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2014/4/8 
 
Ichiro Katayama, M.D., Ph.D. Professor and Chairman
Graduation: 1977
Favorite pursuit: outdoor, gallery viewing, cooking
Specialized area: allergic skin disorders (atopic dermatitis, drug-induced eruption, urticaria, contact dermatitis), collagen diseases (systemic sclerosis, Sjogren’s syndrome, dermatomyositis, lupus erythematosus), vitiligo vulgaris, prurigo/pruritis, skin ulceration
Research interest: allergic skin disorders, pathophysiologic analysis for collagen diseases and development in their treatment, biological interaction among skin resident cells, pathophysiologic analysis for iching, skin biological rhythm, melanocyte immunology, wound healing and skin aging, photobiology
Qualification: Medical doctor (MD), Doctor of medical science (DMSc)
Achievement:

1:Non-pigmenting fixed drug eruption caused by an over-the-counter non-steroidal anti-inflammatory drug: Drug-specific CD8+ T lymphocytes identified in peripheral blood.
Hanafusa T, Azukizawa H, Matsumura S, Murakami Y, Tanaka A, Kurachi K, Katayama I.
Eur J Dermatol. 2012 Aug 2. [Epub ahead of print] No abstract available.
2.:Towards global consensus on outcome measures for atopic eczema research: results of the HOME II meeting.
Schmitt J, Spuls P, Boers M, Thomas K, Chalmers J, Roekevisch E, Schram M, Allsopp R, Aoki V, Apfelbacher C, Bruijnzeel-Koomen C, Bruin-Weller M, Charman C, Cohen A, Dohil M, Flohr C, Furue M, Gieler U, Hooft L, Humphreys R, Ishii HA, Katayama I, Kouwenhoven W, Langan S, Lewis-Jones S, Merhand S, Murota H, Murrell DF, Nankervis H, Ohya Y, Oranje A, Otsuka H, Paul C, Rosenbluth Y, Saeki H, Schuttelaar ML, Stalder JF, Svensson A, Takaoka R, Wahlgren CF, Weidinger S, Wollenberg A, Williams H.
Allergy. 2012 Jul 30. doi: 10.1111/j.1398-9995.2012.02874.x. [Epub ahead of print]
3.:Abnormal Axon Reflex-Mediated Sweating Correlates with High State of Anxiety in Atopic Dermatitis.
Kijima A, Murota H, Matsui S, Takahashi A, Kimura A, Kitaba S, Lee JB, Katayama I.
Allergol Int. 2012 Jul 25. [Epub ahead of print]
4.:Positive link between STAT3 activation and Th17 Cell infiltration to the lesional skin in vitiligo vulgaris.
Tanemura A, Kotobuki Y, Itoi S, Takata T, Sano S, Katayama I.
J Dermatol Sci. 2012 Sep;67(3):207-9. Epub 2012 Jun 28. No abstract available.
5.:Artemin causes hypersensitivity to warm sensation, mimicking warmth-provoked pruritus in atopic dermatitis.
Murota H, Izumi M, El-Latif MI, Nishioka M, Terao M, Tani M, Matsui S, Sano S, Katayama I.
J Allergy Clin Immunol. 2012 Jul 4. [Epub ahead of print]
6.:Systemic allergic contact dermatitis to palladium inlay manifesting as annular erythema.
Hanafusa T, Yoshioka E, Azukizawa H, Itoi S, Tani M, Kira M, Katayama I.
Eur J Dermatol. 2012 Jul 4. [Epub ahead of print] No abstract available.
7.:Upregulation of N-acetylglucosaminyltransferase-V by heparin-binding EGF-like growth factor induces keratinocyte proliferation and epidermal hyperplasia.
Kimura A, Terao M, Kato A, Hanafusa T, Murota H, Katayama I, Miyoshi E.
Exp Dermatol. 2012 Jul;21(7):515-9. doi: 10.1111/j.1600-0625.2012.01515.x.
8.:An extremely rare case of Merkel cell carcinoma metastasized to the duodenum.
Tanemura A, Nakano M, Iwasaki T, Yokomi A, Arase N, Wataya-Kaneda M, Miyazaki M, Yakushijin T, Takehara T, Katayama I.
Eur J Dermatol. 2012 May 29. [Epub ahead of print] No abstract available.
9.:Consumption of the epidermis in acral lentiginous melanoma.
Ohata C, Nakai C, Kasugai T, Katayama I.
J Cutan Pathol. 2012 Jun;39(6):577-81. doi: 10.1111/j.1600-0560.2012.01914.x. Epub 2012 May 11.
