Kadir Caner Akdemir

This study shows that chromosomal instability in esophageal adenocarcinoma drives an inflammatory tumor microenvironment through a cGAS-chemokine-myeloid axis, with CXCL8 as a key mediator.

This study shows KDM6A mutations in bladder cancer improve response to immune checkpoint therapy but worsen chemotherapy outcomes through effects on DNA repair and metabolic reprogramming.

This study uses spatial transcriptomics to identify ECM expression patterns in GBM, revealing region-specific adhesion and signaling networks in the tumor microenvironment.

This study investigates how oncogenic mutations in gliomas influence the tumor microenvironment through integrative multiomic and spatial transcriptomic analysis of glioma samples.

This study shows that SMARCA4 mutations in lung cancer disrupt enhancer landscapes and innate immune gene expression, leading to immunotherapy resistance.

The paper identifies ERBB2 alterations as a recurrent oncogene in esophageal adenocarcinoma brain metastases and links them to monoclonal seeding and treatment response.

The paper analyzes AID-related mutations across cancers and finds they are associated with better outcomes in ICI-treated patients and contribute to immunogenic neoepitopes.

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

This study identifies germline genetic variants influencing somatic mutation patterns in 2,642 cancer genomes across 39 cancer types.

This study characterizes mitochondrial genomes in 2,700 cancer patients across 37 types using whole-genome sequencing and RNA-seq, revealing mutational patterns, truncating mutations, and nuclear transfer of mitochondrial DNA.

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

The paper identifies hundreds of genes deregulated by SVs in cancer, showing increased expression linked to SV breakpoints and enhancer elements.

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