Roel G.W. Verhaak

This paper introduces ecEvol, a method to infer ecDNA emergence time and other parameters from bulk whole-genome sequencing data, finding that ecDNA typically emerges early and is associated with poorer survival.

The paper analyzes spatial gene expression and tumor-microenvironment interactions in IDH-mutant gliomas across malignant transformation, finding reduced proliferation at the infiltrative margin in higher-grade tumors.

This study identifies multicellular spatial molecular programs in meningiomas using multi-omic data and develops a model to infer these programs from histopathology.

The paper identifies DNA methylation changes during IDH-mutant glioma progression, links them to TET enzyme activity, and develops a methylation-based grading system that outperforms WHO grading.

The paper analyzes multi-omics data from IDH-mutant astrocytomas to identify molecular markers of malignant progression linked to cell cycling and DNA methylation changes.

The paper observes that lentiviral infection selectively depletes cells containing extrachromosomal DNA (ecDNA), suggesting potential therapeutic strategies for ecDNA-driven cancers.

This study identifies genetic changes in IDH-mutant gliomas that correlate with treatment response and tumor evolution using longitudinal genomic data from 206 patient samples.

This study shows that ecDNA mis-segregation leads to micronuclei formation, reduced oncogene transcription, and improved patient survival in neuroblastoma.

AmpliconSuite identifies focal amplifications in cancer genomes, showing ecDNA has higher copy numbers and stronger oncogene enrichment compared to other amplification types.

The paper investigates the development and evolution of extrachromosomal DNA (ecDNA) in Barrett's esophagus patients progressing to esophageal adenocarcinoma, finding ecDNA is strongly associated with cancer progression and enriched for oncogenes and immunomodulatory genes.

The paper identifies 407 Master-Regulator proteins that canalize cancer genomics into transcriptional subtypes and links genetic alterations to tumor biology through modular regulatory architectures.

The paper examines how somatic structural variations affect TAD boundaries and gene regulation in human cancers using whole genome sequencing data.

The paper examines how somatic mutation distributions vary across chromatin folding domains in cancer genomes, revealing distinct patterns associated with different mutational processes.

The paper identifies three span intervals of tandem duplications in TDP tumors and links them to specific gene mutations and pathways, showing TP53 and BRCA1 loss drives short-span TDPs.

The paper analyzes tumor-intrinsic gene expression subtypes in IDH wild type glioblastomas and their association with immune microenvironment changes during recurrence.