Expression of Apoptotic vs Antiapoptotic Proteins in Middle Ear Cholesteatoma

Chung, Jae Ho; Lee, Seung Hwan; Park, Chul Won; Kim, Kyung Rae; Tae, Kyung; Kang, Seung Ho; Oh, Young Ha; Pyo, Jung Yoon

doi:10.1177/0194599815591810

Cited by 9 publications

(8 citation statements)

References 28 publications

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“…To evaluate cell proliferation in our study, Ki-67 and NF-κβ were used. Even though many authors show that Ki-67 is upregulated in cholesteatoma [46,47], our results did not show statistically significant results between groups. Similar results with no statistically significant difference of Ki-67 in cholesteatoma compared to skin were presented by Kim et al [48] and Kuczkowski et al [49].…”

Section: Discussioncontrasting

confidence: 99%

Complex Evaluation of Tissue Factors in Pediatric Cholesteatoma

2021

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The aim of this study was to describe the appearance and distribution of tissue remodeling markers (MMP-2, MMP-9, TIMP-2, TIMP-4), Sonic hedgehog gene protein (Shh), pro- and anti-inflammatory cytokines (IL–1, IL–10), transcription factor (NF-κβ), proliferation marker (Ki–67), angiogenetic factor (VEGF), tissue defensins (HβD–2, HβD–4) of the pediatric cholesteatoma. Sixteen cholesteatoma samples were obtained from children, eleven skin controls from cadavers. Tissues were stained for MMP-2, MMP-9, TIMP-2, TIMP-4, Shh, IL–1, IL–10, NF-κβ, Ki–67, VEGF, HβD–2, HβD–4. Non-parametric statistic, Mann–Whitney, and Spearman’s coefficient was used. A statistically significant difference was seen between Shh and HβD–2 in perimatrix and control connective tissue, between NF-κβ in cholesteatoma and control skin, and between HβD–4 in matrix and skin epithelium. Complex intercorrelations between MMPs, NF-κβ and VEGF cause the intensification of angiogenesis in cholesteatoma. The persistent increase in Shh gene protein expression in cholesteatoma perimatrix suggests the stimulation of the cholesteatoma growth in children. Similar expression of IL-1 and IL-10 and their intercorrelation, proves there is a balance between pro- and anti-inflammatory cytokines. NF-κβ, and not Ki-67, seems to be the main inducer of cellular proliferation. The main antimicrobial protection is provided by HβD-2.

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Section: Discussioncontrasting

confidence: 99%

Complex Evaluation of Tissue Factors in Pediatric Cholesteatoma

2021

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“…That probably might suggest the specific stage of disease with a decrease in cellular activity. However, this data was different from other studies where Chung et al[35] and Hamed et al[36] proved overexpression of Ki-67 in cholesteatoma tissue compared to skin epithelium. This might be explained by the fact that Hamed and other authors took control skin from the same patients, who had cholesteatoma.…”

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confidence: 96%

Untitled

2020

BJSTR

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Introduction:The complex appearance of proliferation markers, cytokines, remodelling factors, antimicrobial peptides and genes still have not been studied together despite their possible crucial role in the development of cholesteatoma. Therefore, the aim of this study was complex research of appearance and distribution of proliferation, remodeling markers, pro-and anti-inflammatory cytokines, local tissue defensins and genes of the cholesteatoma tissue.Materials and Methods: Four cholesteatoma tissue samples were obtained from children, 5 cholesteatoma specimens were obtained from adults, and 7 deep external meatal skin controls were obtained from cadavers. Tissues were stained for Ki-67, MMP-2, TIMP-2, IL-1, IL-10, HβD-2, HβD-4 and Shh immunohistochemically. Non-parametric statistic, Mann-Whitney and Spearman's coefficient were used.Results: A statistically significant difference was seen between the numbers of Ki-67, TIMP-2 positive cells in matrix and control group epithelium and between numbers of HβD-2, HβD-4 Shh positive cells in perimatrix in comparison to control group connective tissue. A very strong positive correlation was detected in control tissue epithelium between Ki-67 and TIMP-2, IL-10, Shh; between MMP-2 and TIMP-2, IL-1; between IL-10 and TIMP-2, Shh. In the connective tissue, a very strong correlation was detected between Ki-67 and Shh. A strong correlation was detected in epithelium between Ki-67 and MMP-2, and between MMP-2 and IL-10. Conclusion:Cholesteatoma tissue with the low appearance of Ki-67 proves the indistinct proliferation activity in the already developed tumour, but Ki-67 correlations with HβD-2 and HβD-4 in cholesteatoma indicate the direct link between the proliferation and expression of antimicrobial peptides. HβD-2 seems to be the most important factor for antimicrobial defence, but the correlations between HβD-2 and HβD-4 suggest their common action against chronic middle ear infection in case of choleasteatoma. Higher levels of MMP-2 positive cells in cholesteatoma and lower levels of TIMP-2 positive cells suggest the prevalence of enzymatic processes over their suppression, possibly being characteristic for cholesteatoma of different age patients. Shh gene might play a crucial role in the development of cholesteatoma.