10.:Periostin, a matricellular protein, accelerates cutaneous wound repair by activating dermal fibroblasts.
Ontsuka K, Kotobuki Y, Shiraishi H, Serada S, Ohta S, Tanemura A, Yang L, Fujimoto M, Arima K, Suzuki S, Murota H, Toda S, Kudo A, Conway SJ, Narisawa Y, Katayama I, Izuhara K, Naka T.
Exp Dermatol. 2012 May;21(5):331-6. doi: 10.1111/j.1600-0625.2012.01454.x.
11.:Vitiligo exacerbated after herpes zoster.
Terao M, Tanemura A, Katayama I.
J Dermatol. 2012 Mar 6. doi: 10.1111/j.1346-8138.2012.01514.x. [Epub ahead of print] No abstract available.
12.:Seven cases of vitiligo complicated by atopic dermatitis: suggestive new spectrum of autoimmune vitiligo.
Tanemura A, Yajima T, Nakano M, Nishioka M, Itoi S, Kotobuki Y, Higashiyama M, Katayama I.
Eur J Dermatol. 2012 Mar-Apr;22(2):279-80. No abstract available.
13.:Morphea on the breast after a needle biopsy.
Arase N, Igawa K, Senda S, Terao M, Murota H, Katayama I.
Ann Dermatol. 2011 Dec;23(Suppl 3):S408-10. Epub 2011 Dec 27.
14.:[Atopic dermatitis].
Katayama I.
Arerugi. 2011 Dec;60(12):1598-605. Review. Japanese. No abstract available.
15.:Generalized Lichen Nitidus in Russell-Silver Syndrome.
Kanai C, Terao M, Tanemura A, Miyoshi Y, Ozono K, Katayama I.
Pediatr Dermatol. 2012 Feb 14. doi: 10.1111/j.1525-1470.2011.01613.x. [Epub ahead of print]
16.:Etanercept is safely used for treating psoriatic arthritis in a patient complicated with type 1 hereditary angioedema.
Umegaki N, Kira M, Horiuchi T, Itoi S, Tani M, Yokomi A, Tanemura A, Miyahara H, Hatanaka M, Kitamura H, Kitano E, Katayama I.
Mod Rheumatol. 2012 Feb 5. [Epub ahead of print]
17.:Blaschkitis-like eruptions with hypodontia and low IκB kinase gamma expression.
Oiso N, Kimura M, Tanemura A, Tsuruta D, Itou T, Suzuki T, Katayama I, Kawada A.
J Dermatol. 2012 Feb 2. doi: 10.1111/j.1346-8138.2011.01493.x. [Epub ahead of print] No abstract available.
18.:A novel application of topical rapamycin formulation, an inhibitor of mTOR, for patients with hypomelanotic macules in tuberous sclerosis complex.
Wataya-Kaneda M, Tanaka M, Nakamura A, Matsumoto S, Katayama I.
Arch Dermatol. 2012 Jan;148(1):138-9. No abstract available.
19.:Vaccination with WT-1 (Wilms' tumor gene-1) peptide and BCG-CWS in melanoma.
Nishioka M, Tanemura A, Nishida S, Nakano A, Tsuboi A, Oji Y, Oka Y, Azuma I, Sugiyama H, Katayama I.
Eur J Dermatol. 2012 Mar-Apr;22(2):258-9. No abstract available.
20.:The predominant drug-specific T-cell population may switch from cytotoxic T cells to regulatory T cells during the course of anticonvulsant-induced hypersensitivity.
Hanafusa T, Azukizawa H, Matsumura S, Katayama I.
J Dermatol Sci. 2012 Mar;65(3):213-9. Epub 2011 Dec 17.
 


Hiroyuki Murota, M.D., Ph.D. Assistant PROFESSOR
Graduation: 1995
Favorite pursuit: motorcycle, assembling vacuume tube-audio amplifier, travel, musical instrument (electric bass, electric guitar)
Specialized area: allergic dermatoses, collagen diseases
Research interest: please refer to my recent research theme in another paper.
Achievement:

Unexplained events in patients with dermatoses are topics of my research, especially for…

1. understanding of the abnormal physiology in atopic dermatitis
1) Pruritus and temperature
“My pruritus worsened when I felt warmth!”
This is the complaint frequently heard from patients with atopic dermatitis in our daily practice. Such warmth-provoked itch impairs patients’ QoL, and is difficult to treat. To quest for a cure of this unfavorable symptom, understanding the underlying mechanism of this symptom is required.
Recently, we found a neurotrophic factor, artemin, accumulated in lesional skin of atopic dermatitis, and its involvement in warmth-provoked pruritus.

