Zeynep Kalender Atak

This study identifies immunogenomic drivers of acquired resistance to immunotherapy across multiple cancer types using a large-scale clinicogenomic dataset.

The paper shows that ciliopathy and neonatal ketamine exposure interact to cause motor deficits through non-apoptotic caspase activation, which can be reversed by caspase inhibition.

The paper identifies TZAP as a developmental regulator of mitochondrial homeostasis critical for activity-dependent synaptic connectivity in Drosophila.

The paper uses a deep learning model on melanoma genomes to prioritize enhancer mutations by analyzing allelic imbalance in chromatin accessibility and gene expression.

The paper identifies an intermediate cell state in melanoma through single-cell RNA-seq and ATAC-seq, revealing a gene regulatory network that governs phenotype switching and potential therapeutic targets.

Building gene regulatory networks from scRNA-seq and clustering cells on them identifies stable states robustly to batch effects, applied to mouse and human brain and to melanoma.

The paper introduces a computational pipeline, cisTarget, to identify functional non-coding mutations in cancer genomes by analyzing their impact on personalized gene regulatory networks.