Nature Search

p53 inactivation drives breast cancer metastasis to the brain through SCD1 upregulation and increased fatty acid metabolism

This study associates p53 loss and brain metastasis in breast cancer. Mechanistically, p53-null tumors recruit astrocytes that provide substrates for enhanced fatty acid synthesis via upregulated SCD1 expression, representing a targetable axis in the disease.

Kathrin Laue
Sabina Pozzi
Uri Ben-David
Research29 Dec 2025
Nature Genetics

Volume: 58, P: 116-131
Immunologic and chemical targeting of the tight-junction protein Claudin-6 eliminates tumorigenic human pluripotent stem cells

The potential tumorigenicity of human pluripotent stem cells (hPSCs) limits their application in cell therapies. Ben-David et al.identify the tight-junction protein Claudin-6 as a cell-surface marker of hPSCs, and demonstrate three Claudin-6-based strategies to remove tumorigenic hPSCs from mixed cell cultures.

Uri Ben-David
Neta Nudel
Nissim Benvenisty
Research18 Jun 2013
Nature Communications

Volume: 4, P: 1-8
The landscape of chromosomal aberrations in breast cancer mouse models reveals driver-specific routes to tumorigenesis

Genetically engineered mouse models of cancer are useful in identifying oncogenes and tumour suppressors. Here, the authors use gene expression profiles to generate a catalogue of copy number aberrations in 45 mouse models, and compare mouse and human tumours to identify additional drivers of tumorigenesis.

Uri Ben-David
Gavin Ha
Todd R. Golub
ResearchOpen Access04 Jul 2016
Nature Communications

Volume: 7, P: 1-13
Aneuploidy induces profound changes in gene expression, proliferation and tumorigenicity of human pluripotent stem cells

Trisomy 12 is the most frequent chromosomal abnormality detected in cultures of human pluripotent stem cells. Here the authors show that human pluripotent stem cells carrying this abnormality exhibit gene expression profiles more similar to those of germ cell tumours, and give rise to more aggressive teratomas.

Uri Ben-David
Gal Arad
Juan Carlos Biancotti
Research08 Sept 2014
Nature Communications

Volume: 5, P: 1-11
Human aneuploid cells depend on the RAF/MEK/ERK pathway for overcoming increased DNA damage

Despite being a hallmark of cancer, the identification of targetable vulnerabilities of aneuploid cancer cells remains limited. Here, the authors develop RPE1-hTERT cell lines with varying degrees of aneuploidy to investigate the consequences of chromosomal imbalance, identifying CRAF as an aneuploid-selective therapeutically targetable vulnerability.

Johanna Zerbib
Marica Rosaria Ippolito
Stefano Santaguida
ResearchOpen Access09 Sept 2024
Nature Communications

Volume: 15, P: 1-20
A compendium of Amplification-Related Gain Of Sensitivity genes in human cancer

In cancer, the impact on cellular fitness of copy-number gains affecting collaterally-amplified genes remains poorly understood compared to oncogenes. Here, the authors integrate genomic data from tumours and cell lines and identify a class of ‘Amplification-Related Gain Of Sensitivity’ (ARGOS) genes, with potential therapeutic applications.

Veronica Rendo
Michael Schubert
Floris Foijer
ResearchOpen Access27 Jan 2025
Nature Communications

Volume: 16, P: 1-18
Frequent aneuploidy in primary human T cells after CRISPR–Cas9 cleavage

Aneuploidy and chromosomal truncations are frequent outcomes of CRISPR–Cas9 editing in human T cells.

Alessio David Nahmad
Eli Reuveni
Adi Barzel
Research30 Jun 2022
Nature Biotechnology

Volume: 40, P: 1807-1813
Publisher Correction: DNA-based copy number analysis confirms genomic evolution of PDX models

Anna C. H. Hoge
Michal Getz
Uri Ben-David
Amendments and CorrectionsOpen Access12 Jul 2022
npj Precision Oncology

Volume: 6, P: 1
Genome doubling causes double trouble

Human cancer cells often double their genome through an error in cell division, and this can lead to further genomic instability. A detailed analysis of the first cell cycle after genome doubling sheds light on this phenomenon.

Yonatan Eliezer
Uri Ben-David
News & Views30 Mar 2022
Nature

Volume: 604, P: 44-45
Analysis of chromosomal aberrations and recombination by allelic bias in RNA-Seq

Chromosomal aberrations can be detected by global gene expression analysis. Here, the authors report eSNP-Karyotyping, a new method that can detect chromosomal aberrations by measuring the ratio of expression between the two alleles without comparison to a matched diploid sample.

Uri Weissbein
Maya Schachter
Nissim Benvenisty
ResearchOpen Access07 Jul 2016
Nature Communications

Volume: 7, P: 1-8
Short-term molecular consequences of chromosome mis-segregation for genome stability

Chromosomal instability leads to aneuploidy, a state of karyotype imbalance. By inducing controlled chromosome mis-segregation, Santaguida and colleagues show that aneuploidy can also instigate chromosomal instability.

