Ashani T Weeraratna
Johns Hopkins University, MD·Biology
Melanoma can come back years after apparently successful treatment, because tumor cells that spread early settle in distant organs and sit quietly before waking up. Why they stay dormant, and what rouses them, is largely unknown.
- Fields
Biology
Microbiology & Immunology
Medicine & Clinical Research
- Topics
melanoma
tumor dormancy
metastatic recurrence
- Grants
- 1 known grant, through Jun 2030
What they work on
- Define how the switch between non-canonical and canonical Wnt signaling, secreted signals that direct cell behavior, controls entry into and exit from melanoma cell dormancy in young versus aged lung tissue.
- Test whether aged fibroblasts, the lung's connective-tissue cells, respond to distant cancer cells by proliferating and secreting factors that recruit myeloid-derived suppressor cells, creating an immune-suppressed niche that permits dormant cells to grow out.
- Determine how Wnt5A-driven, senescence-like resistance to BRAF and MEK inhibitors interacts with canonical Wnt signaling, which increases sensitivity to these targeted drugs, and how aging shifts the balance.
- Assess how host factors, including sex and age, influence metastatic spread and treatment response, to establish which patient characteristics predict recurrence from dormant disseminated melanoma cells.
More about the research
Age is one of the strongest predictors of poor melanoma outcome, which points to the surrounding tissue rather than the tumor cell alone: as organs age, their resident support cells and immune cells change, and those changes may both permit reawakening and blunt the effect of therapy. This project asks how the aging tissue environment controls dormancy, recurrence, and drug resistance in melanoma.
Why it matters
Most melanoma deaths follow recurrence at distant sites, and older patients fare worst. Mapping how aged lung fibroblasts and the immune cells they recruit keep dormant tumor cells in check or let them escape could identify treatments aimed at the tissue environment rather than the tumor alone, potentially helping older patients' immune systems hold dormant cells in check and clarifying when BRAF/MEK-targeted therapy will fail.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Julio Aguirre-Ghiso
Albert Einstein College of Medicine, NY·Medicine & Clinical Research
Map the transcriptional and chromatin programs controlled by ZFP281, a gene-regulating protein, in early disseminated breast cancer cells and in human DCIS samples, and test how they drive both dissemination and dormancy in mouse models.
David Tweardy
University of Texas MD Anderson Cancer Center, TX·Medicine & Clinical Research
Determine whether the STAT3 inhibitor TTI-101, alone or combined with anti-PD-1 antibody, treats lung tumors effectively in the K-ras mutant CC-LR mouse model of non-small cell lung cancer.
John McAuliffe
Albert Einstein College of Medicine, NY·Medicine & Clinical Research
Determine whether pancreatic cancer cells circulating in the blood or spread to organs like the liver express NR2F1, a gene-switching receptor linked to dormancy, in mice and in human patients.
The school
Johns Hopkins University: 100 labs on PI Pages, $4.1B a year on research, 622 research doctorates a year.
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