
Nature

Volume: 400, P: 464-468
Widespread chromatin context-dependencies of DNA double-strand break repair proteins

DNA double-strand breaks are repaired by multiple pathways. The balance of these pathways depends on the local chromatin context, but the underlying mechanisms are poorly understood. Here the authors uncover a network of proteins that regulate pathway balance in a chromatin context-dependent manner.

Xabier Vergara
Anna G. Manjón
Bas van Steensel
ResearchOpen Access22 Jun 2024
Nature Communications

Volume: 15, P: 1-14
Old drugs with new tricks

Drug repurposing is an attractive strategy for extending the arsenal of oncology therapies. Screening of a large collection of existing non-oncology compounds against a panel of cancer cell lines now identifies several drugs capable of selectively inhibiting the growth of cancer cells.

Roderick L. Beijersbergen
News & Views28 Jan 2020
Nature Cancer

Volume: 1, P: 153-155
A doxycycline- and light-inducible Cre recombinase mouse model for optogenetic genome editing

Achieving spatial control of gene expression is important. Here the authors report an optimised photoactivatable Cre recombinase system, doxycycline- and light-inducible Cre recombinase (DiLiCre), and generate a DiLiCre mouse line which they use for mutagenesis in vivo and positional cell-tracing.

Miguel Vizoso
Colin E. J. Pritchard
Jacco van Rheenen
ResearchOpen Access28 Oct 2022
Nature Communications

Volume: 13, P: 1-15
A kinome-centered CRISPR-Cas9 screen identifies activated BRAF to modulate enzalutamide resistance with potential therapeutic implications in BRAF-mutated prostate cancer

Sander A. L. Palit
Jeroen van Dorp
Michiel S. van der Heijden
ResearchOpen Access01 Jul 2021
Scientific Reports

Volume: 11, P: 1-8
A loss-of-adhesion CRISPR-Cas9 screening platform to identify cell adhesion-regulatory proteins and signaling pathways

Targeting integrin-mediated retention of malignant B cells in their protective microenvironment is an efficacious treatment for lymphoma and leukemia. Here, the authors present an unbiased loss-of-adhesion CRISPR screening method, identifying therapeutic targets for these B-cell malignancies.

Martin F. M. de Rooij
Yvonne J. Thus
Marcel Spaargaren
ResearchOpen Access19 Apr 2022
Nature Communications

Volume: 13, P: 1-11
EGFR activation limits the response of liver cancer to lenvatinib

EGFR inhibition and lenvatinib treatment of liver cancer cells in vitro and in in vivo mouse models has potent anti-proliferative effects, and lenvatinib plus gefitinib treatment of 12 patients with advanced liver cancer resulted in meaningful clinical responses.

Haojie Jin
Yaoping Shi
René Bernards
Research21 Jul 2021
Nature

Volume: 595, P: 730-734
shRNA libraries and their use in cancer genetics

René Bernards
Thijn R Brummelkamp
Roderick L Beijersbergen
Reviews23 Aug 2006
Nature Methods

Volume: 3, P: 701-706
Glucocorticoid receptor triggers a reversible drug-tolerant dormancy state with acquired therapeutic vulnerabilities in lung cancer

Glucocorticoids (GC) are reported to block cancer cell proliferation, but the mode of action is unclear. Here the authors show that glucocorticoid receptor activation induces cancer cell dormancy in lung cancer by regulating CDKN1C expression through a distal enhancer, and these dormant cells are addicted to IGF-1R signalling pathway.

Stefan Prekovic
Karianne Schuurman
Wilbert Zwart
ResearchOpen Access16 Jul 2021
Nature Communications

Volume: 12, P: 1-18
The ubiquitin-specific protease USP28 is required for MYC stability

Nikita Popov
Michael Wanzel
Martin Eilers
Research10 Jun 2007
Nature Cell Biology

Volume: 9, P: 765-774
Inducing and exploiting vulnerabilities for the treatment of liver cancer

CDC7 inhibition selectively induces senescence in hepatocellular carcinoma cells with TP53 mutations, which enables the selective apoptotic cell death of these senescent cells using inhibitors of mTOR signalling.

Cun Wang
Serena Vegna
René Bernards
Research02 Oct 2019
Nature

Volume: 574, P: 268-272
Intracellular bacterial growth is controlled by a kinase network around PKB/AKT1

Conventional antibiotics, which target the infectious agent, are subject to the development of antibiotic resistance. An alternative approach is to focus on host factors that support pathogen growth. A kinase inhibitor screen identified AKT1 as a central molecule essential for intracellular survival of Salmonella typhimurium and Mycobacterium tuberculosis and thus presenting a putative drug target.

