Christopher R. Vakoc

This study shows that targeting inflammatory myeloid progenitors in the bone marrow with CAR T cells reduces neuroinflammation and cognitive decline in aging and Alzheimer's models.

This study identifies POU2AF2 as a lineage-specific dependency in DLBCL, showing it coactivates POU2F2 to sustain malignant transcriptional networks and innate-like B-cell identity.

The paper identifies POU2F1 as a key regulator of DLL3 and neuroendocrine identity in SCLC through CRISPR screens and epigenomic analysis.

This study shows SS18-SSX sustains oncogenic transcription without needing SWI/SNF activity, identifies P300 as a critical co-factor, and demonstrates targeting P300 or SWI/SNF as therapeutic strategies.

This study reveals that PAC-1, a clinical-stage oncology compound, targets drug-resistant cancers by disrupting iron homeostasis and exploiting MDR1 expression to induce iron depletion.

This study identifies MARK2/3 as essential kinases for YAP/TAZ function in cancer and shows their inhibition can restore Hippo pathway tumor suppression.

This study identifies a therapeutic vulnerability in POU2F-POU2AF-driven cancers by showing that targeting the mSWI/SNF complex with a PROTAC degrader reduces tumor growth in preclinical models.

This study identifies mSWI/SNF complex activity as a targetable dependency in POU2F3-positive small cell lung cancer, showing that inhibiting mSWI/SNF or BRD9 reduces tumor growth and improves survival.

The paper identifies MED12-p63 interaction as a driver of basal identity in PDAC through genetic screens and biochemical analysis.

ACE introduces a probabilistic model to assess gene essentiality in CRISPR screens, identifying differential essentiality across samples and uncovering genotype-specific essentiality.

This study shows ORC subunits and CDC6 are essential for pre-RC assembly, mitosis, and nuclear structure in human cells.