Related article
Murota H, et al. Artemin causes hypersensitivity to warm sensation, mimicking warmth-provoked pruritus in atopic dermatitis. J Allergy Clin Immunol. 2012

2) Is sweat exacerbating factor of atopic dermatitis?
For the dermatologist and its related researchers in outside of Japan might feel strange to hear this question. In Japan, sweat is thought to be an exacerbating factor, and is introduced as major exacerbating factor in Japanese guideline for atopic dermatitis. However, sweating is important to maintain skin in healthy condition. Thus, we are confusing how should we instruct possible countermeasures to sweat to the patients with atopic dermatitis. To investigate the pathogenic role of sweat in atopic dermatitis, we are measuring sweating volume in patients with atopic dermatitis using quantitative axon reflex test (originally generated by Prof. Jeong-Beom Lee) .

Related article
Kijima A, Murota H, et al. Abnormal Axon Reflex-Mediated Sweating Correlates with High State of Anxiety in Atopic Dermatitis. Allergol Int. 2012

3) The role of cholesterol in skin barrier function and keratinocyte biology.
As you all know, lipids play important role in skin barrier function and skin homeostasis. Although the role of ceramide has been well documented in many literatures, the role of cholesterol remains obscure.
Now, we are investigating the role of cholesterol in keratinocyte and stratum corneum.

Related article
Abd El-Latif MI, Murota H, et al. Effects of a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor and low-density lipoprotein on proliferation and migration of keratinocytes. Br J Dermatol. 2010 163:128-37.

4) Ecomonic impact, medical cost, health related Quality of life, and work and classroom productivity in allergic skin diseases.
The impairment that pruritic skin diseases have on patient productivity at work, in the classroom, and in daily activities is substantial and needs to be characterized. The objective of this study was to determine how pruritic skin diseases impact patient productivity and quality of life (QOL), in order to improve the measurement of these endpoints to allow the influence of treatment options

Related article
Murota H, et al. Impact of sedative and non-sedative antihistamines on the impaired productivity and quality of life in patients with pruritic skin diseases. Allergol Int. 2010 59:345-54
Murota H, et al. Effects of nonsedative antihistamines on productivity of patients with pruritic skin diseases. Allergy. 2010 65:929-30.

5) Tissue remodeling in chronic allergic dermatitis.
The process known as tissue remodeling and repair is thought to be an underlying cause of refractory allergic diseases such as asthmatic diseases and atopic dermatitis. Based on a generally accepted definition by the Global Initiative for Asthma, it has been proposed that tissue remodeling contributes to (1) reconstitution and repair of inflammatory tissue injuries, (2) irreversibility or intractability of the process, and (3) persistence of allergic inflammation. In view of these considerations, tissue remodeling appears to participate in the prolongation of chronic allergic reactions rather than in repair of tissue damaged by allergic inflammation.
Histamine has distinct effects on dermal fibroblasts, which are characterized by increased synthesis of type 1 collagen and glycosaminoglycans, and augmentation of fibrogenic cytokine-induced fibroblast proliferation. However, there has been little or no direct evidence as to whether the effects of histamine on fibroblasts derived from different tissues are expressed at the same level. Now, we are confirming the involvement of histamine in tissue remodeling of atopic dermatitis lesional skin.

Related article
Murota H, et al. Emedastine difumarate inhibits histamine-induced collagen synthesis in dermal fibroblasts. J Investig Allergol Clin Immunol. 2008;18:245-52
Murota H, Katayama I. Emedastine difumarate: a review of its potential
ameliorating effect for tissue remodeling in allergic diseases. Expert Opin
Pharmacother. 2009 10:1859-67

2. Pathogenesis of scleroderma and its therapeutic perspectives
Scleroderma is characterized by broad area skin sclerosis and internal organ involvement including pulmonary fibrosis, esophageal dysfunction, pulmonary arterial hypertension, renal crisis, and heart failure. These symptoms dramatically affect the prognosis for scleroderma patients. Autoaggressive immunological activation and continuous activation of fibroblasts are the key components of scleroderma, yet the mechanisms underlying these are incompletely understood. We focused on the role of several inflammatory cytokines (e.g. TNF and IL-6), proteases (e.g. TACE), and matrix protein (e.g. periostin) in pathogenesis of scleroderma, and believe we could contribute to formulating novel therapeutic approach for patients with scleroderma.

