Expression of parathyroid hormone‐related protein (PTHrP), osteoclast differentiation factor (ODF)/receptor activator of nuclear factor‐κB ligand (RANKL) and osteoclastogenesis inhibitory factor (OCIF)/osteoprotegerin (OPG) in ameloblastomas

Kumamoto, Hiroyuki; Ooya, Kiyoshi

doi:10.1111/j.1600-0714.2004.00204.x

Cited by 44 publications

(39 citation statements)

References 53 publications

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“…These features suggest that these IAP family proteins might have a role in terminal differentiation of these neoplastic cells in ameloblastoma variants. We reported that some osteolytic cytokines and stromal microvessel densities clearly differed between follicular and plexiform patterns of ameloblastomas [20,22]. In the present study, XIAP mRNA levels were significantly greater in follicular ameloblastomas than in plexiform ameloblastomas, and expression of survivin protein tended to be higher in follicular ameloblastomas than in plexiform ameloblastomas.…”

Section: Discussioncontrasting

confidence: 54%

Expression of survivin and X chromosome-linked inhibitor of apoptosis protein in ameloblastomas

Kumamoto

Ooya

2004

Virchows Archiv

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To clarify the role of apoptosis in oncogenesis and cytodifferentiation of odontogenic epithelium, expression of survivin and X chromosome-linked inhibitor of apoptosis protein (XIAP), inhibitor of apoptosis protein (IAP) family proteins, was examined in tooth germs and in benign and malignant ameloblastomas by means of immunohistochemistry and reverse-transcription polymerase chain reaction. Immunoreactivity for survivin and XIAP was detected in developing and neoplastic odontogenic epithelium. In tooth germs, survivin expression was evident in inner enamel epithelium. Follicular, plexiform and metastasizing ameloblastomas showed survivin reactivity chiefly in neoplastic cells neighboring the basement membrane, and most neoplastic cells in basal cell and desmoplastic ameloblastomas and ameloblastic carcinomas were positive for survivin. Survivin mRNA levels were slightly higher in ameloblastomas than in tooth germs, suggesting that elevation of survivin expression might be involved in oncogenesis of odontogenic epithelium. Immunoreactivity for XIAP was detected in most odontogenic epithelial cells in tooth germs and in benign and malignant ameloblastomas, and XIAP mRNA levels were significantly higher in follicular ameloblastomas than in plexiform ameloblastomas. The expression of survivin and XIAP in odontogenic tissues suggests that these IAP family proteins contribute to the biological properties of ameloblastomas, such as cell survival, proliferation, differentiation and tissue structuring, as well as to cellular regulation during tooth development.

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Section: Discussioncontrasting

confidence: 54%

Expression of survivin and X chromosome-linked inhibitor of apoptosis protein in ameloblastomas

Kumamoto

Ooya

2004

Virchows Archiv

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“…Moreover, they may be involved in regulation of the immune system, arterial calcification, and a number of metabolic bone diseases [1]. Some studies have also examined the roles of osteoclast regulatory factors in progression of odontogenic lesions [9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

The Role of RANK/RANKL/OPG Signalling Pathways in Osteoclastogenesis in Odontogenic Keratocysts, Radicular Cysts, and Ameloblastomas

Tekkeşın

Mutlu

Olgaç

2011

Head and Neck Pathol

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The aim of this study was to evaluate the immunohistochemical expression of molecules involved in osteoclastogenesis, including the receptor activator of nuclear factor kappa B (RANK), RANK ligand (RANKL) and osteoprotegerin (OPG) in odontogenic keratocysts (OKCs), which has been named as a keratocystic odontogenic tumour by the WHO, and compare their expression with radicular cysts and ameloblastomas. RANK is a member of tumour necrosis factor receptor family and it is activated by RANK ligand. OPG binds to RANKL and inactivates it. The imbalance of these factors could cause the differential bone resorption activity in some diseases and tumours. The expression of these molecules was evaluated in ameloblastomas (n = 20), OKCs (n = 20), and radicular cysts (n = 20) by immunohistochemistry. Immunohistochemical reactivity for RANK, RANKL, and OPG was detected in neoplastic and nonneoplastic epithelium and connective tissue cells. RANK showed the greatest expression in OKCs followed by ameloblastomas, with the lowest expression seen in radicular cysts. Expression of RANKL was detected in all lesions and no significant differences were observed between groups. OPG was expressed very low in all groups. In the stroma, the number of RANK positive cells was higher in OKCs when compared with ameloblastomas and radicular cysts but radicular cyst had higher numbers of RANKL positive cells in the stroma than ameloblastomas. The molecular system of RANK/RANKL/OPG is variably expressed in OKCs, radicular cysts, and ameloblastomas and this system may be involved in the osteoclastogenic mechanisms in OKCs and ameloblastomas. Advanced studies could further clarify the role of RANK, RANKL, and OPG in mediating tumour associated bone osteolysis.

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“…Several cases of malignant ameloblastic tumor with hypercalcemia have been attributed to parathyroid hormonerelated protein (PTHrP) implicated in malignancy-associated hypercalcemia (162)(163), and expression of PTHrP has been detected in neoplastic cells of ameloblastomas and keratocystic odontogenic tumors unassociated with hypercalcemia (59,(164)(165)(166). Macrophage colony-stimulating factor (M-CSF), receptor activator of nuclear factor-kappaB ligand (RANKL), and osteoprotegerin (OPG), which regulate osteoclast differentiation and activation, have been identified in ameloblastomas and keratocystic odontogenic tumors (46,(166)(167)(168)(169)(170).…”

Section: Osteolytic Cytokinesmentioning

confidence: 99%

“…Macrophage colony-stimulating factor (M-CSF), receptor activator of nuclear factor-kappaB ligand (RANKL), and osteoprotegerin (OPG), which regulate osteoclast differentiation and activation, have been identified in ameloblastomas and keratocystic odontogenic tumors (46,(166)(167)(168)(169)(170). These observations suggest that osteolytic cytokines have a role in local bone resorption during the progression of odontogenic tumors.…”

Section: Osteolytic Cytokinesmentioning

confidence: 99%

Molecular alterations in the development and progression of odontogenic tumors

Kumamoto

2010

Oral Med Pathol

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Odontogenic tumors are lesions derived from the elements of the tooth-forming apparatus and are found exclusively within the jawbones. This review presents a contemporary outline of our current understanding of the molecular and genetic alterations associated with the development and progression of odontogenic tumors, including apoptosis-related factors, telomerase, cell cycle regulators, growth 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.

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Expression of parathyroid hormone‐related protein (PTHrP), osteoclast differentiation factor (ODF)/receptor activator of nuclear factor‐κB ligand (RANKL) and osteoclastogenesis inhibitory factor (OCIF)/osteoprotegerin (OPG) in ameloblastomas

Cited by 44 publications

References 53 publications

Expression of survivin and X chromosome-linked inhibitor of apoptosis protein in ameloblastomas

Expression of survivin and X chromosome-linked inhibitor of apoptosis protein in ameloblastomas

The Role of RANK/RANKL/OPG Signalling Pathways in Osteoclastogenesis in Odontogenic Keratocysts, Radicular Cysts, and Ameloblastomas

Molecular alterations in the development and progression of odontogenic tumors

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