Samuel Tzen-yue Hwang MD, PhD
USA
Chairman and Professor, Department of Dermatology, UC Davis School of Medicine
Current Position: Chair and Professor of Dermatology
Institution: Univ. California Davis School of Medicine – since 2016
Prior positions:
Chair and Professor of Dermatology, Medical College of Wisconsin, 2008-2015
Senior Investigator: Dermatology Branch, National Cancer Institute, Bethesda, MD, 1997-2007
Residency: Dermatology, Univ. California San Francisco, CA
Internship: Brigham and Women’s Hospital, Boston, MA
Medical School: Harvard Medical School, Boston, MA
Graduate School: University of Basel Switzerland, PhD Biochemistry
Undergraduate: Harvard College, Cambridge, MA
Contributions to Science:
Dr. Hwang’s major contribution to dermatologic and medical science has been the elucidation of the role of chemokine receptors in trafficking of leukocytes and cancers to inflammatory tissues (skin) and sites of metastasis, respectively (T Kakinuma and ST Hwang. Chemokines, chemokine receptors, and cancer metastasis. J. Leuk. Biol., 2006).
Among the first to explore the role of chemokine receptors in antigen-presenting cell trafficking, his early work focused on the migratory chemotactic trafficking of dendritic cells from the skin to regional lymph nodes via CCR7 (Saeki H, et al. Cutting Edge: Secondary Lymphoid-tissue Chemokine (SLC) and CCR7 participate in the emigration pathway of mature dendritic cells from the skin to regional lymph nodes. J. Immunol.1999).
In paradigm shifting later work, he showed that melanoma cells could express CCR7 and used this receptor to facilitate nodal metastasis, one of the major negative prognostic factors in melanoma as well as many other solid tumors (HE Wiley, et al. Expression of CC chemokine receptor-7 (CCR7) enhances regional lymph node metastasis of B16 murine melanoma. J. Natl. Cancer Inst., 2001). This work was among the first to demonstrate that cancer cells could usurp physiologic mechanisms of cellular trafficking, resulting in metastasis to distant sites.
Since 2009, his interests have shifted toward understanding the pathogenesis of psoriasis using murine models of this disease. His laboratory was the first to describe the critical role of CCR6 in trafficking of gamma-delta T cells to the epidermis in psoriasis (MN Hedrick et al. CC chemokine receptor-6 (CCR6) is essential for IL-23-mediated psoriasiform dermatitis in mice. J. Clin. Invest. 2009; Mabuchi T, Takekoshi T, Hwang ST Epidermal CCR6+ γδ T Cells Are Major Producers of IL-22 and IL-17 in a Murine Model of Psoriasiform Dermatitis. J Immunol. 2011; Mabuchi T et al. CCR6 Is Required for Epidermal Trafficking of γδ-T Cells in an IL-23-Induced Model of Psoriasiform Dermatitis. J Invest Dermatol. 2012). This body of work demonstrated that CCR6 was vital in order for T helper 17 cells that heavily express CCR6 to migrate to skin and to the epidermis where they produced IL-22 and IL-17, major drivers of psoriatic inflammation. Dr. Hwang continues to advance the field in the area of psoriasis pathogenesis through studies on the role of the itch/pain receptor TRPV1 (Zhou et al. TRPV1 mediates inflammation and hyperplasia in imiquimod (IMQ)-induced psoriasiform dermatitis (PsD) in mice. J. Dermatol. Sci. 2018) and dietary influences (Yu S et al. A Western Diet, but Not a High-Fat and Low-Sugar Diet, Predisposes Mice to Enhanced Susceptibility to Imiquimod-Induced Psoriasiform Dermatitis. J. Invest Dermatol. 2018) in psoriasiform dermatitis. He is considered an expert in the use of IL-23 and imiquimod murine models of psoriasis (Singh TP et al. IL-23- and imiquimod-induced models of experimental psoriasis in mice. Curr Protoc Immunol. 2019).
Dr. Hwang has also made significant strides in improving our understanding of the pathophysiology of cutaneous T cell lymphoma, a rare form of non-Hodgkin’s T cell lymphoma that primarily affects the skin. Because of the lack of spontaneous mou
Institution: Univ. California Davis School of Medicine – since 2016
Prior positions:
Chair and Professor of Dermatology, Medical College of Wisconsin, 2008-2015
Senior Investigator: Dermatology Branch, National Cancer Institute, Bethesda, MD, 1997-2007
Residency: Dermatology, Univ. California San Francisco, CA
Internship: Brigham and Women’s Hospital, Boston, MA
Medical School: Harvard Medical School, Boston, MA
Graduate School: University of Basel Switzerland, PhD Biochemistry
Undergraduate: Harvard College, Cambridge, MA
Contributions to Science:
Dr. Hwang’s major contribution to dermatologic and medical science has been the elucidation of the role of chemokine receptors in trafficking of leukocytes and cancers to inflammatory tissues (skin) and sites of metastasis, respectively (T Kakinuma and ST Hwang. Chemokines, chemokine receptors, and cancer metastasis. J. Leuk. Biol., 2006).