Related article
Yang L, et al. Periostin Facilitates Skin Sclerosis via PI3K/Akt Dependent Mechanism in a Mouse Model of Scleroderma. PLoS ONE 2012 7: e41994.
Kitaba S, Murota H, et al. Blockade of interleukin-6 receptor alleviates disease in mouse model of scleroderma. Am J Pathol. 2012 180:165-76.
Terao M, Murota H, et al. Tumor necrosis factor-alpha processing inhibitor-1 inhibits skin fibrosis in a bleomycin-induced murine model
of scleroderma. Exp Dermatol. 2010 19:38-43
Murota H, et al. Disruption of tumor necrosis factor receptor p55 impairs collagen turnover in experimentally induced sclerodermic skin fibroblasts. Arthritis Rheum. 2003 48:1117-25.

3. Temperature and circulatory disorder
1) Livedo reticularis with summer ulceration; Why in summer?
Livedo reticularis with summer ulceration (LRSU) was origin- ally defined as a syndrome associated with idiopathic livedo reticularis in which ulcerations occur only or especially during the warmer months of the year. Typical histopathological findings of LRSU are endothelial proliferation and hyaline degeneration along with thrombosis of dermal vessels and necrosis of the epidermis. The pathogenesis of livedo reticularis is partly explained by a genetic disorder, venous abnormalities and dysfunction of coagulant proteins. Although these results imply that disorder of anticoagulant process might trigger this disease, they cannot explain why LRSU occurs only in summer. Now, we are searching the thermo-sensitive disease-associated protein using proteomics.

Related article
Murota H,et al. Heat-inductible turbidity precipitates in plasma samples of livedo reticularis with summer ulceration: hypothesis for abnormal coagulation in summer. Thromb Haemost. 2005 94:222-3

2) Raynaud phenomenon
Now, we are searching the thermo-sensitive disease-associated protein using proteomics.

 


Mari Kaneda, M.D., Ph.D. Assistant PROFESSOR
Graduation: 1980
Favorite pursuit: Associate professor of Department of Dermatology, Graduate School of Medicine, Osaka University.
Membership: Japanese Society of Dermatology
Board member of Japanese Society for Investigative Dermatology
Japanese Society of Human Genetics
Japanese Society for Familial Tumor
Japanese Society for von Recklinghausen Disease
Board member of The Japanese Society of Tuberous Sclerosis Complex
Achievement:


1) Research field
Genetics of skin diseases
Pathogenesis of hereditary skin tumors
Therapeutics for neuro-cutaneous syndrome
Molecular pathogenesis of tuberous sclerosis complex

2) Special areas of interest
In the Osaka University hospital, I have treated many patients of genetic skin diseases including approximately 250 patients of tuberous sclerosis complex (TSC) and more than 300 patients of von Recklinghausen disease. Since the abnormality of the PI3K-mTOR pathway is often found in the neuro-cutaneous syndrome including TSC and von Recklinghausen disease, the regulation of mTOR signaling may make a break-through in the treatment of the neuro-cutaneous syndrome. Then, I have been focusing on the factors regulating mTOR. Recently, I have treated patients using an mTOR inhibitor by not only topical use but also systemic administration. Until now, the clinical trial is going well. Now, we are preparing an investigator-initiated clinical trial to treat TSC skin manifestations using topical formulations of the mTOR inhibitor with the aid of the Ministry of Health, Labor and Welfare.
I discovered a new protein which was involved in the pathogenesis of the TSC. This protein is likely related to the PI3K-mTOR pathway. So, another interest is the characterization of the protein and the development of a new drug for TSC based on the protein.

