Anton George Henssen

The paper shows ecDNA localizes to the nuclear periphery in cancer, resisting silencing and enhancing transcriptional output through interactions with the nuclear lamina.

This study develops a method to detect minimal residual disease in neuroblastoma using ecDNA breakpoints, achieving high sensitivity and specificity in bone marrow samples.

TOPAS converts phosphoproteomic data into patient-specific reports for molecular tumor boards, focusing on clinically relevant signaling and therapeutic targets.

The paper introduces ec3D, a method to reconstruct 3D structures of ecDNA from Hi-C data, revealing spherical configurations and unique long-range interactions in cancer.

This paper develops CancerPAM, a bioinformatics pipeline for identifying CRISPR knock-in sites to remodel the tumor microenvironment, enhancing CAR T cell therapy in solid tumors.

A genome-wide plasmid screen, Retain-seq, identifies thousands of CpG-rich promoter-like human elements that tether episomes to mitotic chromosomes, shape ecDNA structure, and lose function when methylated.

The paper shows that extrachromosomal circular DNA (eccDNA) from micronuclei promotes inflammation and hepatocellular carcinoma (HCC) development through the cGAS-STING pathway.

This study shows lineage history and developmental context jointly shape tumor-state architecture in MYCN-driven zebrafish neuroblastoma.

The paper investigates how extrachromosomal DNA (ecDNA) inheritance mechanisms influence cancer evolution through mitotic segregation and micronuclei formation.

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

The paper introduces interSeg, a deep learning tool that accurately predicts oncogene amplification status from interphase FISH images, achieving high accuracy in detecting ecDNA and chromosomal amplifications.

The paper identifies chromothripsis-induced amplification of DYRK1A in blast phase MPN as a driver of aggressive disease and a potential therapeutic target.

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

This paper shows that high MYCN levels in neuroblastoma reduce L1CAM expression, limiting CAR T cell efficacy, and that inhibiting MYCN with MLN8237 restores L1CAM and enhances CAR T cell activity.

This paper introduces FUDGE, a method for detecting fusion genes using CRISPR/Cas9 enrichment and long-read sequencing, achieving high sensitivity and specificity across various cancer types.