Research: Cancer Cell
Pictured: Mouse fibroblasts expressing a sensor to detect cellular levels of hydrogen peroxide. Lighter green colors indicate areas of increased peroxided levels. Red are mitochondria. Credit: Cory Raymond, Ph.D. candidate in Cunniff Lab.
Cancer Cell is a fundamental science program with a focus on processes intrinsic to the cancer cell.
Research members are focused on cancer genetics/epigenetics, DNA damage and repair, and REDOX biology, and how these processes affect cancer initiation and progression.
Theme One
Genetic and epigenetic alterations in cancer
Theme Two
Redox and metabolic dysregulation in cancer
Theme Three
DNA damage and repair in cancer
in grant funding awarded in 2025.
Program Impact
Novel Mechanism for ER Movement Revealed in New Publication
In a new study published in Molecular Biology of the Cell, John Salogiannis, Ph.D., and trainee Allison Langley discovered a surprising new way the endoplasmic reticulum (ER) moves through the cell, a process they call “hitchhiking.” Instead of traveling on its own, the ER can latch onto moving Golgi vesicles to get where it needs to go—a finding that could reshape how scientists think about cell organization. This opens the door to future studies aimed at uncovering the key proteins involved and understanding how cells decide which movement strategy to use.
Video: Instead of traveling on its own, the ER (magenta in movie) can latch onto moving Golgi vesicles (green) to get where it needs to go
New Study From the Roberts Lab Identifies Multiple Factors That Impact Oxidation-induced Mutational Landscapes
In a new study published in Nature Communications, Steven Roberts, Ph.D., and graduate student Cameron Cordero, together with collaborators at the University of Kansas and Vanderbilt University, uncovered how oxidative DNA damage leads to mutations in multiple ways—not just by changing single bases, but also through insertions and deletions. By combining Cryo‑EM and genome‑wide analyses, they showed that tightly packed regions of DNA are harder for repair proteins to reach, making them more prone to mutation. This work offers exciting new insight into how oxidative stress shapes cancer‑related mutations and sets the stage for future efforts to trace the origins of this damage and explore its potential as a target for immunotherapy.
Pictured: Cryo-EM structures (A) show the DNA repair enzyme, OGG1 can find damage in histone-bound DNA when the lesion faces away from the histones, but not when the lesion is close to the proteins. This difference in lesion accessibility influences where mutations occur in human cells and cancers (B). Credit: the Roberts Lab at UVMCC and the Freudenthal Lab at KUMC
New Publication Reveals Gene Expression Changes Upon Loss of the Cancer-implicated Protein Miro1
New findings from Nathaniel Shannon, Ph.D., in the laboratory of Brian Cunniff, Ph.D., published in the Journal of Cell Science, reveal how the loss of the mitochondrial‑trafficking protein Miro1 disrupts normal cell behavior. The team discovered that without Miro1, key growth‑regulating proteins (ERK1/2) become abnormally activated, suggesting a link between mitochondrial positioning and cell‑signaling changes. These insights pave the way for future optogenetics‑based studies designed to pinpoint how mitochondrial clustering influences gene expression—work that could guide the development of new therapeutic strategies.
Pictured: Immunofluorescent image of mouse fibroblasts to visualize intracellular structures. Red = Actin Cytoskeleton, Blue = Nucleus, Green = Mitochondria. Credit: Nate Shannon, Ph.D., Postdoctoral Scholar in Cunniff Lab
Pictured: An analysis of gene expression after administration of LNPs differing in their ionizable lipid that shows how the structure of the ionizable lipid (C) determines the inflammatory capacity for any given LNP (B). Credit: the Majumdar Lab
Majumdar Lab Shows Vaccine Inflammatory Responses Can Be Tailored for Specific Therapeutic Purpose
Research from Dev Majumdar, Ph.D.'s lab featured in ACS Nano reveals that the ionizable lipid inside lipid nanoparticles—the delivery vehicle for RNA medicines—is a key driver of vaccine‑induced inflammation. By fine‑tuning the chemistry of this lipid, the team shows it may be possible to design cancer vaccines that spark just the right level of immune activation. Their next steps will explore how these nanoparticles interact with cellular recycling pathways to further improve the precision of RNA‑based therapies.
Fellowships
Reem Aboushousha, Ph.D.: Parker B. Francis Fellowship
Reem Aboushousha, Ph.D., received a Parker B. Francis Fellowship to investigate how the protein GSTP drives chemotherapy resistance in lung adenocarcinoma, with the goal of developing strategies to make tumors more responsive to Cisplatin. This three‑year award—supported by UVM Shared Resources and a UVM Cancer Center Pilot Grant—will advance Dr. Aboushousha's work toward improving outcomes for patients in Vermont and northern New York, where lung cancer rates are especially high.
Maggie Trout: ChadTough Defeat DIPG 2025 Pre-Doctoral Fellowship
Maggie Trout, a UVM Cancer Center pre‑doctoral candidate, has been awarded a Pre‑Doctoral Fellowship from ChadTough Defeat DIPG to advance research on diffuse midline glioma (DMG), an aggressive childhood brain cancer with no cure and very limited survival. Her work will investigate whether blocking mitochondrial reactive oxygen species (ROS) scavenging can weaken DMG cells and improve the effectiveness of existing chemotherapies, with the long‑term goal of identifying new therapeutic strategies for this devastating disease.
Inter-programmatic Pilot Award
Pilot Study to Investigate Vermonters' High Skin Cancer Risk
The UVM Cancer Center’s Interprogram Pilot Awards foster collaboration across research programs. Among the projects selected in 2025 is one led by Melanie Bui, M.D., Ph.D., (Population Science and Cancer Outcomes member) and Steven Roberts, Ph.D., (Cancer Cell co-leader) to better understand Vermont's high melanoma rates. By analyzing mutation patterns in UV‑exposed skin—from patients and individuals with high‑UV occupational exposure—the team aims to determine whether environmental factors or differences in DNA repair contribute to this elevated risk.
Brian Eckenroth, Ph.D.
Faculty Scientist, Microbiology and Molecular Genetics
Noelle Gillis, Ph.D.
Faculty Scientist, Pharmacology
Matthew Hannaford, Ph.D.
Assistant Professor, Molecular Physiology and Biophysics
Christopher Landry, Ph.D.
Professor, Chemistry Cellular, Molecular, and Biomedical Sciences
Princess Rodriguez Ramirez, Ph.D.
Assistant Professor, Microbiology and Molecular Genetics
