Ross L. Levine

This paper evaluates generalist large language models (LLMs) in tumor genomic interpretation tasks, finding they can complement or outperform task-specific models in some cases.

This study uses single-cell multiomic analysis to reveal genotype-immunophenotype relationships and clonal evolution in NPM1-mutant AML across disease stages.

This study identifies CEBPD as a tumor suppressor gene in acute myeloid leukemia through functional experiments and genomic analyses.

This study shows that TET2 and TP53 mutations work together to promote leukemic transformation by altering inflammatory responses and chemotherapy tolerance in hematopoietic stem cells.

scDNA is a toolkit for analyzing single-cell DNA data to identify subclonal structures, mutation trajectories, and sample quality, with applications in cancer research.

This study characterizes myeloid sarcoma through multi-omic profiling, identifies RAS pathway activation as a hallmark, and shows RAS inhibition reduces tumor burden in mouse models.

Decipher is a deep generative model that integrates single-cell RNA-seq data to visualize and characterize transitions between normal and perturbed cell states across different diseases.

The paper identifies CXCL1-CXCR2 signaling as a mediator of leptomeningeal metastasis resistance to radiation therapy and presents it as a potential therapeutic target.

This study identifies TET2-mutant clonal hematopoiesis in thyroid cancer microenvironments and shows that TGFβ signaling from these macrophages mediates resistance to BRAF/MEK inhibition, with TGFβ inhibition restoring sensitivity.

This study identifies two sphingolipidomic subtypes in AML, with one subtype associated with poor clinical outcomes and high-risk features.

This study presents a paired tumor:normal sequencing dataset for hematologic malignancies, showing improved identification of somatic variants and their clinical relevance.

This study shows that Tet2 loss-of-function in AML cells alters cell-state transitions, improving survival during drug treatment and contributing to relapse.

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

The paper shows Stag2 loss in HSPCs impairs B-cell lineage commitment by reducing chromatin accessibility, while Stag1 cannot restore this function despite rescuing topological domains.