Meydan LabSystems and Computational Biomedicine · Weill Cornell Medicine

Meydan Lab

Projects

Chromatin remodeling and lymphoma

Nature, 2026 · Cancer Cell, 2024

Mutations in subunits of the SWI/SNF (BAF) chromatin-remodeling complex occur in about one in five human cancers, and ARID1A is frequently mutated in lymphoma. BAF complexes open chromatin so that transcription factors can bind, but how their loss reshapes gene regulation, and why mutations in different subunits converge on cancer, has remained unclear.

This project follows BAF disruption from transcription-factor binding to the 3D organization of the genome and to B-cell fate, and asks whether the dependencies it creates can be targeted therapeutically.

Aims

  • Determine how ARID1A loss changes B-cell fate decisions and contributes to lymphoma.
  • Connect BAF chromatin remodeling to CTCF and cohesin binding and to 3D genome organization.
  • Identify therapeutic vulnerabilities created by BAF disruption.

Key findings

  • ARID1A coordinates the sequential binding of transcription factors through SWI/SNF; its loss drives pre-memory B-cell fate and lymphoma development (Cancer Cell, 2024).
  • ARID1A-deficient lymphoma is vulnerable to SMARCA2/SMARCA4 inhibition, the basis of an international patent application for these inhibitors in lymphoma.
  • BAF disruption alters CTCF and cohesin binding and 3D chromatin architecture, a shared mechanism for cancer-driving mutations across SWI/SNF subunits (Nature, 2026).

Approach

Integrative multiomic analysis of chromatin accessibility, transcription-factor binding, gene expression, single-cell multiome and 3D genome data from genetic models, with computational models of transcription-factor regulatory potential and chromatin structure.

Selected papers

More in the complete bibliography →

Portals, code and data (5)

An integrated view of human spaceflight

Science, 2019 · Cell, 2020 · Nature, 2024

Spaceflight exposes the body to microgravity, radiation, isolation and disrupted daily rhythms. As missions grow longer and more people fly, understanding these effects at the molecular level matters for astronaut health and for human biology on Earth.

This project builds an integrated molecular picture of the human response to spaceflight, from one year-long mission with a twin on the ground, to a synthesis across astronauts and model organisms, to multi-mission atlases and shared data infrastructure.

Aims

  • Measure molecular, physiological and cognitive changes during long-duration spaceflight against a genetically matched control.
  • Identify biological responses shared across astronauts and experimental models.
  • Build shared data resources and a biobank so that spaceflight studies can be compared across missions.

Key findings

  • Many changes measured during the year-long mission returned toward baseline after landing, while a subset, including some gene-expression changes, persisted (NASA Twins Study, Science, 2019).
  • Mitochondrial stress emerged as a central biological hub of the spaceflight response across astronauts and model organisms (Cell, 2020).
  • SOMA connected molecular and clinical measurements across missions, including the Inspiration4 crew, and paired them with an international astronaut biobank (Nature, 2024).
  • Immune changes, mitochondrial stress and host–microbiome responses recur across longitudinal, single-cell and multiomic measurements.

Approach

Longitudinal multiomics (transcriptomics, epigenomics, proteomics, metabolomics and microbiome) and single-cell profiling, integrated with clinical and physiological measurements and with model-organism data. The data are shared through interactive portals, public repositories and a biobank.

Selected papers

More in the complete bibliography →

Portals, code and data (15)

Targeted therapy in acute myeloid leukemia

Preclinical studies, 2014–2017 · First IDH2 inhibitor approved, 2017

Acute myeloid leukemia (AML) is an aggressive cancer of the blood and bone marrow in which immature myeloid cells fail to mature and crowd out normal blood production. In some patients, mutations in the IDH2 gene produce an abnormal metabolite that disrupts DNA demethylation and blocks differentiation.

This project studied how targeted inhibition of mutant IDH2 reverses that epigenetic dysfunction, alone and in combination with inhibition of oncogenic signaling, and how cooperating mutations shape the epigenome of AML. The preclinical work was cited in the clinical development of enasidenib, the first IDH2 inhibitor, which the FDA approved in 2017 for relapsed or refractory IDH2-mutant AML.

Aims

  • Determine whether inhibiting mutant IDH2 reverses aberrant DNA methylation and restores differentiation in leukemia models.
  • Test combination strategies that pair epigenetic therapy with inhibition of oncogenic signaling in IDH2- and TET2-mutant AML.
  • Understand how cooperating mutations in epigenetic regulators combine to drive leukemia.

Key findings

  • Inhibiting mutant IDH2 with AG-221, the compound later named enasidenib, reduced abnormal DNA methylation and restored differentiation in leukemia models (2014).
  • Combination targeted therapy disrupted aberrant oncogenic signaling and reversed epigenetic dysfunction in IDH2- and TET2-mutant AML models (Cancer Discovery, 2017).
  • The original enasidenib clinical publications cited this preclinical mechanism.

