Laura Y. McGirt, M.D.
Assistant Professor of Medicine (Dermatology)
- Clinical Trials Information
- Clinical Trials: 1-800-811-8480
- Online Self-Referral Form
- Other Telephone NumbersVanderbilt Dermatology, One Hundred Oaks
- FaxesVanderbilt Dermatology, One Hundred Oaks Fax
Vanderbilt Dermatology, One Hundred Oaks
719 Thompson Lane, Suite 26300
Nashville, TN 37204-3609
Vanderbilt University Medical Center
1161 21st Avenue S.
Nashville, TN 37232-2600
Dr. McGirt has a clinical interest in cutaneous oncology and follows patients with cutaneous lymphoma, melanoma, and other non-melanoma skin cancers (squamous cell carcinoma and basal cell carcinoma) in dermatology clinic.
Dr. McGirt's primary research interest is cutaneous T-cell lymphoma (CTCL) with an emphasis on the most common form, mycosis fungoides (MF).
Dr. McGirt has a clinical interest in cutaneous oncology and follows patients with cutaneous lymphoma, melanoma, and other non-melanoma skin cancers (squamous cell carcinoma and basal cell carcinoma) in dermatology clinic.Dr. McGirt's primary research interest is cutaneous T-cell lymphoma (CTCL) with an emphasis on the most common form, mycosis fungoides (MF). She aims to better understand what drives the development and progression of MF, as well as identify improved diagnostic and prognostic markers. Additionally, she is working to characterize targets for novel therapeutics to enhance survival in MF/CTCL.
- M.D. - Duke University School of Medicine, 2003
- Internship (Internal Medicine) - Johns Hopkins, 2004
- Clinical Research Immunology Fellowship - Johns Hopkins, 2006
- Residency (Dermatology) - Johns Hopkins, 2009
Pathogenesis and diagnosis/prognosis of Cutaneous T-cell lymphoma
We are interested in elucidating the oncogenic mechanisms by which cutaneous T-cell lymphoma (CTCL) develops. To address this, we are studying altered microRNA (miRNA) in CTCL. miRNA are small, 18-22bp, non-coding single stranded RNA that most commonly cause inhibition of translation through the binding of the 3' UTR of its target mRNA. We have identified specific miRNA that are up and down regulated in CTCL and amelioration of their aberrant expression has led to slowed growth in CTCL cell lines. We are currently identifying the regulatory processes as well as the targeted genes of these altered miRNA and exploring what role they play in CTCL.
We are utilizing these miRNA as potential diagnostic and prognostic markers in the blood of early and advanced stage CTCL. We will be enrolling subjects and isolating PBMC from subjects with all stages of CTCL. The subjects will be followed longitudenally and PBMC isolated yearly for a minimum of 5 years or until they are lost to follow up. miRNA signatures will be compared between early stage CTCL without disease progression, early CTCL with progression, and advanced disease.
Additionally, we are interested in the identification of genetic mutations (translocations, insertion/deletions) that are found in CTCL. To date, there have not been any mutations found in a majority of CTCL and often the mutations identified (eg. p53) have an ultraviolet induced signature which likely developed from the commonly utilized ultraviolet-based therapy. We have initiated a whole-genome sequencing project and will shortly be starting validation of identified mutations in CTCL.
Cutaneous T-cell lymphoma, cutaneous oncology