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“…Many previous reports found that Ki-67 was overexpressed in the cholesteatoma epithelium compared to the normal retroauricular and meatal skin [ 8 , 19 - 22 ]. In contrast to these results, Kuczkowski et al [ 23 ] failed to find any significant difference in Ki-67 expression between 51 cholesteatomas and 6 meatal skin tissues.…”

Section: Discussionmentioning

confidence: 99%

Cytokeratin 13, Cytokeratin 17, and Ki-67 Expression in Human Acquired Cholesteatoma and Their Correlation With Its Destructive Capacity

Hamed

Nakata

Shiogama

et al. 2017

Clin Exp Otorhinolaryngol

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Objectives Cholesteatoma is a nonneoplastic destructive lesion of the temporal bone with debated pathogenesis and bone resorptive mechanism. Both molecular and cellular events chiefly master its activity. Continued research is necessary to clarify factors related to its aggressiveness. We aimed to investigate the expression of Ki-67, cytokeratin 13 (CK13) and cytokeratin 17 (CK17) in acquired nonrecurrent human cholesteatoma and correlate them with its bone destructive capacity.Methods A prospective quantitative immunohistochemical study was carried out using fresh acquired cholesteatoma tissues (n=19), collected during cholesteatoma surgery. Deep meatal skin tissues from the same patients were used as control (n=8). Cholesteatoma patients were divided into 2 groups and compared (invasive and noninvasive) according to a grading score for bone resorption based upon clinical, radiologic and intraoperative findings. To our knowledge, the role of CK17 in cholesteatoma aggressiveness was first investigated in this paper.Results Both Ki-67 and CK17 were significantly overexpressed in cholesteatoma than control tissues (P<0.001 for both Ki-67 and CK17). In addition, Ki-67 and CK17 were significantly higher in the invasive group than noninvasive group of cholesteatoma (P=0.029, P=0.033, respectively). Furthermore, Ki-67 and CK17 showed a moderate positive correlation with bone erosion scores (r=0.547, P=0.015 and r=0.588, P=0.008, respectively). In terms of CK13, no significant difference was found between cholesteatoma and skin (P=0.766).Conclusion Both Ki-67 and CK17 were overexpressed in cholesteatoma tissue and positively correlated with bone resorption activity. The concept that Ki-67 can be a predictor for aggressiveness of cholesteatoma was supported. In addition, this is the first study demonstrating CK17 as a favoring marker in the aggressiveness of acquired cholesteatoma.

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Expression of Apoptotic vs Antiapoptotic Proteins in Middle Ear Cholesteatoma

Abstract: The upregulation of c-FLIP together with unchanged p53 suggests an altered equilibrium between apoptosis and antiapoptosis, favoring antiapoptosis, and may play a role in the pathogenesis of cholesteatoma.

Cited by 9 publications

References 28 publications

Complex Evaluation of Tissue Factors in Pediatric Cholesteatoma

Complex Evaluation of Tissue Factors in Pediatric Cholesteatoma

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Cytokeratin 13, Cytokeratin 17, and Ki-67 Expression in Human Acquired Cholesteatoma and Their Correlation With Its Destructive Capacity

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