Coenraad Kuijl
Nigel D. L. Savage
Jacques Neefjes
Research29 Nov 2007
Nature

Volume: 450, P: 725-730
Reversible and adaptive resistance to BRAF(V600E) inhibition in melanoma

Patients with melanomas carrying an activating BRAF mutation respond to treatment with BRAF inhibitors although resistance to the inhibitor usually emerges; this resistance is shown to arise through increased expression of receptor tyrosine kinases such as EGFR; however, these changes decrease cell fitness and during a break from inhibitor treatment these cells are selected against, revealing that some patients who acquire EGFR expression may benefit from inhibitor re-treatment after a drug holiday.

Chong Sun
Liqin Wang
Rene Bernards
Research26 Mar 2014
Nature

Volume: 508, P: 118-122
Unresponsiveness of colon cancer to BRAF(V600E) inhibition through feedback activation of EGFR

Inhibition of activated BRAF has been ineffective in colon cancers with the mutation; here, this is shown to be due to the feedback activation of the epidermal growth factor receptor (EGFR) in response to BRAF inhibition.

Anirudh Prahallad
Chong Sun
René Bernards
Research26 Jan 2012
Nature

Volume: 483, P: 100-103
Statistical methods for analysis of high-throughput RNA interference screens

Amanda Birmingham
Laura M Selfors
Caroline E Shamu
Reviews30 Jul 2009
Nature Methods

Volume: 6, P: 569-575
ARID1A mutation sensitizes most ovarian clear cell carcinomas to BET inhibitors

Katrien Berns
Joseph J. Caumanns
René Bernards
ResearchOpen Access15 May 2018
Oncogene

Volume: 37, P: 4611-4625
The lethal response to Cdk1 inhibition depends on sister chromatid alignment errors generated by KIF4 and isoform 1 of PRC1

Erik Voets
Judith Marsman
Rob Wolthuis
ResearchOpen Access01 Oct 2015
Scientific Reports

Volume: 5, P: 1-12
A CRISPR screen identifies CDK7 as a therapeutic target in hepatocellular carcinoma

Cun Wang
Haojie Jin
René Bernards
Correspondence05 Mar 2018
Cell Research

Volume: 28, P: 690-692
SMARCE1 suppresses EGFR expression and controls responses to MET and ALK inhibitors in lung cancer

Andreas I Papadakis
Chong Sun
Sidong Huang
ResearchOpen Access06 Feb 2015
Cell Research

Volume: 25, P: 445-458

Search

Inducible CRISPR–Cas9 screening platform to interrogate non-proliferative cellular states

cFLIP suppression and DR5 activation sensitize senescent cancer cells to senolysis

Inhibition of telomerase limits the growth of human cancer cells

An shRNA barcode screen provides insight into cancer cell vulnerability to MDM2 inhibitors

CRISPR knockout screening outperforms shRNA and CRISPRi in identifying essential genes

A large-scale RNAi screen in human cells identifies new components of the p53 pathway

Creation of human tumour cells with defined genetic elements

Widespread chromatin context-dependencies of DNA double-strand break repair proteins

Old drugs with new tricks

A doxycycline- and light-inducible Cre recombinase mouse model for optogenetic genome editing

A kinome-centered CRISPR-Cas9 screen identifies activated BRAF to modulate enzalutamide resistance with potential therapeutic implications in BRAF-mutated prostate cancer

A loss-of-adhesion CRISPR-Cas9 screening platform to identify cell adhesion-regulatory proteins and signaling pathways

EGFR activation limits the response of liver cancer to lenvatinib

shRNA libraries and their use in cancer genetics

Glucocorticoid receptor triggers a reversible drug-tolerant dormancy state with acquired therapeutic vulnerabilities in lung cancer

The ubiquitin-specific protease USP28 is required for MYC stability

Inducing and exploiting vulnerabilities for the treatment of liver cancer

Intracellular bacterial growth is controlled by a kinase network around PKB/AKT1

Reversible and adaptive resistance to BRAF(V600E) inhibition in melanoma

Unresponsiveness of colon cancer to BRAF(V600E) inhibition through feedback activation of EGFR

Statistical methods for analysis of high-throughput RNA interference screens

ARID1A mutation sensitizes most ovarian clear cell carcinomas to BET inhibitors

The lethal response to Cdk1 inhibition depends on sister chromatid alignment errors generated by KIF4 and isoform 1 of PRC1

A CRISPR screen identifies CDK7 as a therapeutic target in hepatocellular carcinoma

SMARCE1 suppresses EGFR expression and controls responses to MET and ALK inhibitors in lung cancer

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