Research

The Viny Lab studies how chromatin architecture and DNA methylation define the rules of genome interpretation, shaping when and where transcription factors act. We investigate how disruption of these rules in hematopoietic stem cells drives myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML), and leverage these insights to develop epigenetically informed therapeutic strategies. 
Mutations in chromatin regulators—including cohesin complex members—are among the most common lesions in MDS and AML, highlighting the central role of genome organization in hematologic malignancies. 
 
Our Lab studies how chromatin rules dictate when and how transcription factors become oncogenic—and how to therapeutically exploit that dependence. 

Active Research Areas
Chromatin Architecture and Lineage Specification
We study how 3D genome organization establishes lineage-specific transcriptional programs and how disruption of chromatin architecture alters hematopoietic differentiation.
Key questions include:

• How cohesin regulates chromatin accessibility and insulation
• How lineage-specific transcription factor cistromes are established and maintained
• How altered chromatin structure impairs differentiation or promotes stemness

Pioneer Factors and Chromatin Licensing
We investigate how chromatin accessibility is established and how pioneer transcription factors engage regulatory DNA.
Current work focuses on:

• Cohesin–BAF cooperation in enabling pioneer factor activity
• Mechanisms governing the initiation and maintenance of accessibility
• Chromatin-dependent constraints on transcription factor function

  

DNA Methylation as a Regulatory Gate
We study how DNA methylation interacts with chromatin accessibility to stabilize or restrict regulatory elements.
Current directions include:

• Single-molecule resolution of accessibility–methylation relationships
• Effects of mutations such as TET2 loss on epigenetic state
• Methylation-dependent control of transcription factor binding

  

Transcription Factor Rewiring in Leukemia
We investigate how transcription factors are rewired in altered chromatin contexts to drive leukemogenesis.
Areas of focus include:

• FLI1-driven programs in cohesin-mutant hematopoietic stem cells
• FLI1–MENIN cooperation as an oncogenic dependency
• Loss of transcription factor specificity, including GATA1 cistrome disruption in erythropoiesis

Translational Epigenomics and Therapeutic Targeting
We leverage mechanistic insights to define biomarkers and therapeutic vulnerabilities in myeloid malignancies.
Key efforts include:

• Predictors of response to hypomethylating agents in MDS
• Synthetic lethal dependencies in cohesin-mutant cancers
• Targeting transcription factor–cofactor interactions, including menin sensitivity

Technology Development and Systems-Level Profiling
We develop and apply genomic platforms to study chromatin regulation in primary human samples.
Capabilities include:

• Low-input and automated ATAC-seq and CUT&RUN
• Nanopore-based chromatin and methylation profiling
• Single-cell and proteomic approaches
• Rapid diagnostic pipelines for leukemia genomics

Long-Term Goals
Our goal is to define the principles by which chromatin states govern transcription factor activity and cell identity, and to apply these insights to:

• Predict disease evolution in clonal hematopoiesis and leukemia
• Identify context-specific therapeutic vulnerabilities
• Develop precision epigenetic therapies

Ultimately, we seek to move beyond cataloging mutations toward defining—and targeting—the rules of genome regulation in cancer.