3) Clinical Experience:
In 1992, at the department of dermatology of Osaka university hospital, I started medical examination for hereditary neuro-cutaneous syndrome. I have treated many patients of hereditary skin diseases including approximately 250 patients of TSC and more than 300 patients of von Recklinghausen disease. In Japan, there is no clinics specialized for TSC. So, I treated TSC patients with doctors of urology, respiratory medicine, pediatrics, radiology, psychiatry and so on. After I diagnose patients as TSC, I follow up the generalized condition of those patients. If I find lesions which need to be treated, I consult doctors of the special field. If the lesions are renal angiomyolipoma, I consult urologist and/or radiologist who are experts for trans-arterial embolization. In the case of manifest skin lesions, I treated patients by myself with surgical treatments, laser treatment, topical formulations or internal medicines. Although I have treated patients of various ages, more than half of the patients are older than 20 years old.
Although many previous reports on TSC handle juvenile patients, many of my patients are adult. So, the prevalence of symptoms and the severity of each symptom in my patients are different from previous reports. I make an effort to enlighten the doctors of the world as to this fact through international meetings.
 


Atsushi Tanemura, M.D., Ph.D. Assistant PROFESSOR
Graduation: 1997
Scientific position: Assistant professor and chief in the department of dermatology, Osaka University Graduate School of Medicine
Specific clinical field in dermatology: Skin oncology, skin surgery, acquired hypopigmented disorders
Specific research field: Melanoma and melanocyte biology, melanocyte immunology, anti-tumor immune therapy
Achievement:

Recent publications;
1. Tanemura A, Kotobuki Y, Itoi S, Takata T, Sano S, Katayama I.: Positive link between STAT3 activation and Th17 Cell infiltration to the lesional skin in vitiligo vulgaris. J Dermatol Sci 2012. [Epub ahead of print]

2. Kotobuki Y, Tanemura A, Yang L, Itoi S, Wataya-Kaneda M, Murota H, Fujimoto M, Serada S, Naka T, Katayama I. Dysregulation of melanocyte function by Th17-related cytokines: significance of Th17 cell infiltration in autoimmune vitiligo vulgaris. Pigment Cell Melanoma Res, 25(2):219-230, 2012. (co-1st author)

3: Namiki T, Tanemura A, Valencia JC, Coelho SG, Passeron T, Kawaguchi M, Vieira WD, Ishikawa M, Nishijima W, Izumo T, Kaneko Y, Katayama I, Yamaguchi Y, Yin L, Polley EC, Liu H, Kawakami Y, Eishi Y, Takahashi E, Yokozeki H, Hearing VJ. AMP kinase-related kinase NUAK2 affects tumor growth, migration, and clinical outcome of human melanoma. Proc Natl Acad Sci, 108(16):6597-6602, 2011.
 


Mamori Tani, M.D. Assistant PROFESSOR
Graduation: 1992
Achievement:

Artemin causes hypersensitivity to warm sensation, mimicking warmth-provoked pruritus in atopic dermatitis.
Murota H, Izumi M, El-Latif MI, Nishioka M, Terao M, Tani M, Matsui S, Sano S, Katayama I.
J Allergy Clin Immunol. 2012 Jul 4. [Epub ahead of print]

Systemic allergic contact dermatitis to palladium inlay manifesting as annular erythema.
Hanafusa T, Yoshioka E, Azukizawa H, Itoi S, Tani M, Kira M, Katayama I.
Eur J Dermatol. 2012 Jul 4. [Epub ahead of print] No abstract available.

Etanercept is safely used for treating psoriatic arthritis in a patient complicated with type 1 hereditary angioedema.
Umegaki N, Kira M, Horiuchi T, Itoi S, Tani M, Yokomi A, Tanemura A, Miyahara H, Hatanaka M, Kitamura H, Kitano E, Katayama I.
Mod Rheumatol. 2012 Feb 5. [Epub ahead of print]
 


Azukizawa Hiroaki, M.D., Ph.D. Assistant PROFESSOR
Graduation: 1997
Achievement:

In our lab, a K5-mOVA transgenic (Tg) mouse expressing a membrane-bound ovalbumin (mOVA) driven by the keratin 5(K5) promoter was established for studying the presentation of epidermal self-antigen by migratory dendritic cells (mDCs). By using this Tg mouse, we have established an autoimmune skin disease model mouse reproducing devastating skin damage of toxic epidermal necrolysis (TEN) by a combination of transgenic mice expressing an epidermal model antigen and its specific CD8+ T cell receptor (Azukizawa H. Eur J Immunol 2003 & 2005). In this model mouse, we found that thymus-derived CD4+CD25+ regulatory T cell (Treg) is a critical regulator of cytotoxic T lymphocyte (CTL)
causing TEN.

