Cheng‐Zhong Zhang

The paper identifies clustered structural variant hotspots in osteosarcoma, linking them to oncogenic addiction and plasticity through transcriptional changes and clinical detectability.

This study identifies fusion-driven oncogenic programs in translocation renal cell carcinoma (tRCC) that shape an immunosuppressive tumor microenvironment, explaining its reduced immunotherapy response.

This paper introduces refLinker, a method for haplotype-resolved analysis of cancer karyotypes, revealing transcriptional consequences of somatic Xi rearrangements.

SCANBIT identifies tumor cell populations in scRNA-seq data by using pseudobulked SNV calls, showing that mutational burden affects identification accuracy.

This study links ionizing radiation-induced nuclear abnormalities to delayed proliferative death and genomic instability through single-cell and bulk genome analysis.

The paper identifies breakage-replication/fusion as a mechanism causing DNA duplications and insertions, unifying explanations for complex rearrangements and enabling rapid DNA amplification.

This paper presents a computational method to determine complete chromosomal haplotypes using bulk long-range sequencing and Hi-C data, achieving high precision and completeness in diploid human genomes.

This paper shows that CRISPR-Cas9-induced DNA breaks can lead to chromothripsis, a catastrophic chromosomal rearrangement, which is an on-target toxicity in genome editing.

This study identifies genomic signatures of chromosomal instability in Barrett's esophagus progressing to esophageal adenocarcinoma, showing sloping copy-number variation as a precursor to complexity.

The paper analyzes whole-genome sequencing data from cancer samples to identify genomic footprints of telomere maintenance mechanisms, finding specific telomere variant repeat patterns associated with ATRX/DAXX mutations.

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

This study analyzes chromothripsis in 2,658 cancers using whole-genome sequencing, finding it prevalent across multiple cancer types with complex structural alterations.

SvABA detects structural variants and indels using genome-wide local assembly, showing improved sensitivity and specificity, especially for small variants and complex rearrangements in cancer genomes.

The paper analyzes somatic rearrangements in cancer genomes using whole-genome sequencing data, identifying recurrent breakpoints and their genomic features.