Ryan Wilcox
University of Michigan, MI·Medicine & Clinical Research
T-cell lymphomas are aggressive blood cancers that arise from T cells, a type of white blood cell. Standard chemotherapy rarely cures them, and patients whose disease returns after treatment have few good options.
- Fields
Medicine & Clinical Research
Pharmacology
Microbiology & Immunology
- Topics
T-cell lymphoma
PTCL, NOS
enhancers
- Grants
- 6 known grants, through Feb 2031
What they work on
- Characterize a newly found enhancer, a DNA region that boosts gene activity, that controls the cancer-driving transcription factor GATA-3, and test its role in chemotherapy-resistant T-cell lymphoma using primary patient specimens.
- Identify GATA-3-dependent enhancers that drive cancer genes such as c-Myc, and follow how they change as lymphoma develops from a pre-malignant state in genetically engineered mouse models.
- Test whether a p300/CBP bromodomain inhibitor, a drug that blocks enhancer activation, works alone or with targeted agents against patient-derived lymphomas grown in NSG mice.
- Test whether the cell-death blocker BCL-xL is needed by both malignant T cells and their supporting macrophages, using newly developed BCL-xL antagonists and drug combinations in PDX and GEM models.
- Identify the Notch ligands, the signals that switch on the Notch pathway, and the stromal cells such as fibroblastic reticular cells that present them in PTCL, NOS, using mouse models and patient specimens.
- Define the gene-activity programs triggered by environment-dependent Notch signaling, and test whether blocking it with antibody-based or genetic approaches slows T-cell lymphoma growth.
- Evaluate the multikinase inhibitor pacritinib, which blocks JAK, CSF-1R and Src family kinases, in a multicenter phase II trial in several groups of patients with relapsed or refractory T-cell lymphoma.
- Study predictive and pharmacodynamic biomarkers during the pacritinib trial to learn which patients respond and how the drug acts on lymphoma cells and lymphoma-associated macrophages.
More about the research
The projects here ask what keeps these cancer cells alive and growing, and how those weak points could be targeted. They look at two sides of the problem. One is inside the cancer cell: the genetic switches that keep cancer-promoting genes turned on. The other is the cancer's surroundings, called the tumor microenvironment (TME). This includes nearby macrophages, immune cells that normally clear debris, and stromal cells, the supporting tissue cells. Both are studied in mice and patient samples, and one project carries the ideas into a clinical trial.
Why it matters
Patients with T-cell lymphomas, especially those whose disease resists chemotherapy or comes back after treatment, have poor outcomes and few effective options. This work could provide non-chemotherapy treatment strategies for them. It points to targets in both the cancer cells and their supporting environment: p300/CBP and GATA-3-controlled enhancers, BCL-xL, and Notch ligands. It also tests whether pacritinib, a drug already studied in other blood disorders, helps patients with relapsed disease, and looks for biomarkers that may predict who will respond.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Novel Multi-targeted Strategies Targeting T-cell Lymphomas and their Microenvironment
NIH · Mar 2026 – Feb 2031
Notch ligands as oncogenic drivers and therapeutic targets in T-cell lymphomas
NIH · Jan 2024 – Dec 2028
Novel therapeutic strategies targeting the enhancer landscape in high-risk T-cell lymphomas.
NIH · Jul 2026 – Jun 2028
Closest labs
Jason Yustein
Emory University, GA·Medicine & Clinical Research
Map single-cell protein and RNA signatures and cell-cell communication in MYC-amplified human and mouse osteosarcoma, using patient-derived xenografts and engineered mice, and disrupt candidate metastasis-linked signals genetically.
Suryavathi Viswanadhapalli
University of Texas Health Science Center at San Antonio, TX·Medicine & Clinical Research
Determine how LIF/LIFR signaling, a growth-factor pathway linked to poor survival, drives endometrial cancer progression, using global genomic approaches in endometrial cancer cells.
Lili Wang
Columbia University, NY·Medicine & Clinical Research
Determine how the MGA/MYC/NME1 pathway, a growth program switched on when the gene Mga is silenced, changes tumor-cell properties during the CLL-to-Richter's transformation, using the lab's mouse RT model.
The school
University of Michigan: 124 labs on PI Pages, $2.1B a year on research, 963 research doctorates a year.
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