University of Vermont

The University of Vermont Cancer Center

M.D.-Ph.D. Student Damsky Publishes Melanoma Study in Cancer Cell

William Damsky, Ph.D.
Third-year medical student William Damsky, Ph.D. (UVM Medical Photography/Raj Chawla)

Current third-year University of Vermont medical student William Damsky, Ph.D., is first author of a melanoma study featured on the cover and in the December 13, 2011 Cancer Cell.

The most deadly form of skin cancer, melanoma is caused by changes in melanocytes – cells that are responsible for skin and hair color. Because melanoma is highly metastatic and very difficult to treat, researchers are eager to gain a clearer understanding of how the genetic changes that occur in melanoma relate to the metastatic process.

Mentored by Marcus Bosenberg, M.D., Ph.D., former UVM assistant professor of pathology and current Yale associate professor of dermatology and pathology, Damsky focused on the Wnt signaling pathway, which previous research has demonstrated is frequently altered in melanoma, to clarify the role of this dysregulation in melanoma metastasis. He and colleagues engineered a unique mouse model of melanoma that allowed them to evaluate several key pathways involved in cell proliferation and survival in melanoma.

In this study, Damsky and colleagues were able to demonstrate that beta-catenin – a key component in the Wnt pathway – is a central mediator of melanoma metastasis to the lymph nodes and lungs, and also discovered that in addition to altering metastasis, beta-catenin levels control tumor differentiation and regulate two signaling processes – MAPK/Erk, which is involved in proliferation and differentiation, and PI3K/Akt, which is involved in cell growth and metabolism.

“Understanding metastasis at a fundamental level will be important in helping to design new generations of cancer drugs that might help patients with metastatic melanoma,” says Damsky.

To read the study article and view the journal cover image by M. Charles, go to β-Catenin Signaling Controls Metastasis in Braf-Activated Pten-Deficient Melanomas.