|Ganna Bilousova||My laboratory has a long-standing interest in induced pluripotent stem cells (iPSCs) and their differentiation capacity into a variety of cell types. I am particularly interested in developing experimental stem cell-based therapies for skin blistering diseases, such as Epidermolysis Bullosa, and connective tissue diseases, such as Ehlers-Danlos Syndrome. My group also studies mechanisms of aging and the pathways that trigger rejuvenation during reprogramming into iPSCs.|
|Stanca Birlea||The purpose of my research is to characterize the stem cell populations of the skin in pigmentary disorders and hair follicle disorders. My lab is focused on finding strategies to directly isolate the melanocyte stem cells in important functional sites of hair follicle, and how they interact with keratinocytes. We try to understand, using a human vitiligo model receiving standard and new treatments, the cellular and molecular basis of repigmentation process, an example of regenerative medicine. This model facilitates identification of signals and pathways driving the lack of treatment response in vitiligo and enables discovery of drug targets that overcome the treatment resistance.|
|Neil Box||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.|
Dr. Fujita is a tenured professor of Dermatology and Immunology & Microbiology, and a dermatologist at the Univ. of Colorado School of Medicine and VA Eastern Colorado Healthcare System, as well as a Director of Research Services, Dermatology RC-1S. The Fujita Lab studies biological roles and molecular regulations of 1) IL-1b, inflammasomes and autoinflammation in human melanoma, 2) IL-37 in adaptive immunity, 3) tumor heterogeneity in melanoma and its therapeutic resistance, and 4) damages to melanocytes and keratinocytes. The Lab is currently funded by NIH/NCI R01 (as a PI), VA Merit Awards (one as a PI and the other two as a co-I), and the Cancer League of Colorado (as a PI), and Dr. Fujita produced 97 peer-reviewed publications.
The research of the Huang group focuses on mechanistic understanding and therapeutic targeting of hyperactive proinflammatory responses in several disease conditions including traumatic brain injury (TBI), inflammatory skin disorders and Alzheimer’s disease. Dr. Hong Li’s contribution is essential to our recent discovery of the role of the transcriptional coregulators CtBP1 and CtBP2 in the modulation of innate immune responses and our ongoing efforts on the development of a novel class of anti-inflammatory agents.
My laboratory is investigating the mechanisms leading to cellular reprogramming and aging, as well as induced Pluripotent Stem Cell (iPSC)-associated cellular rejuvenation. My group’s expertise in producing mRNA and manipulating RNA transfections was crucial for identifying and optimization of a cocktail of factors that can “rejuvenate” human somatic cells, which we can now deliver into cells via non-integrating clinically-relevant RNA molecules. My group is currently exploring the applicability of this somatic cell rejuvenation approach in improving outcomes of skin transplantation.In addition, my laboratory works extensively with genetically corrected patient iPSCs and skin cells derived from these iPSCs as a potential therapeutic tool for the treatment of Epidermolysis Bullosa (EB), a group of severe inherited skin blistering diseases.
|David Norris||Dr. Norris is Chairman of the Department of Dermatology at the University of Colorado School of Medicine. He is an internationally renowned investigator in cutaneous immunology and cell biology, and melanoma research. He has been continuously funded for 40 years by the NIH, studying mechanisms of cell death in photosensitive lupus, vitiligo, and alopecia areata and has made seminal discoveries regarding the role of ultraviolet light in inducing translocation of autoantigens to the plasma membrane in keratinocytes in photosensitive lupus. His interest in immune mechanisms in vitiligo lead to many years of research in pigment cell biology, which eventually developed into studies of the resistance of melanocytes and melanoma to apoptosis. Over the past 17 years, Dr. Norris has been funded by a VA Merit Award to study drug combinations that kill melanoma by overcoming anti-apoptotic defenses, especially in melanoma initiating cells, and recently served on the Board of Scientific Councilors to the NCI Director.|
|Yosef Refaeli||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.|
|Dennis Roop||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.|
The research focus in Dr. Shellman’s lab is on the study of melanoma and melanocytes, with the aim of bench-to-bedside. With a deep understanding of molecular and biochemical pathways, we aim to develop treatments to thwart melanomas’ anti-apoptotic defenses. We also study the cell death pathways, proliferation, differentiation, maintenance and development of melanocyte lineage, as well as the etiology of pigmentation disorders. We use complementary in vitro and in vivo models, including human patient-derived iPSCs, transgenic mice, and mouse xenograft studies with patient relapsed melanomas. With these models, we aim to decipher the mechanisms of melanocyte lineage regulation in health and disease, and have identified potential treatments for difficult-to-treat melanomas.
|Tamara Terzian||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.|