Mathijs Arnoud Sanders

scRIPT: a rapid, high-coverage single-cell lineage-tracing method applied to the hematoendothelial differentiation of embryonic stem cells

scRIPT is a single-cell lineage-tracing method that improves coverage and reliability in differentiation protocols by integrating rapid barcoding, sorting, and sequencing with quality control.

Single-Cell Roadmap of Early Hemato-Endothelial Development: Functions of Atf3, Zfp711 and Bcl6b

The paper investigates the roles of Atf3, Zfp711, and Bcl6b in early hemato-endothelial lineage specification using scRNA-seq and KO mESCs, finding distinct effects on mesodermal and hematopoietic lineages.

G-quadruplexes are a source of vulnerability in BRCA2 deficient granule cell progenitors and medulloblastoma

This study identifies G-quadruplexes as a source of genome instability in BRCA2-deficient granule cell progenitors and medulloblastoma, suggesting PIF1 helicase as a therapeutic target.

Hematological phenotypes in GATA2 deficiency syndrome arise from secondary injuries and maladaptation to proliferation

This study shows that GATA2 deficiency leads to hematological issues through bone marrow failure and maladaptation, with leukemia arising from genomic instability and proliferation defects.

Widespread chromatin context-dependencies ofDNA double-strand break repair proteins

A multiplexed screen reveals how dozens of proteins sense the local chromatin context to tune the balance between two DNA repair pathways.

Gata2-regulated Gfi1b expression controls endothelial programming during endothelial-to-hematopoietic transition

This study shows that Gata2 regulates Gfi1b to control endothelial-to-hematopoietic transition and HSPC maturation, with reduced Gata2 leading to impaired hematopoietic programming.

The mutational landscape of human somatic and germline cells

This study compares mutational landscapes in somatic and germline cells across 29 anatomical structures, identifying key mutational signatures and their contributions to different cell types.

Inherited MUTYH mutations cause elevated somatic mutation rates and distinctive mutational signatures in normal human cells

This study shows that inherited MUTYH mutations increase somatic mutation rates and specific mutational signatures in normal human cells, contributing to cancer risk without causing premature aging.

Somatic mutation rates scale with lifespan across mammals

This study finds that somatic mutation rates per year decrease with species lifespan across mammals, suggesting evolutionary constraints on mutagenesis and its role in ageing.

Elevated somatic mutation burdens in normal human cells due to defective DNA polymerases

The paper shows that germline mutations in POLE or POLD1 lead to elevated mutation burdens in normal human cells and tissues, but do not cause premature aging or other phenotypic features beyond early-onset cancer.

Genome-wide mutational signatures of immunological diversification in normal lymphocytes

The paper analyzes the mutational landscape of normal lymphocytes, revealing off-target effects of programmed genome engineering and the impact of differentiation and microenvironment exposure.

Germline loss-of-function variants in the base-excision repair gene MBD4 cause a Mendelian recessive syndrome of adenomatous colorectal polyposis and acute myeloid leukaemia

Life without mismatch repair

The paper quantifies mismatch repair (MMR) activity in human tissues by analyzing mutation rates in individuals with constitutional MMR deficiency, revealing genotype-specific mutational signatures and the role of MMR components in DNA repair.

Somatic evolution in non-neoplastic IBD-affected colon

The paper analyzes somatic mutations in colonic crypts of IBD patients and controls, finding higher mutation rates and clonal expansions in IBD-affected tissue.

An integrated genomic analysis of anaplastic meningioma identifies prognostic molecular signatures

This study identifies two molecular subgroups of anaplastic meningioma with distinct survival outcomes and links them to specific genetic mutations.