Symposium
October 7 – 9, 2011
Hampton University Skin of Color Research Institute Symposium 2011
From Bench to Bedside: Future Directions
www.symposium.huscri.com
We are proud to announce The Hampton University Skin of Color Research Institute (HUSCRI) is hosting its second annual symposium: From Bench to Bedside: Future Directions scheduled for the weekend of October 7-9, 2011 in Hampton Roads, Virginia. The Symposium will qualify for CME credits through Eastern Virginia Medical School. The 2010 inaugural symposium attracted approximately 150 attendees and was well received by both meeting faculty and attendees.
Hampton University, one of the nation’s top historically black colleges, is an ideal organizer for the Symposium. Hampton University has established a dedicated research facility and is providing significant funding for the HUSCRI, the first multi-disciplinary enterprise of its kind in Virginia and perhaps the East Coast
The inaugural symposium (2010 meeting website symposium.huscri.com) was a dynamic hybrid of clinical, research, and industry participants creating a synergy that yielded excellent feedback from attendees. This years’ symposium will continue to build on that foundation. The objectives of the 2011 symposium will be to: 1) promote the dissemination of the latest research findings to the scientific and medical community; 2) foster the enthusiasm of novice researchers and clinicians; 3) increase the attendance of underrepresented minorities at dermatologic conferences; 4) nurture collaborative relationships within the field.
The Symposium will consist of two days of didactic sessions, interactive panel discussions utilizing an audience response system, and a social networking event on the evening of Saturday October 8, 2011. The program will bring together a group of national and international experts- with a broad range of expertise pertaining to different aspects of skin of color. The meeting will comprise a total of seven morning and afternoon sessions and will start the morning of Saturday October 8, 2011. Session topics will focus on health disparities/cultural competence, systemic diseases with cutaneous manifestations, melanocytic disorders, keloids/wound healing, aging, and advanced imaging and optical properties of the skin. The Symposium will be preceded by a half-day grant writing mini-seminar designed specifically for young investigators in the early stages of their career development, particularly targeted to minority researchers. The seminar will include a presentation by representatives from the National Institute of Health to inform potential PIs of funding mechanisms within NIH, and a focused grant-writing workshop coordinated by Dr. Donald Frazier at the University of Kentucky National Institute of General Medical Sciences program, a national leader helping predominantly minority institutions improve their competitiveness in writing grant proposals. Objectives of this session are: 1) to identify funding sources / agencies and determine which one is the most appropriate for a specific proposal. 2) to gain knowledge on how proposals are reviewed and what reviewers expect, and 3) to learn how to build a fundable grant proposal.
Treatment of Keloids and Scars
BRIAN BERMAN, MD, PHD
Department of Dermatology
University of Miami School of Medicine
New treatments are emerging for keloids, based on recent research. Dr. Brian Berman presented theses new treatment modalities at the 2011 HUSCRI Skin of Color Symposium. Treatments presented were immune response modifiers, specifically interferon and imiquimod and new and emerging anti-fibrotics. Interferon normalizes collagen and collagenase, reducing keloid volume, and is most effective when used as prophylaxis after surgery. In two studies, use of imiquimod 5% immediately after excision lowered reccurrence of keloids after excision significantly and was well-tolerated by patients.
In addition, new and emerging anti-fibrotics show some promise. Dr. Berman presented the results of several studies utilizing rhTGFβ3,e-Matrix, AZX100, and EXC 001 . The injection of AZX100 3.0 mg into keloid excision sites showed significant benefits in scarring after 12 months over the placebo. A randomized, double blind study of intradermal EXC 001 for surgical revision of hypertrophic breast scars, showed significantly improved outcomes when compared to placebo at 24 weeks. Anti-fibrotics, in general yield significant improvement in scarring over time and were well-tolerated by patients. While much is still not understood about how and why keloids form, these new and emerging treatments offer patients new and effective alternatives.
The Pathological Stem Cell Niche Governs Keloid Growth
ANH LEE, DDS, PHD
Associate Professor
Oral and Maxillofacial Surgery
University of Southern California
Dr. Anh Lee and colleagues at the University of California have made real progress in identifying a stem cell niche that governs keloid growth. Dr. Lee, speaking at the 2011 HUSCRI Skin of Color Symposium, presented the results of research targeting this mechanism to better understand keloid formation.
Keloid scarring is a serious condition, particularly affecting people of African descent, with genetic predisposition. Keloids are particularly troublesome since they are difficult to treat, subject to recurrence and no one treatment appears to work for all keloids. In addition, there is a lack of both animal models and clinical trials in this area that limits the development of effective treatments. Genome-wide linkage analysis identifies the keloid susceptibility locus on chromosome 7p11 for African American families and on 2q23 for Japanese families with a disequilibrium existing between synthesis and catabolism of extracellular matrix proteins (ECM). Dr. Lee’s objectives were to develop a murine model of human keloid-like disease, define the pathologic niche, and test feasibility of targeting inflammatory niche components for anti-scarring therapy. In vitro and in vivo studies were conducted and the resulting keloid animal model shows that IL-6 drives growth of transplanted KPCs.
