"Surgical Pathology of the Head and Neck, Third Edition " is a complete stand-alone reference dealing with head and neck pathology. Providing an interdisciplinary approach to the diagnosis, treatment, and management of head and neck diseases, and covering all aspects of general pathology - this is the reference of choice for head and neck pathologists, head and neck surgeons and pathologists promoting clear communication between pathologists and surgeons. With over 1200 photographs, micrographs, drawings, and tables - over 200 more illustrations than the second edition - head and neck pathologists, head and neck surgeons, otolaryngologists and pathologists will find this updated bestseller a valid reference for any practice. Unparalleled in scope and content than any other book available on the subject, "Surgical Pathology of the Head and Neck, Third Edition" is a must-have resource for oral, surgical, and general pathologists; otolaryngologists; oral, maxillofacial, plastic, reconstructive, general, head, neck, and orthopedic surgeons; and neurosurgeons, oncologists, hematologists, ophthalmologists, radiologists, endocrinologists, dermatologists, dentists, and residents and fellows in these disciplines.

Surgical Pathology of the Head and Neck

Forty-five examples of epithelial odontogenic lesions (9 ameloblastomas (AB): 13 odontogenic keratocysts (OKC): 15 dentigerous cysts (DC): 6 radicular cysts (RC): and 2 odontogenic carcinomas (OC)) were immunohistochemically analyzed for the presence of p53 protein (p53P) and proliferative activity as indicated by positivity for Ki-67 antigen. p53P+ cells, detected as dense and/or faint nuclear staining, were found in 42 of the 45 odontogenic lesions examined. Dense p53P reactivity was most commonly detected in OKC, AB and OC, with other lesions generally exhibiting only weak nuclear reactivity. Numbers of Ki-67 positive cells as well as p53P+ cells were scored semiquantitatively. Although the presence/absence of densely stained p53P+ cells was broadly related to Ki-67+ cell numbers, there were no differences in p53P+ cell numbers between lesions exhibiting differences in proliferative activity. These results suggest that overexpression of p53P, rather than increased numbers of p53P+ cells, is related to proliferation in odontogenic epithelial lesions.

p53 protein and Ki‐67 reactivity in epithelial odontogenic lesions. An immunohistochemical study

Expression of proliferating cell nuclear antigen in ameloblastomas and odontogenic cysts

Odontogenic tumors are lesions derived from the elements of the tooth-forming apparatus and are found exclusively within the jawbones. This review represents a contemporary outline of our current understanding of the molecular and genetic alterations associated with the development and progression of odontogenic tumors, including oncogenes, tumor-suppressor genes, oncoviruses, growth factors, telomerase, cell cycle regulators, apoptosis-related factors, regulators of tooth development, hard tissue-related proteins, cell adhesion molecules, matrix-degrading proteinases, angiogenic factors, and osteolytic cytokines. It is hoped that better understanding of related molecular mechanisms will help to predict the course of odontogenic tumors and lead to the development of new therapeutic concepts for their management.

Molecular pathology of odontogenic tumors

Immunohistochemical evaluation of PCNA and Ki-67 in ameloblastoma

The aim of this study is to evaluate the proliferating activity of ameloblastomas and its correlation to the biological behaviour according to each histological type. 38 cases of solid and unicystic ameloblastomas were reviewed including 1 case of ameloblastic carcinoma and 1 recurrent case. An anti-PCNA antibody, PC10(Dako), was applied for the detection of proliferating cell nuclear antigen (PCNA) in paraffin embedded tissue sections. Also 20 cases of dentigerous cysts were reviewed. In conclusion, we observed that there was no difference between the proliferating activities of the different histological types of solid ameloblastomas. Because 1 case of ameloblastic carcinoma and one recurrent case revealed remarkably high PCNA reactivity, we believe that PCNA would be useful in showing the differentiation between benign and malignant ameloblastomas. In unicystic ameloblastomas, plexiform intraluminal growth was considered to be an important feature in tumorous transformation of cystic epithelium.

Immunohistochemical study on proliferating cell nuclear antigen expression in ameloblastomas.

Activation of the epidermal growth factor receptor (EGFR) and downstream signaling pathways have been implicated in causing resistance to EGFR-targeted therapy in solid tumors, including the head and neck tumors. To investigate the mechanism of antiproliferation to EGFR inhibition in oral cancer, we compared EGFR tyrosine kinase inhibitor (Gefitinib, Iressa, ZD1839) with respect to its inhibitory effects on three kinases situated downstream of EGFR: MAPK, Akt, and glycogen synthase kinase-3β (GSK-3β). We have demonstrated that ZD1839 induces growth arrest and apotosis in oral cancer cell lines by independent of EGFR-mediated signaling. An exposure of oral cancer cells to ZD1839 resulted in a dose dependent up-regulation of the cyclin-dependent kinase inhibitor p21 and p27, down regulation of cyclin D1, inactivation of GSK-3β and of active MAPK. In resistant cells, GSK-3β is constitutively active and its activity is negatively regulated primarily through Ser 9 phosphorylation and further enhanced by Tyr216 phosphorylation. These results showed that the resistance to the antiproliferative effects of ZD1839, in vitro was associated with uncoupling between EGFR and MAPK inhibition, and that GSK-3β activation and degradation of its target cyclin D1 were indicators of high cell sensitivity to ZD1839. In conclusion, our data show that the uncoupling of EGFR with mitogenic pathways can cause resistance to EGFR inhibition in oral cancer.

The GSK-3β/Cyclin D1 Pathway is Involved in the Resistance of Oral Cancer Cells to the EGFR Tyrosine Kinase Inhibitor ZD1839

The present invention relates to a novel use of bisphosphonate, and more
particularly to a composition for increasing collagen synthesis comprising
bisphosphonate as an active ingredient, as well as the use thereof. The inventive
composition comprising the bisphosphonate promotes collagen synthesis, and thus, when
it is applied to the skin, it reduces wrinkles of the skin and makes the skin elastic. For
this reason, the inventive composition will be useful as cosmetics for the prevention or
improvement of skin aging or a wound-healing agent. Furthermore, the inventive
composition can remarkably increase the collagen synthesis of fibroblasts in vitro , and
thus, can be effectively used in the production of products containing collagen.

The use of bisphosphonates for treating skin by stimulating of collagen synthesis

The present invention relates to a method for manufacturing a tungsten oxide electrode having the high production efficiency of active oxygen species, and comprising the steps of: preparing a tungsten base material; anodizing the tungsten base material to form a preliminary tungsten oxide; heat-treating the preliminary tungsten oxide; and applying reducing current to electrically reduce the heat-treated tungsten oxide.

Method of manufacturing tungsten oxide

Bazarsad Shadavlonjid , Eunae Cho, Woong Nam , Hyun Sil Kim , Jong In Yook , Jin Kim Department of Oral Pathology, Oral Cancer Research Institute, Yonsei University College of Dentistry, Seoul, South Korea Department of Oral and Maxillofacial Surgery, Yonsei University College of Dentistry, Seoul, South Korea. Dental School of Mongolian National University of Medical Science, Ulaanbaatar, Mongolia

Jin Kim

Papers

Immunohistochemical study on proliferating cell nuclear antigen expression in ameloblastomas.

The GSK-3β/Cyclin D1 Pathway is Involved in the Resistance of Oral Cancer Cells to the EGFR Tyrosine Kinase Inhibitor ZD1839

The use of bisphosphonates for treating skin by stimulating of collagen synthesis

Method of manufacturing tungsten oxide

A case of Ameloblastic Fibrosarcoma Transformed from Ameloblastic Fibro-odontoma