Rosalie C. Sears

Designed protein binders to conserved MYC regions reach low-nanomolar affinity, reduce MYC-MAX proximity in cells, and are depleted from MYC-dependent cancer cells in culture and mouse pancreatic tumors.

The paper identifies subtype-intermediate progenitor cells in pancreatic cancer with distinct epigenetic profiles linked to clinical outcomes and lineage reprogramming.

This study shows that GNL3 SUMOylation is essential for homologous recombination repair of DNA double-strand breaks and identifies potential therapeutic targets in breast cancer.

ACCREDIT improves cross-modal image registration by detecting failures and automatically recovering alignments, outperforming existing methods in accuracy and robustness.

The paper identifies spatially distinct epithelial states in PDAC that correlate with immunosuppressive myeloid niches and poor prognosis.

The paper identifies global 3'UTR lengthening in SCNC through APA and develops a neural network model to classify SCNC using APA signatures.

The paper identifies resistance mechanisms to KRAS-MEK pathway targeting in PDAC by analyzing clinical trial data and multi-omics profiles, showing that KRAS/MYC co-gain correlates with resistance and that co-targeting these genes is synergistic.

This paper introduces a dual-contrast microCT protocol to track tumor growth, metastasis, and cachexia in murine PDAC models over time.

This study shows that HuR promotes immune evasion in PDAC by inhibiting T cell infiltration and function, suggesting HuR as a therapeutic target with immunotherapy.

This study shows that MHC-II expression in pancreatic cancer cells correlates with immune infiltration and improves immunotherapy response in mouse models.

S3R models spatially varying associations in spatial transcriptomics data by estimating location-specific coefficients with structured sparsity and smoothness penalties, showing effectiveness in synthetic and real datasets.

This study develops a novel pancreatic cancer mouse model by expressing Myc and mutant Kras in adult acinar cells, showing metastasis and therapeutic resistance similar to human PDAc.

This study identifies long noncoding RNAs as key regulators of pancreatic cancer identity and resistance to reprogramming.

PIVOT is an open-source tool for nonlinear registration of multi-omic spatial data, demonstrating improved throughput compared to existing workflows.

This study shows PIN1 promotes cellular plasticity and immune changes in chronic pancreatitis, with genetic or pharmacological inhibition reducing disease severity.

The paper identifies a negative feedback loop where MYC suppresses KDM5B, leading to increased cell survival and tumor progression.

This study shows alpha-synuclein regulates nucleolar DNA double-strand break repair in melanoma cells, affecting genomic stability and cancer progression.

This study analyzes clonal heterogeneity in human pancreatic ductal adenocarcinoma using single-cell and spatial transcriptomics, revealing transcriptional continua, clonal transitions, and spatially dispersed clones associated with metastasis.

This study shows that HuR in pancreatic cancer cells enhances angiogenesis by modulating extracellular vesicle signaling to endothelial cells, increasing their migratory and tube-forming abilities while reducing ICAM-1 expression.

The paper shows hypoxic fibroblasts in pancreas cancer use histone methylation and ROS-mediated NF-κB activation to produce growth factors that drive epithelial-mesenchymal transition in malignant cells.

This study shows HBP1 protects against acute pancreatitis but promotes pancreatic cancer progression in the presence of KRAS mutations.

The paper shows that metaplastic tuft cells in pancreatic cancer transdifferentiate into neural-like progenitor cells, driven by Myc activity, and this transition is linked to poor patient survival.

This study constructs the Prostate Cancer Cell Atlas by analyzing ~710,000 single cells from 197 human samples to characterize cell states and dynamics across prostate cancer progression stages.

This paper introduces a novel adaptor-switching strategy, s3, that significantly improves usable reads per cell in single-cell genomics assays while maintaining high-throughput capabilities.