Dr. Lee’s team has made real progress. “We have derived a new population of stem cells, named keloid
derived precursor cells (KPC)” summarizes Lee, “capable of clonogenicity, self-renewal, distinct embryonic and mesenchymal stem cell surface markers, and multipotent differentiation. Using KPCs we have developed a human keloid-like tumor model that is driven by the in vivo inflammatory niche
governed by IL-6.” Furthermore, research shows that elevated telomerase activity and upregulated proliferation capability are tightly regulated by the inflammatory niche mediated by an autocrine/paracrine cytokine IL-17/IL-6 axis. This human keloid-like tumor model driven by the in
vivo inflammatory niche allows testing of the anti-tumor therapeutic effect of antibodies targeting distinct niche components, specifically IL-6 and IL-17, and will likely lead to new insights and subsequent treatment modalities.
Ethnic Differences in Genetic Predisposition to Dermal Wound Healing Disorders and Keloid Formation
ERNST REICHENBERGER, PHD
University of Connecticut Health System
Center for Regenerative Medicine and Skeletal Development
Dermal wound healing disorders and formation of keloids due either to injury to the skin or secondary to acne is a key medical issue for patients with skin of color. Keloids, consisting of tumor like tissue which proliferates beyond the original wound margins, occur in 5-16% of patients from South Africa, Zaire as compared with 0.1% of those of English descent. Keloids are a complex disorder, and Dr. Reichenberger presents several hypotheses for the initiation of this disfiguring condition. Hypoxia, hormonal regulation, insufficient protein degradation, decreased apoptosis, and immune response have all been implicated as possible causes. In addition, keloids are associated with other conditions such as hypertension with 25% of African Americans with hypertension also forming keloids.
Numerous new genetic studies seek to identify keloid genes, but more focused studies are needed. New keloid loci have been identified by Genome wide linkage, and epigenetic studies are underway with Dr. Shirley Russell. A combined effort is needed in order to identify genes, study mechanisms leading to keloid formation, create cell culture, organ culture and animal models needed to study fibrosis, and keloid diagnosis at the molecular level to enhance treatment.
Keloid Development Structure, Differential Diagnosis and Matrix Remodeling
SHIRLEY RUSSELL, PHD
Center for Human Genetics Research
Division of Dermatology
Department of Medicine
Vanderbilt University School of Medicine
Fibrosis which occurs when fibroblasts remain active giving rise to excessive extracellular matrix and disruption of normal tissue architecture, is a leading cause of morbidity and mortality worldwide. It is a major component of many disorders, including several that are more prevalent and severe in individuals of African ancestry. Fibrosis can occur in most tissues, but the most commonly affected sites are liver, kidney, lungs, and skin. Despite this significant unmet medical need, currently no satisfactory treatments directly target the process of fibrosis. Dr. Shirley Russell, at the HUSCRI Symposium 2011, presented data on genetic studies examining keloid scars, their formation and potential for therapeutic strategies.
Keloids are benign dermal tumors occurring during a prolonged wound healing in genetically susceptible individuals. Keloids extend beyond the margin of the original wound, they do not routinely regress, and they are resistant to treatment and occur predominantly in individuals of African, Hispanic and Asian descent. Keloid fibroblasts are characterized by increased accumulation of extracellular matrix (ECM) components apparently due to increased synthesis and a decreased rate of degradation of these components.
Multiple biochemical pathways associated with fibrosis are misregulated in the indefinitely prolonged period of wound healing. An epigenetically altered program in fibroblasts cultured from keloids is supported by: 1) misregulation of gene expression is seen only in lesional fibroblasts, 2) the altered program is maintained throughout the culture lifetime, and 3) there are alterations in the pattern of DNA methylation and histone acetylation that appear to play a role in the pattern of altered gene expression. There is currently no routinely satisfactory treatment for keloids although strategies aimed at specific pathways are being tested. The findings that many pathways are misregulated suggest that epigenetic modifiers could be an effective therapeutic strategy for keloids and other fibrotic disorders, including a group that is more severe and prevalent in individuals of African ancestry.
Symposium 2011 Agenda
Symposium 2011 Brochure
Symposium 2011 Abstracts
Symposium 2011 Impressions
Funding for this conference was supported in part by National Institutes of Health, NIAMS Grant Number R13AR061973.
HUSCRI would also like to thank the following companies for their generous support:
SILVER SPONSOR: $10,000‐$14,999
L’Oreal
BRONZE SPONSOR: $5,000‐$9,999
Medicis
COPPER SPONSOR $2,001‐4,999
Allergan
Olympus
Sanofi-Aventis
Sentara Healthcare
EXHIBIT: $2,000
Janssen Biotech
Stiefel, a GSK Company
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Beautiful Kids Non-Profit Organization
Cicatricial Alopecia Research Foundation
Inflammatory Skin Disease Institute
Lupus Foundation of America DC/MD/VA Chapter
