G. J. Murphy

Abnormal global longitudinal strain and reduced serum inflammatory markers in cardiac AL amyloidosis patients without significant amyloid fibril deposition

The paper identifies early molecular and functional signatures in cardiac AL amyloidosis patients with abnormal GLS and reduced inflammatory markers despite no significant amyloid fibril deposition.

A heterozygous CEBPA mutation disrupting the bZIP domain causes MDS disease progression

This study shows a heterozygous CEBPA mutation in the bZIP domain causes MDS progression by altering chromatin structure and clonal composition, using patient-derived iPSCs.

Intertumoral lineage diversity and immunosuppressive transcriptional programs in well-differentiated gastroenteropancreatic neuroendocrine tumors

This study analyzes single-cell transcriptomes of gastroenteropancreatic neuroendocrine tumors to identify lineage diversity and immunosuppressive programs in tumor and immune cells.

Mapping Cellular Response to Destabilized Transthyretin Reveals Cell- and Amyloidogenic Protein-Specific Signatures

The paper exposes cells to destabilized TTR variants and analyzes transcriptional and epigenetic responses to identify cell- and protein-specific signatures of amyloidogenic stress.

Multi-modal profiling of peripheral blood cells across the human lifespan reveals distinct immune cell signatures of aging and longevity

The paper analyzes immune cell changes in centenarians and younger individuals to identify aging and longevity signatures in peripheral blood cells.

Multi-Modal Profiling of Human Fetal Liver-Derived Hematopoietic Stem Cells Reveals the Molecular Signature of Engraftment Potential

The paper profiles human fetal liver hematopoietic stem cells using multi-modal data to identify a molecular signature associated with engraftment potential.

Amyloidogenic Proteins Drive Hepatic Proteostasis Remodeling in an Induced Pluripotent Stem Cell Model of Systemic Amyloid Disease

This study uses iPSC-derived hepatic cells to show that liver proteostasis factors and UPR signaling correlate with TTR amyloid production and can reduce amyloid secretion through ER stress-independent activation.