Charles L. Sawyers

Loss of extracellular matrix-integrin signaling switches off YAP/TEAD and lets prostate adenocarcinoma organoids turn neuroendocrine; LATS inhibition reverses it, and combined YAP, NOTCH and AR inhibition fully reprograms them.

This study identifies an IL-1β/IL-6 signaling circuit in the tumor microenvironment that drives prostate cancer progression from pre-invasive to invasive stages.

The paper identifies a TIP60 coactivator switch in neuroendocrine prostate cancer, revealing a therapeutic target for MYC-driven diseases.

The paper integrates single-cell multiomics and CRISPR screening in prostate cancer organoids to reveal lineage-specific dependencies and heterogeneity effects on gene essentiality.

This study identifies FOXA1 mutations in prostate cancer, showing they alter chromatin accessibility and promote tumorigenicity by reprogramming cell fate through interactions with androgen receptor and POU2F1.

This study identifies loss of function mutations in the DNA pre-replication complex as a mechanism for PARP inhibitor resistance in BRCA-mutant prostate cancer, independent of reversion mutations.

This study develops an in vivo platform called SETs to reconstruct tumor evolution without chromosomal instability, identifying therapeutic response determinants in prostate cancer.

This study identifies ASCL1 as a critical driver of neuroendocrine lineage transition in prostate cancer using an in vivo model and spatial transcriptomics.

The paper uses single-cell analysis to study how cell surface antigen expression changes in treatment-resistant prostate cancer, revealing transcriptional heterogeneity and shared gene regulatory networks between NEPC and SCLC.

This study shows that treatment timing affects the path to androgen receptor signaling inhibitor resistance in prostate cancer, with resistance arising through different mechanisms depending on the tumor context.

The paper predicts cancer cell-of-origin from DNA sequences by matching mutational landscapes to chromatin modification patterns in normal tissues.