My group has an interest in understanding the skin pigmentary system and the potential role of melanocyte stem cells in hyperpigmentation and in pigmentation diseases such as vitiligo or premature graying where melanocyte loss is observed. We are focused on finding effective therapies for these conditions.
The goal of our laboratory is to elucidate the role of desmosomal genes and proteins in the normal development of the skin and its appendages (hair follicles, mammary glands). Furthermore, we are investigating how mutations in desmosomal genes lead to diseases (skin fragility disorders, skin cancer). To accomplish these goals, we are generating and characterizing genetically engineered mice which either lack expression of certain desmosomal genes (knockout mice) or which express mutant versions of these genes (transgenic mice, knockin mice). In order to understand how desmosomal genes are regulated during embryonic development of the skin and its appendages, we are also analyzing the role of epidermal signal transduction pathways (e.g. Wnt and NFкB) in regulating the expression of the desmosomal genes.
My research is aimed at identifying the signaling pathways that control
epidermal development and differentiation. A key regulator of epidermal
development is p63, a transcription factor that is expressed as six
different isoforms. Mice lacking all p63 isoforms do not develop an
epidermis or skin appendages, such as hair follicles and mammary
glands. Using genetically engineered mice, my laboratory studies the
role of p63 isoforms during embryonic development and postnatal
differentiation of the skin. In addition, p63 is mutated in a subset of
ectodermal dysplasias, inherited disorders that are characterized by
abnormalities of the skin and skin appendages. One of our other research
objectives is to use mouse models to identify the pathogenic mechanisms
that underlie skin fragility in patients with these disorders.
Our laboratory is interested in defining the molecular mechanisms
involved in the initiation, establishment and maintenance of lymphoid
tumors. We have based our work on the hypothesis that lymphoid neoplasms
arise as a result of the dysregulation of signals that normally control
lymphoid function and homeostasis.
My research focuses on understanding the role of cancer stem cells in the maintenance and resistance of skin cancer. We are developing stem cell therapies for inherited skin blistering diseases. We are also developing stem cell therapies for wound repair.
My research is focused on the mechanisms involved in melanoma
chemoresistance and to develop methods to reverse the resistance of
melanoma to therapy. My goal is to determine the mechanisms through which survivin functions
in melanoma and whether survivin expression is associated with
progression of melanoma.
The purpose of my research is to understand the cellular and molecular basis of repigmentation process in human vitiligo following various therapies including UV light. I have also been involved in researching genes that can be involved in the ocurrance of vitiligo.
The main focus of our current research is: (1) to understand subpopulations of cancer cells, such as cancer stem cells from human melanoma, (2) to study biological roles of inflammatory or anti-inflammatory molecules (particularly IL-1, IL-37 and AAT, inflammasome components) in the progression of human malignant melanoma, (3) to understand biological roles of a new cytokine, IL-37, (4) to identify melanoma-related and host response-related biomarker profiling from blood of melanoma patients, and (5) to identify metastasis-related genetic/genomic changes in human melanoma. The experiments utilize in vitro methodologies (cellular and molecular biology, immunology, pathology) and in vivo animal study (xenotransplantation, direct in vivo xenograft and genetically-engineered mouse models).
My laboratory is interested in the regulation of a key tumor suppressor, the transcription factor p53. p53 is mutated in over 50% of human cancers and has therefore been the subject of intensive basic and preclinical investigation. In the hope of improving cancer therapies that specifically target p53 mutations, we are investigating the role of different p53 mutations in driving tumorigenesis. For this we are using novel combinations of extant mouse models of cancer, murine xenografts and sophisticated tissue culture systems.