Nathan A. Lack

This study uses longitudinal scRNA-seq to track neuroendocrine transdifferentiation in a prostate cancer model, identifying transcriptional changes and key regulators during treatment-induced NEPC progression.

The paper develops a motif-based model to predict sequence variant effects in AR enhancers and identifies functional classes of transcription factors, validated against mutagenesis data and GWAS risk alleles.

This study shows that the androgen receptor and MYC work together to control the production of Siglec-7 ligands in prostate cancer by regulating sialylation and glycopeptide profiles.

The paper identifies BRPF1 as a key regulator of Taxol resistance in TNBC through genetic and chemical screens, showing its inhibition sensitizes resistant cells to chemotherapy.

This study uses longitudinal single-cell RNA sequencing to identify RUNX1T1 as a key regulator in the transition and maintenance of treatment-induced neuroendocrine prostate cancer.

The paper introduces a method to infer functional regulatory sites in enhancer sequences using STARR-seq data, showing it can identify local regulatory sites missed by global approaches.

This paper evaluates B7-H3 expression across prostate cancer subtypes and identifies it as a stable target for ADC and ICI due to its low heterogeneity and negative regulation by androgen signaling.

This study shows AR-V7 forms condensates independently of androgens and AR-FL in CRPC, driving oncogenic transcription through both condensate-dependent and -independent mechanisms.

The paper investigates how AR-bound CREs influence gene expression through epigenetic changes and chromatin looping, finding that contact frequency with promoters drives expression.

The paper identifies breast cancer risk SNPs that overlap with estrogen receptor binding sites, showing their role in altering estrogen signaling through chromatin interactions.

This study develops snpSTARRseq, a high-throughput method to test non-coding variants from GWAS, showing 37% of prostate cancer risk loci alter enhancer activity.

The paper introduces CWAS, a method linking genetic variation to chromatin states, identifying novel prostate cancer risk loci and regulatory mechanisms not detectable by eQTLs.

The paper develops multimeric sACE2 decoys using SunTag or MoonTag systems, showing >100-fold increased SARS-CoV-2 neutralization compared to monomeric sACE2.