Lorenza Garribba
Giuseppina De Feudis
Stefano Santaguida
ResearchOpen Access11 Mar 2023
Nature Communications

Volume: 14, P: 1-17
Patient-derived xenografts undergo mouse-specific tumor evolution

This large-scale analysis of copy number alterations (CNAs) in patient-derived xenografts (PDXs) across 24 cancer types shows that new CNAs accumulate quickly and that the specific CNAs acquired during passaging differ from those acquired during tumor evolution in patients, suggesting that PDX tumors are under distinct selection pressures from tumors in human hosts.

Uri Ben-David
Gavin Ha
Todd R Golub
Research09 Oct 2017
Nature Genetics

Volume: 49, P: 1567-1575
DeepTarget predicts anti-cancer mechanisms of action of small molecules by integrating drug and genetic screens

Sanju Sinha
Neelam Sinha
Eytan Ruppin
ResearchOpen Access05 Nov 2025
npj Precision Oncology

Volume: 9, P: 1-14
SMRT compounds abrogate cellular phenotypes of ataxia telangiectasia in neural derivatives of patient-specific hiPSCs

Ataxia telangiectasia is a genetic disease that results in various pathological disorders. In this study, the authors develop an in vitromodel of Ataxia telangiectasia using human induced pluripotent stem cells, and find that physiological defects can be alleviated by small molecule read-through compounds.

Peiyee Lee
Nathan T. Martin
William E. Lowry
Research07 May 2013
Nature Communications

Volume: 4, P: 1-8
A palmitate-rich metastatic niche enables metastasis growth via p65 acetylation resulting in pro-metastatic NF-κB signaling

Fendt and colleagues find that pre-metastatic niche formation and a high-fat diet increase palmitate availability in future organs of metastases and show that breast cancer cells use palmitate to generate acetyl-CoA, acetylate the NF-κB subunit p65 and induce pro-metastatic signaling.

Patricia Altea-Manzano
Ginevra Doglioni
Sarah-Maria Fendt
Research02 Feb 2023
Nature Cancer

Volume: 4, P: 344-364
Aneuploidy as a driver of human cancer

This Review discusses recurrent aneuploidies driving human cancer, methods to identify them and strategies to uncover underlying driver genes. It highlights genomic and experimental approaches to study and ultimately target driver aneuploidies.

Eran Sdeor
Hajime Okada
Uri Ben-David
Reviews02 Oct 2024
Nature Genetics

Volume: 56, P: 2014-2026
Aneuploidy renders cancer cells vulnerable to mitotic checkpoint inhibition

Aneuploid cancer cell lines show increased dependence on the spindle assembly complex (SAC); initially they are resistant to SAC perturbations, but over time they accumulate chromosomal aberrations that impair their fitness.

Yael Cohen-Sharir
James M. McFarland
Uri Ben-David
Research27 Jan 2021
Nature

Volume: 590, P: 486-491
Genetic and transcriptional evolution alters cancer cell line drug response

The extent, origins and consequences of genetic variation within human cell lines are studied, providing a framework for researchers to measure such variation in efforts to support maximally reproducible cancer research.

Uri Ben-David
Benjamin Siranosian
Todd R. Golub
Research08 Aug 2018
Nature

Volume: 560, P: 325-330
DNA-based copy number analysis confirms genomic evolution of PDX models

Anna C. H. Hoge
Michal Getz
Uri Ben-David
ResearchOpen Access28 Apr 2022
npj Precision Oncology

Volume: 6, P: 1-7
Author Correction: Cas9 activates the p53 pathway and selects for p53-inactivating mutations

Oana M. Enache
Veronica Rendo
Uri Ben-David
Amendments and Corrections25 Jun 2020
Nature Genetics

Volume: 52, P: 748-749
Discovering the anticancer potential of non-oncology drugs by systematic viability profiling

Golub and colleagues tested thousands of drugs not originally developed for oncology across 578 human cancer cell lines, revealing growth-inhibitory effects and providing a resource to identify drugs with the potential to be repurposed for cancer.

Steven M. Corsello
Rohith T. Nagari
Todd R. Golub
Research20 Jan 2020
Nature Cancer

Volume: 1, P: 235-248
The tumorigenicity of human embryonic and induced pluripotent stem cells

The unique ability of human pluripotent stem cells to self-renew and to differentiate into cells of the three germ layers makes them an invaluable tool for the future of regenerative medicine and tumorigenic research. It was assumed that human induced pluripotent stem cells (HiPSCs) would behave like their embryonic counterparts in respect to their tumorigenicity, but a rapidly accumulating body of evidence suggests that there are important differences.

Uri Ben-David
Nissim Benvenisty
Reviews10 Mar 2011
Nature Reviews Cancer

Volume: 11, P: 268-277
Cas9 activates the p53 pathway and selects for p53-inactivating mutations

Cas9 expression induces DNA damage and activates the p53 pathway, and it can lead to the selection of cells with p53-inactivating mutations. Cas9 is less active in wild-type TP53 cell lines than in TP53-mutant cell lines.

