Frank UreñaPhD · MD Candidate

Research

Molecular science in service of patients.

It started with preclinical models. As a pathology technician and then a CRO researcher, I learned how disease looks at the cellular level before I understood why. That gap between observation and mechanism became the engine of everything that followed.

My doctoral work on miR-15a/16 regulation of T-cell proliferation gave me the first answer: microRNAs are rheostats, not switches — and the signaling cascades they control (MEK1–ERK1/2–Elk1) are the same ones that fail in autoimmunity, exhaustion, and cancer immune evasion. The Nature Biomedical Engineering paper on biomaterial vaccines followed the same logic in reverse: instead of studying how the immune system fails, design a material that teaches it to succeed.

The Harvard / MGH postdoc extended that thread into the tumor microenvironment — how cancer-associated fibroblasts remodel the immune landscape in pancreatic cancer, and how alveolar type 2 organoids can become patient-specific platforms for testing immune hypotheses. Medical school is not a departure from this arc. It is the deliberate acquisition of the clinical context that makes the science honest.

Focus Areas

Three research pillars

T-Cell Biology & Immunoengineering

Investigating how microRNAs and signaling cascades — particularly the miR-15a/16–MEK1–ERK1/2–Elk1 axis — govern T-cell activation and proliferative capacity, with implications for autoimmunity, oncology, and post-surgical immune regulation.

Biomaterial & Organoid Platforms

Designing immune-instructive biomaterials and patient-derived organoid systems that recapitulate disease microenvironments — bridging bench discoveries to testable therapeutic hypotheses.

Translational Immunology

Connecting molecular-level discoveries in immune signaling to measurable clinical outcomes — spanning oncology, infectious disease, and chronic inflammatory conditions.


Research approach

What question drives you?

How do T cells decide between activation, exhaustion, and tolerance — and can we learn to tip that decision in a patient's favor? My doctoral work on miR-15a/16 regulation of T-cell proliferation is one answer. I expect the full answer will span multiple diseases and a career.

What is your translational model?

Discovery at the molecular level (miRNA regulation, signaling cascades, single-cell approaches) → organoid and animal validation → clinical hypotheses testable in human cohorts. A finding earns its place only when it could change what a physician offers a patient.

What is next?

I am in medical school deliberately — to earn the clinical context that makes translational science honest. I have not committed to a specialty, and I intend to let the clinical exposure guide that decision. Whatever field I choose will have a research arm.

Publications

Representative work

Nature Biomed Eng · 2022 · 62 citations

Biomaterial vaccines capturing pathogen-associated molecular patterns protect against bacterial infections and septic shock.

J Biol Chem · 2022 · 18 citations

T-cell activation decreases miRNA-15a/16 levels to promote MEK1–ERK1/2–Elk1 signaling and proliferative capacity.

J Leukoc Biol · 2022 · 11 citations

Selenoprotein I deficiency in T cells promotes differentiation into tolerant phenotypes while decreasing Th17 pathology.