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P53蛋白在牙囊、含牙囊肿、牙源性角化囊肿及囊肿炎症亚型中的表达:一项免疫组织化学研究

P53 Protein Expression in Dental Follicle, Dentigerous Cyst, Odontogenic Keratocyst, and Inflammatory Subtypes of Cysts: An Immunohistochemical Study.

作者信息

Fatemeh Mashhadiabbas, Sepideh Arab, Sara Bagheri Seyedeh, Nazanin Mahdavi

机构信息

Department of Oral and Maxillofacial Pathology, School of Dentistry, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Department of Orthodontics, School of Dentistry, Tehran University of Medical Sciences, Tehran, Iran.

出版信息

Oman Med J. 2017 May;32(3):227-232. doi: 10.5001/omj.2017.42.

Abstract

OBJECTIVES

An odontogenic keratocyst (OKC) is a developmental odontogenic cyst with aggressive clinical behavior. This cyst shows a different growth mechanism from the more common dentigerous cyst and now has been renamed as a keratocystic odontogenic tumor (KCOT). Inflammation can assist tumor growth via different mechanisms including dysregulation of the p53 gene. This study aims to assess and compare the expression of tumor suppressor gene p53 in inflamed and non-inflamed types of OKC and dentigerous cyst.

METHODS

Immunohistochemical expression of p53 was assessed in 14 cases of dental follicle, 34 cases of OKC (including 18 inflamed OKCs), and 31 cases of dentigerous cyst (including 16 inflamed cysts).

RESULTS

The mean percentage of p53 positive cells was 0.7% in dental follicles, 5.4% in non-inflamed OKCs, 17.3% in inflamed OKCs, 1.2% in non-inflamed dentigerous cysts, and 2.2% in inflamed dentigerous cysts. The differences between the groups were statistically significant ( < 0.050) except for the difference between inflamed and non-inflamed dentigerous cysts, and between dental follicle and non-inflamed dentigerous cyst.

CONCLUSIONS

The difference in p53 expression in OKC and dentigerous cyst can explain their different growth mechanism and clinical behavior. Inflammation is responsible for the change in behavior of neoplastic epithelium of OKC via p53 overexpression.

摘要

目的

牙源性角化囊肿(OKC)是一种具有侵袭性临床行为的发育性牙源性囊肿。该囊肿与更常见的含牙囊肿具有不同的生长机制,现已重新命名为角化囊性牙源性肿瘤(KCOT)。炎症可通过包括p53基因失调在内的不同机制促进肿瘤生长。本研究旨在评估和比较肿瘤抑制基因p53在炎症性和非炎症性OKC及含牙囊肿中的表达。

方法

对14例牙囊、34例OKC(包括18例炎症性OKC)和31例含牙囊肿(包括16例炎症性囊肿)进行p53免疫组化表达评估。

结果

牙囊中p53阳性细胞的平均百分比为0.7%,非炎症性OKC中为5.4%,炎症性OKC中为17.3%,非炎症性含牙囊肿中为1.2%,炎症性含牙囊肿中为2.2%。除炎症性和非炎症性含牙囊肿之间以及牙囊和非炎症性含牙囊肿之间的差异外,各组之间的差异具有统计学意义(<0.050)。

结论

OKC和含牙囊肿中p53表达的差异可以解释它们不同的生长机制和临床行为。炎症通过p53过表达导致OKC肿瘤上皮行为的改变。

相似文献

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P53 protein expression in odontogenic cysts.牙源性囊肿中的P53蛋白表达
J Endod. 2001 Jul;27(7):459-61. doi: 10.1097/00004770-200107000-00006.

本文引用的文献

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Caught in the cross fire: p53 in inflammation.深陷交叉火力:炎症中的p53
Carcinogenesis. 2014 Aug;35(8):1680-90. doi: 10.1093/carcin/bgu134. Epub 2014 Jun 18.

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