Oana M. Enache
Veronica Rendo
Uri Ben-David
Research18 May 2020
Nature Genetics

Volume: 52, P: 662-668
AI driven decision support reduces antibiotic mismatches and inappropriate use in outpatient urinary tract infections

Shirley Shapiro Ben David
Roni Romano
Uri Lerner
ResearchOpen Access27 Jan 2025
npj Digital Medicine

Volume: 8, P: 1-10
Genomic evolution of cancer models: perils and opportunities

Genomic instability in cancer models presents a major challenge in the design and reproducibility of research and its clinical translation. This Opinion article discusses the causes and consequences of intra-tumour genomic heterogeneity and instability in commonly used models and implications thereof.

Uri Ben-David
Rameen Beroukhim
Todd R. Golub
Reviews21 Dec 2018
Nature Reviews Cancer

Volume: 19, P: 97-109
Context is everything: aneuploidy in cancer

Aneuploidy contributes to tumorigenesis, but the underlying processes are not well understood. This Review explains the context dependency of aneuploidy in cancer and discusses its clinical potential as a prognostic marker and a therapeutic target.

Uri Ben-David
Angelika Amon
Reviews23 Sept 2019
Nature Reviews Genetics

Volume: 21, P: 44-62
Optimizing cancer immunotherapy response prediction by tumor aneuploidy score and fraction of copy number alterations

Tian-Gen Chang
Yingying Cao
Eytan Ruppin
ResearchOpen Access03 Jun 2023
npj Precision Oncology

Volume: 7, P: 1-8
FOXM1 repression increases mitotic death upon antimitotic chemotherapy through BMF upregulation

Sara Vaz
Fábio J. Ferreira
Elsa Logarinho
ResearchOpen Access25 May 2021
Cell Death & Disease

Volume: 12, P: 1-14
Virtual karyotyping of pluripotent stem cells on the basis of their global gene expression profiles

Uri Ben-David
Yoav Mayshar
Nissim Benvenisty
Protocols25 Apr 2013
Nature Protocols

Volume: 8, P: 989-997
Chemical ablation of tumor-initiating human pluripotent stem cells

Uri Ben-David
Nissim Benvenisty
Protocols27 Feb 2014
Nature Protocols

Volume: 9, P: 729-740
Somatic loss of WWOX is associated with TP53 perturbation in basal-like breast cancer

Suhaib K. Abdeen
Uri Ben-David
Rami I. Aqeilan
ResearchOpen Access06 Aug 2018
Cell Death & Disease

Volume: 9, P: 1-13

Search

p53 inactivation drives breast cancer metastasis to the brain through SCD1 upregulation and increased fatty acid metabolism

Immunologic and chemical targeting of the tight-junction protein Claudin-6 eliminates tumorigenic human pluripotent stem cells

The landscape of chromosomal aberrations in breast cancer mouse models reveals driver-specific routes to tumorigenesis

Aneuploidy induces profound changes in gene expression, proliferation and tumorigenicity of human pluripotent stem cells

Human aneuploid cells depend on the RAF/MEK/ERK pathway for overcoming increased DNA damage

A compendium of Amplification-Related Gain Of Sensitivity genes in human cancer

Frequent aneuploidy in primary human T cells after CRISPR–Cas9 cleavage

Publisher Correction: DNA-based copy number analysis confirms genomic evolution of PDX models

Genome doubling causes double trouble

Analysis of chromosomal aberrations and recombination by allelic bias in RNA-Seq

Short-term molecular consequences of chromosome mis-segregation for genome stability

Patient-derived xenografts undergo mouse-specific tumor evolution

DeepTarget predicts anti-cancer mechanisms of action of small molecules by integrating drug and genetic screens

SMRT compounds abrogate cellular phenotypes of ataxia telangiectasia in neural derivatives of patient-specific hiPSCs

A palmitate-rich metastatic niche enables metastasis growth via p65 acetylation resulting in pro-metastatic NF-κB signaling

Aneuploidy as a driver of human cancer

Aneuploidy renders cancer cells vulnerable to mitotic checkpoint inhibition

Genetic and transcriptional evolution alters cancer cell line drug response

DNA-based copy number analysis confirms genomic evolution of PDX models

Author Correction: Cas9 activates the p53 pathway and selects for p53-inactivating mutations

Discovering the anticancer potential of non-oncology drugs by systematic viability profiling

The tumorigenicity of human embryonic and induced pluripotent stem cells

Cas9 activates the p53 pathway and selects for p53-inactivating mutations

AI driven decision support reduces antibiotic mismatches and inappropriate use in outpatient urinary tract infections

Genomic evolution of cancer models: perils and opportunities

Context is everything: aneuploidy in cancer

Optimizing cancer immunotherapy response prediction by tumor aneuploidy score and fraction of copy number alterations

FOXM1 repression increases mitotic death upon antimitotic chemotherapy through BMF upregulation

Virtual karyotyping of pluripotent stem cells on the basis of their global gene expression profiles

Chemical ablation of tumor-initiating human pluripotent stem cells

Somatic loss of WWOX is associated with TP53 perturbation in basal-like breast cancer

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