Benjamin L. Ebert

This study identifies transcriptional changes in stromal and endothelial cells during MGUS to myeloma progression and treatment response, revealing a tumor-permissive BME signature that is modulated by therapy.

The paper discovers a charged molecular glue, c-Glue, through targeted degron display, enabling the development of Molecular Glue Degraders (MGDs) for protein degradation.

This paper identifies a bifunctional small molecule that can induce both transactivation and repression of gene expression depending on cellular context.

The paper identifies plasma proteins associated with clonal hematopoiesis and links them to cardiovascular disease through proteomic and genetic analyses.

This paper develops chemical probes for FBXO22, including a degrader and a recruitment ligand, to enable targeted protein degradation applications.

This study develops electrophilic degraders using SNAr chemistry, enabling selective protein degradation without requiring a defined E3 ligase recruiter.

This study analyzes 4,187 participants over 21 years to identify factors influencing the development of clonal hematopoiesis, finding age, sex, and dyslipidemia as significant predictors.

The paper identifies IL1RAP and AIM2 as key modifiers of CHIP-associated cardiovascular risk using UK Biobank data and CRISPR experiments in mice.

This study analyzes clonal hematopoiesis in over a million diverse individuals, identifying 72 genome-wide significant loci and linking CHIP to various phenotypes.

This study shows that clonal hematopoiesis, especially with DDR gene mutations, increases the risk of peripheral artery disease and atherosclerosis.

The paper investigates the association between age-related mosaic chromosomal alterations and infection risk in 767,891 individuals without blood cancer, finding increased infection susceptibility linked to mCAs.

The paper examines TP53 allelic states in MDS patients, finding that bi-allelic targeting is linked to worse outcomes, while mono-allelic targeting does not differ from wild-type patients.

The paper shows oncologic therapy increases clonal hematopoiesis with DDR mutations, which predicts risk of therapy-related myeloid neoplasms.

The paper performs a pooled loss-of-function screen in hematopoietic cells to identify genes underlying GWAS loci associated with red blood cell traits, finding 77 genes at 38 loci with biological relevance.