C. A. Iacobuzio-Donahue

This study shows pancreatic tumors co-evolve with retrotransposons to modulate immune responses by regulating viral mimicry through SINEs and L1 retrotransposition.

This study identifies subclonal copy number alterations in relapsed osteosarcoma, showing MYC gain/amplification in treatment-resistant clones and their emergence before chemotherapy.

The paper investigates how 9p21.3 deletions in cancer disable both cell intrinsic and extrinsic tumor suppression by co-deleting CDKN2A/B and type I interferons, leading to immune evasion and metastasis.

This study develops a scalable workflow for targeted single-nucleus DNA sequencing in pancreatic cancer, enabling high-resolution genomic analysis of tumor subclones and normal cells.

The paper analyzes genomic data from 25,000 patients to identify associations between genomic alterations and metastatic patterns across 50 tumor types, finding chromosomal instability correlates with metastatic burden in some cancers.

This study shows BRCA mutations in pancreatic cancer alter CAF subtypes, specifically increasing CLU+ CAFs, and links this to HSF1 signaling.

The paper develops ATAC-Array, a low-cost chromatin accessibility assay, and shows it predicts pancreatic cancer prognosis based on chromatin accessibility patterns.

This study identifies MYC as a key driver of metastatic heterogeneity in pancreatic cancer by linking its activity to increased metastasis through TAM recruitment.

The paper identifies molecular mechanisms of neuroendocrine transformation in lung cancer using multi-omic analysis of tumors and clinical samples.

The paper identifies a human-specific BRCA2 variant that reduces DNA repair ability, suggesting positive selection for decreased BRCA2 function in human evolution.

This study investigates the evolutionary dynamics of non-coding regions in pancreatic cancer, finding higher mutational burden in noncoding DNA and similar mutational spectra between enhancers and coding DNA.

This study uses whole genome sequencing to show that relapsed multiple myeloma exhibits accelerated systemic seeding driven by chemotherapy-induced mutations and clonal expansion of single myeloma cells.

This study identifies genetic features of recurrent pancreatic cancer through sequencing and finds that treatment-induced genetic changes and potential second primary tumors influence recurrence.

The paper shows that endoplasmic reticulum stress enables pancreatic cancer cells to evade immune detection and form latent metastases.