Among the first to explore the role of chemokine receptors in antigen-presenting cell trafficking, his early work focused on the migratory chemotactic trafficking of dendritic cells from the skin to regional lymph nodes via CCR7 (Saeki H, et al. Cutting Edge: Secondary Lymphoid-tissue Chemokine (SLC) and CCR7 participate in the emigration pathway of mature dendritic cells from the skin to regional lymph nodes. J. Immunol.1999).
In paradigm shifting later work, he showed that melanoma cells could express CCR7 and used this receptor to facilitate nodal metastasis, one of the major negative prognostic factors in melanoma as well as many other solid tumors (HE Wiley, et al. Expression of CC chemokine receptor-7 (CCR7) enhances regional lymph node metastasis of B16 murine melanoma. J. Natl. Cancer Inst., 2001). This work was among the first to demonstrate that cancer cells could usurp physiologic mechanisms of cellular trafficking, resulting in metastasis to distant sites.
Since 2009, his interests have shifted toward understanding the pathogenesis of psoriasis using murine models of this disease. His laboratory was the first to describe the critical role of CCR6 in trafficking of gamma-delta T cells to the epidermis in psoriasis (MN Hedrick et al. CC chemokine receptor-6 (CCR6) is essential for IL-23-mediated psoriasiform dermatitis in mice. J. Clin. Invest. 2009; Mabuchi T, Takekoshi T, Hwang ST Epidermal CCR6+ γδ T Cells Are Major Producers of IL-22 and IL-17 in a Murine Model of Psoriasiform Dermatitis. J Immunol. 2011; Mabuchi T et al. CCR6 Is Required for Epidermal Trafficking of γδ-T Cells in an IL-23-Induced Model of Psoriasiform Dermatitis. J Invest Dermatol. 2012). This body of work demonstrated that CCR6 was vital in order for T helper 17 cells that heavily express CCR6 to migrate to skin and to the epidermis where they produced IL-22 and IL-17, major drivers of psoriatic inflammation. Dr. Hwang continues to advance the field in the area of psoriasis pathogenesis through studies on the role of the itch/pain receptor TRPV1 (Zhou et al. TRPV1 mediates inflammation and hyperplasia in imiquimod (IMQ)-induced psoriasiform dermatitis (PsD) in mice. J. Dermatol. Sci. 2018) and dietary influences (Yu S et al. A Western Diet, but Not a High-Fat and Low-Sugar Diet, Predisposes Mice to Enhanced Susceptibility to Imiquimod-Induced Psoriasiform Dermatitis. J. Invest Dermatol. 2018) in psoriasiform dermatitis. He is considered an expert in the use of IL-23 and imiquimod murine models of psoriasis (Singh TP et al. IL-23- and imiquimod-induced models of experimental psoriasis in mice. Curr Protoc Immunol. 2019).
He and collaborators at MCW have developed and characterized novel structural variants of chemokines that block the function of chemokine receptors in the hope of using them for the treatment of inflammatory skin disease as well as cancer (Drury LJ et al. Monomeric and dimeric CXCL12 inhibit metastasis through distinct CXCR4 interactions and signaling pathways. Proc Natl Acad Sci U S A. 2011:17655-60;Takekoshi T et al. A locked, dimeric CXCL12 variant effectively inhibits pulmonary metastasis of CXCR4-expressing melanoma cells due to enhanced serum stability. Mol Cancer Ther. 2012). Most recently, Dr. Hwang and Dr. Volkman collaborated to show that an engineered, dimeric CCL20 molecule could block IL-23-mediated psoriasiform dermatitis (Getchman et al. Protein engineering of the chemokine CCL20 prevents psoriasiform dermatitis in an IL-23-dependent murine model. PNAS 2017).
Dr. Hwang has also made significant strides in improving our understanding of the pathophysiology of cutaneous T cell lymphoma, a rare form of non-Hodgkin’s T cell lymphoma that primarily affects the skin. Because of the lack of spontaneous mou