In humans, Delayed hypersensitivity is responsible for severe cutaneous adverse drug reactions (cADRs), especially in Stevens-Johnson syndrome (SJS), TEN, and drug-induced hypersensitivity syndrome (DIHS) (also known as drug rash with eosinophilia and systemic symptoms [DRESS] syndrome). The drug-induced lymphocyte stimulation test (DLST), or lymphocyte transforma- tion test (LTT), is used to identify the culprit drug in severe cADR cases. drug-specific proliferating cells were identified by a flow cytometric DLST (FCM-DLST) protocol that combines CFSE dilution and BrdU incorporation and utilizes them as a substitute for 3H-thymidine incorporation. We established the combination of the CFSE and BrdU assays that allows for the clear identification of the very small proliferating cell population as CFSElow BrdUhigh cells. By using this method, we demonstrated that different subsets of drug-specific T cells are induced during different disease stages of a cADR.
(Hanafusa T. et al. Journal of Dermatological Science 2012)

 


Toshifumi Yamaoka, M.D., Ph.D. Assistant PROFESSOR
Graduation: 2003
Scientific position: Assistant professor in the department of dermatology, Osaka University Graduate School of Medicine
Specialized area: collagen disease, psoriasis
Research interest: psoriasis, anti-centromere antibody
Achievement:

A case of toxic epidermal necrolysis complicated by sepsis, haemophagocytic syndrome, and severe liver dysfunction associated with elevated interleukin-10 production.
Yamaoka T, Azukizawa H, Tanemura A, Murota H, Hirose T, Hayakawa K, Shimazu T, Wada N, Morii E, Katayama I. Eur J Dermatol. In press

The roles of P- and E-selectins and P-selectin glycoprotein ligand-1 in primary and metastatic mouse melanomas.
Yamaoka T, Fujimoto M, Ogawa F, Yoshizaki A, Bae SJ, Muroi E, Komura K, Iwata Y, Akiyama Y, Yanaba K, Shimizu K, Sato S. J Dermatol Sci. 2011 Nov;64(2):99-107.

Autoantibody against a protease domain of caspase-8 in patients with systemic sclerosis.
Yamaoka T, Ogawa F, Muroi E, Hara T, Komura K, Iwata Y, Takenaka M, Shimizu K, Hasegawa M, Fujimoto M, Sato S. Clin Exp Rheumatol. 2008 Nov-Dec;26(6):998-1004.

 


Eiji Kiyohara, M.D., Ph.D. Assistant PROFESSOR
Graduation: 2003
Scientific position: Assistant professor in the department of dermatology, Osaka University Graduate School of Medicine
Specialized area: Skin Oncology (Lymphoma and Melanoma)
Research interest: Cancer Immunotherapy
Achievement:

Recent Publications:
Genome-Wide Characterization of Circulating Tumor Cells Identifies Novel Prognostic Genomic Alterations in Systemic Melanoma Metastasis. Chiu CG, Nakamura Y, Chong KK, Huang SK, Kawas NP, Triche T, Elashoff D, Kiyohara E, Irie RF, Morton DL, Hoon DS. Clin Chem. 2014 Apr 9. [Epub ahead of print]
Circulating tumor cells as prognostic biomarkers in cutaneous melanoma patients. Kiyohara E, Hata K, Lam S, Hoon DS. Methods in molecular biology. 1102:513-22 2014
Recent advances and developments in the antitumor effect of the HVJ envelope vector on malignant melanoma: from the bench to clinical application. Tanemura A, Kiyohara E, Katayama I, Kaneda Y. Cancer gene therapy. 20(11):599-605 2013
The combination of chemotherapy with HVJ-E containing Rad51 siRNA elicited diverse anti-tumor effects and synergistically suppressed melanoma. Kiyohara E, Tamai K, Katayama I, Kaneda Y. Gene therapy 19(7):734-41 2012
 



Aya Tanaka, M.D., Ph.D. Assistant PROFESSOR
Graduation: 1997
Scientific position: Assistant professor in the department of dermatology, Osaka University Graduate School of Medicine
Specific clinicalt: Skin oncology, skin surgery
Achievement:


 


Misa HAYASHI, M.D. Assistant PROFESSOR
Graduation: 2008
Scientific position:
Specific clinical: collagen disease, psoriasis
Achievement:



 






Staff 2014
Staff 2012