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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
Exploiting loss of heterozygosity for allele-selective colorectal cancer chemotherapy

Allelic losses occurring in cancer cells have been suggested as potential targets for therapy. Here, the authors show how recurring loss of heterozygosity of a drug metabolic gene in colorectal cancers can be exploited using a low molecular weight compound.

Veronica Rendo
Ivaylo Stoimenov
Tobias Sjöblom
ResearchOpen Access11 Mar 2020
Nature Communications

Volume: 11, P: 1-10
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
Cancer aneuploidies are shaped primarily by effects on tumour fitness

A study reports the development of an algorithm, BISCUT, that detects genomic loci under selective pressure by relying on the distribution of breakpoints across chromosome arms, and uses it to explore how aneuploidies affect tumorigenesis.

Juliann Shih
Shahab Sarmashghi
Rameen Beroukhim
Research28 Jun 2023
Nature

Volume: 619, P: 793-800
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
PPM1D mutations are oncogenic drivers of de novo diffuse midline glioma formation

PPM1D is a known mediator of p53 signalling, and has been linked to treatment resistance in glioma. In this work, the authors utilise genomics, proteomics, and mouse models to determine the role of PPM1D in the development of diffuse midline glioma.

Prasidda Khadka
Zachary J. Reitman
Pratiti Bandopadhayay
ResearchOpen Access01 Feb 2022
Nature Communications

Volume: 13, P: 1-18
Defining eligible patients for allele-selective chemotherapies targeting NAT2 in colorectal cancer

Veronica Rendo
Snehangshu Kundu
Tobias Sjöblom
ResearchOpen Access31 Dec 2020
Scientific Reports

Volume: 10, P: 1-13

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

Exploiting loss of heterozygosity for allele-selective colorectal cancer chemotherapy

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

Cancer aneuploidies are shaped primarily by effects on tumour fitness

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

PPM1D mutations are oncogenic drivers of de novo diffuse midline glioma formation

Defining eligible patients for allele-selective chemotherapies targeting NAT2 in colorectal cancer

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

Exploiting loss of heterozygosity for allele-selective colorectal cancer chemotherapy

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

Cancer aneuploidies are shaped primarily by effects on tumour fitness

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

PPM1D mutations are oncogenic drivers of de novo diffuse midline glioma formation

Defining eligible patients for allele-selective chemotherapies targeting NAT2 in colorectal cancer

Search

Quick links