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恶性黑色素瘤、发育异常痣和普通痣中基质金属蛋白酶-9、基质金属蛋白酶-13、基质金属蛋白酶-21和基质金属蛋白酶组织抑制因子-1表达的评估。

Evaluation of MMP-9, MMP-13, MMP-21, and TIMP-1 expressions in malign melanom, dysplastic nevi, and banal nevi.

作者信息

Yuvruk Meryem, Girgin Rabia Burcin, Zemheri Ebru

机构信息

Department of Pathology, Sancaktepe Prof. Dr. Ilhan Varank Training and Research Hospital, Istanbul, Turkiye.

Department of Pathology, Inonu University Faculty of Medicine, Turgut Ozal Medical Center, Malatya, Turkiye.

出版信息

North Clin Istanb. 2024 Apr 25;11(2):158-166. doi: 10.14744/nci.2023.69009. eCollection 2024.

DOI:10.14744/nci.2023.69009
PMID:38757103
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11095330/
Abstract

OBJECTIVE

Although the role of MMPs in the pathogenesis of melanoma is known, few studies have investigated their role in the development of nevi and dysplastic nevi. This study aims to search the expression differences of MMP-9, MMP-13, MMP-21, and TIMP-1 between malignant melanoma (MM), intradermal nevi (IDN), and dysplastic nevi (DN).

METHODS

MMP-9, MMP-13, MMP-21, and TIMP-1 antibodies were studied immunohistochemically for 60 cases in our pathology clinic archive between 2013 and 2014.

RESULTS

The MM group had the highest expression percentage and intensity for MMP-9 (p<0.001). There was no statistical significance between MMP-13 expression intensities of lesion cells and stromal cells and stromal expression intensities (p>0.05). MMP-21 lesion staining intensities in DN and MM compared to IDN were statistically significant (p=0.001, p=0.011, respectively). For TIMP-1, there was a significant difference between the IDN and the MM group regarding the staining proportion of lesion cells (p<0.01). There was a statistically significant difference in all groups according to lesion cells' expression intensity. (IDN-DN p<0.001, IDN-MM p=0.044, DN-MM p<0.001).

CONCLUSION

The following markers can be helpful when lesions cannot be differentiated; increased staining proportions and intensity of MMP-9 in both lesion and stromal cells favor MM in cases where MM and IDN cannot be differentiated. The increased MMP-13 staining proportion of lesion cells can favor DN in cases where the pathologist cannot differentiate DN and MM. Intense expression of MMP-21 by lesion cells can be a potential marker for evaluating the lesion in favor of DN in cases where DN and IDN cannot be differentiated. The high expression intensity of TIMP-1 in lesion cells can favor DN in cases where there is ambiguity between DN and MM. High expression proportion and intensity of stromal cells of TIMP-1 can be useable in favor of MM in cases where MM and DN cannot be differentiated.

摘要

目的

尽管基质金属蛋白酶(MMPs)在黑色素瘤发病机制中的作用已为人所知,但很少有研究探讨它们在痣和发育异常痣发展中的作用。本研究旨在探寻基质金属蛋白酶-9(MMP-9)、基质金属蛋白酶-13(MMP-13)、基质金属蛋白酶-21(MMP-21)和基质金属蛋白酶组织抑制因子-1(TIMP-1)在恶性黑色素瘤(MM)、皮内痣(IDN)和发育异常痣(DN)之间的表达差异。

方法

对2013年至2014年我们病理科门诊存档的60例病例进行免疫组织化学研究,检测MMP-9、MMP-13、MMP-21和TIMP-1抗体。

结果

MM组MMP-9的表达百分比和强度最高(p<0.001)。病变细胞和基质细胞的MMP-13表达强度与基质表达强度之间无统计学意义(p>0.05)。与IDN相比,DN和MM中MMP-21病变染色强度具有统计学意义(分别为p=0.001,p=0.011)。对于TIMP-1,IDN和MM组在病变细胞染色比例方面存在显著差异(p<0.01)。根据病变细胞的表达强度,所有组之间存在统计学显著差异。(IDN-DN p<0.001,IDN-MM p=0.044,DN-MM p<0.001)。

结论

当病变难以鉴别时,以下标志物可能会有所帮助;在无法区分MM和IDN的情况下,病变细胞和基质细胞中MMP-9染色比例和强度增加有利于诊断MM。在病理学家无法区分DN和MM的情况下,病变细胞中MMP-13染色比例增加有利于诊断DN。病变细胞中MMP-21的强烈表达可能是在无法区分DN和IDN时评估病变有利于DN的潜在标志物。在DN和MM之间存在模糊性的情况下,病变细胞中TIMP-1高表达强度有利于诊断DN。在无法区分MM和DN的情况下,TIMP-1基质细胞的高表达比例和强度可用于支持诊断MM。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72e7/11095330/69c98328fe37/NCI-11-158-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72e7/11095330/bddf0621bb0f/NCI-11-158-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72e7/11095330/77c12ad34914/NCI-11-158-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72e7/11095330/7e80fea5a3f7/NCI-11-158-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72e7/11095330/69c98328fe37/NCI-11-158-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72e7/11095330/bddf0621bb0f/NCI-11-158-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72e7/11095330/77c12ad34914/NCI-11-158-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72e7/11095330/7e80fea5a3f7/NCI-11-158-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72e7/11095330/69c98328fe37/NCI-11-158-g004.jpg

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