Approach

Genome-wide DNA methylation and gene-expression profiling of genetically defined leukemia models before and after treatment, with computational analysis of epigenomic change.

Selected papers

More in the complete bibliography →

COVID-19 in New York: testing, viral genomics and host response

2020–2022 · Nature Medicine · Nature Communications · Nature · Cell Reports Medicine

In spring 2020, New York’s clinical laboratories faced testing backlogs and shortages of PCR reagents, and fully at-home self-testing was not yet available in the United States. Clinicians and researchers also needed to know which viral lineages were spreading and how infection injured the body.

This project developed and validated a rapid RT-LAMP test that needs little equipment, sequenced the virus across the first wave, and profiled host responses from nasal swabs to autopsy tissues.

Aims

  • Expand molecular testing capacity with an assay that runs at a constant temperature and needs minimal instrumentation.
  • Track the viral lineages circulating during New York’s first wave.
  • Characterize host responses and tissue damage associated with infection and severe outcomes.
  • Test whether ACE inhibitors and angiotensin receptor blockers, drugs that can raise expression of the viral entry receptor ACE2, increased susceptibility to infection or worsened outcomes.

Key findings

  • The RT-LAMP assay produced a color-based readout in about 30 minutes; its validation against RT-PCR contributed to Color’s FDA emergency authorization in May 2020 (Nature Communications, 2021).
  • Sequencing of clinical specimens from 669 patients tracked the lineage that dominated New York’s early outbreak.
  • In health records of 50,821 patients at two New York hospitals, ACE inhibitor or angiotensin receptor blocker use was associated with lower risk of intubation and death after adjustment for demographics, drug indications and comorbidities. The authors described the result as preliminary and called for clinical trials before any change to guidelines (Nature Communications, 2021).
  • Complement and coagulation activation were linked to ventilation and death (Nature Medicine, 2020).
  • Spatial profiling of autopsy lungs mapped infected alveolar cells and the inflammation and repair that followed (Nature, 2021).
  • COVID-19 disrupted transcriptional programs and tissue identity across many organs; in the lung, these changes tracked viral load and disease stage (Cell Reports Medicine, 2022).

Approach

RT-LAMP assay design with statistical validation against RT-PCR, shotgun sequencing and clinical records; viral genome sequencing; host transcriptomics of swabs and autopsy tissues; spatial transcriptomics; and integration with health records.

Selected papers

More in the complete bibliography →

Portals, code and data (3)

Urban microbiome mapping

Cell Systems, 2015 · Cell, 2021

Cities host dense microbial communities that people encounter every day but that had rarely been measured. This earlier project mapped the DNA found on urban transit surfaces, first across the New York City subway and then worldwide through the International MetaSUB Consortium, including genes for antimicrobial resistance.

Aims

  • Create a city-scale molecular map of the microbes in a subway system.
  • Extend standardized sampling to cities worldwide and catalogue urban microbiomes and antimicrobial-resistance markers.

Key findings

  • PathoMap sampled all 466 open New York subway stations, producing the first city-scale DNA map of a subway system (Cell Systems, 2015).
  • The MetaSUB global atlas covered 60 cities and mapped urban microbiomes and antimicrobial resistance (Cell, 2021).

Approach

Shotgun metagenomic sequencing of standardized surface swabs, with taxonomic and functional profiling and interactive maps.

Selected papers

More in the complete bibliography →

Portals, code and data (3)
  • MetaSUB Map Urban microbiome sampling and visualization. The portal credits Cem Meydan and David Danko. Open portal.
  • StuckOnU 2017 Visualization of a 48-hour phone-swabbing experiment. The page credits the website and visualizations to Cem Meydan. Open page.
  • PathoMap New York City subway microbiome map (2015). Availability varies.

Portals, code and data

Interactive portals, maps and biobanks from these projects, with their access conditions.

Study code and data indexes

External work & Ventures

Dr. Meydan’s company work. The companies are separate from the Meydan Lab and Weill Cornell Medicine.

Onegevity → Thorne HealthTech: GutBio

Dr. Meydan joined Onegevity as a founding employee and built the GutBio product and analytical platform from the ground up. He continued to lead research and microbiome product development at Thorne HealthTech after the merger. His work spanned the company’s 2021 IPO and its 2023 acquisition by L Catterton. GutBio supported commercial microbiome testing in the United States and Japan.

GutBio paired stool metagenomic sequencing with an analytical platform for metagenome-guided interventions. Research from this work includes an intervention study in irritable bowel syndrome and later multiomic studies.

ARQ

Dr. Meydan is a co-founder of ARQ. The company develops data-driven approaches to human performance. onearq.com

Dr. Meydan’s contribution to each study, with historical context and primary sources: Contributions and sources

Content reviewed 2026-10-31.