Immunohistochemical evaluation of PCNA and Ki-67 in ameloblastoma

Sandra, Ferry; Mitsuyasu, Takeshi; Nakamura, Norifumi; Shiratsuchi, Yuji; Ohishi, Masamichi

doi:10.1016/s1368-8375(00)00079-8

Cited by 84 publications

(71 citation statements)

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“…Many studies comparing with malignant, benign and normal tissue using Ki-67 have been reported that Ki-67 labeling index corresponds with the degree of malignancy (17)(18)(19). In oral lesions, ameloblastoma, which is the most common benign odontogenic tumor, was from 4.3 to 6.8% of Ki-67 labeling index (20)(21). On the other hand, Kimi et ale reported Ki-67 labeling index in OKC was 11.2% and OOC was 7.8%(3).…”

Section: Discussionmentioning

confidence: 99%

“…Material and Methods: Fourteen cases of OKC, nine cases of DOC and eighteen cases ofEDC were examined immunohistochemically using antibodies against cytokeratins (CK7,10, 10/13,17,18,19,20) and apoptosis related factors (bcl-2 and Bax).…”

Section: Introductionmentioning

confidence: 99%

“…This study was to compare with cell proliferation, cell differentiation and apoptosis related factors in OKC, DOC and EDC in order to clarify the characters and category of three hitstopathologically similar cysts.Material and Methods: Fourteen cases of OKC, nine cases of DOC and eighteen cases ofEDC were examined immunohistochemically using antibodies against cytokeratins (CK7,10, 10/13,17,18,19,20) and apoptosis related factors (bcl-2 and Bax).Results: Ki-67 labeling index in OKC was statistically higher than that in DOC and EDC (p<0.05). And that in DOC was higher in EDC (p<0.05).…”

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confidence: 99%

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Odontogenic Keratocyst, Orthokeratinized Odontogenic Cyst and Epidermal Cyst: An Immunohistochemical Study Including Markers of Proliferation, Cytokeratin and Apoptosis Related Factors

Koizumi

2004

Int J Oral-Med Sci

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Objective: There are microscopic similarities among odontogenic keratocyst (OKC), orthokeratinized odontogenic keratocyst (DOC) and epidermal cyst (EDC). This study was to compare with cell proliferation, cell differentiation and apoptosis related factors in OKC, DOC and EDC in order to clarify the characters and category of three hitstopathologically similar cysts.Material and Methods: Fourteen cases of OKC, nine cases of DOC and eighteen cases ofEDC were examined immunohistochemically using antibodies against cytokeratins (CK7,10, 10/13,17,18,19,20) and apoptosis related factors (bcl-2 and Bax).Results: Ki-67 labeling index in OKC was statistically higher than that in DOC and EDC (p<0.05). And that in DOC was higher in EDC (p<0.05). In OKC, CKs and bcl-2 expression patterns were different from DOC and EDC, while both DOC and EDC showed similar reactivity with CKs and bcl-2.Conclusions: The present results suggested that OKC had high cellular proliferation and was relatively low differentiation as compare with DOC and EDC. In addition, there was participation of apoptosis suppressor in OKC. The character of DOC occupied an intermediate position between OKC and EDC. Therefore, it was possible to consider DOC as a distinct entity from OKC. EDC had the lowest cellular activity in the three cysts and it was comparatively maturated lesion.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Odontogenic Keratocyst, Orthokeratinized Odontogenic Cyst and Epidermal Cyst: An Immunohistochemical Study Including Markers of Proliferation, Cytokeratin and Apoptosis Related Factors

Koizumi

2004

Int J Oral-Med Sci

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“…In accordance with the expressions of apoptotic ligand and receptor in central cells, expressions of p53 (8,15), phosphatase and tensin homolog (PTEN) (16), phosphorylated-PTEN (16), phosphorylated-Jun N-terminal kinase (JNK) (17), Bcl-2 associated X protein (Bax) (3,6), Bcl-2 homologous antagonist killer (Bak) (3,5,7), caspase 9 (18), apoptotic protease activating factor-1 (APAF-1) (18), caspase 3 (19), terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) (14,20) were observed in central cells as well. Hence, some reports suggested that central cells have higher apoptotic activity than peripheral cells.…”

Section: Introductionmentioning

confidence: 93%

“…(3,(5)(6)(7)(8)(9)(10)(11)(12)(13) The peripheral cells were further classified into basal, columnar and cuboidal cell types. (5,7,8,10) Immunohistochemical studies have shown that B cell lymphoma (Bcl)-2 (3,5,7), Bcl-x (3,6) proliferating cell nuclear antigen (PCNA) (5), Ki-67 (5), murine double minute 2 (MDM2) (8,9), Midkine (10) and protein (p)65 nuclear factor (NF) kB (13) were highly expressed in peripheral than in central cells. Meanwhile, tumor necrosis factor (TNF)-α (11), Fas ligand (FasL) (14), TNF receptor (TNFR)1/death receptor (DR)1 (11), TNFR2/DR2 (11), DR4 (12), DR5 (12) and Fas (14) were highly expressed in central than peripheral cells.…”

Section: Introductionmentioning

confidence: 99%

Targeting Ameloblatoma into Apoptosis

Sandra

2018

Indones Biomed J

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BACKGROUND: Generally ameloblastoma is a locally aggressive, slow growing, non-metastatic epithelial odontogenic benign tumor. However, rarely some ameloblastoma can metastasize in spite of a benign histologic appearance. Targeting ameloblastoma by inducing it into apoptosis could be a beneficial strategy, since many ameloblastoma cases were reported recurrent after surgical therapy.CONTENT: To investigate ameloblastoma in cellular aspect,cytological pattern of ameloblastoma was divided intoouter layer/peripheral and inner layer/central cells. Tumor necrosis factor (TNF)-α, Fas ligand (FasL), TNF receptor (TNFR)1/death receptor (DR)1, TNFR2/DR2, DR4, DR5andFas were highly expressed in central than peripheral cells. Despite inducing apoptosis, TNF-α can induce PI3K leading to Akt and p44/42 mitogen-activated protein kinases (MAPK) activation in AM-1 cells, which later induce cell survival and proliferation. Therefore apoptotic induction in ameloblastoma should be suggested in higher TNF-α concentration. Expression of FasL and Fas are closely associated with squamous metaplasia and granular transformation of the tumor cells, suggesting that apoptosis induced by FasL may play a role in the terminally differentiated or degenerative ameloblastoma cells. TNF-related apoptosis-inducing ligand (TRAIL) has emerged as an apoptotic inducing anticancer agent in tumor cells specifically. TRAIL induced activation of caspases, lowering mitochondrial membrane potential, high number of apoptotic cells in ameloblastoma cells. Therefore, TRAIL could be a potential agent for targeting ameloblastoma, although further study should be explored.SUMMARY: Targeting ameloblastoma by inducing it into apoptosis could be achieved effectively, although some criteria should be considered. Therefore understanding the underlying apoptosis signaling pathways are necessary for inducing ameloblasotma into apoptosis. Investigations on other apoptosis-related molecules, potential apoptosis-inducing natural products, and novel approach in reprogramming, are important in the future for a better anagement of ameloblastoma.KEYWORDS: ameloblastoma, apoptosis, TNF, Fas, TRAIL, Akt, MAPK, caspase

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