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c-Kit 在黑色素细胞病变免疫组织化学评估中的作用。

The usefulness of c-Kit in the immunohistochemical assessment of melanocytic lesions.

机构信息

Department of Cytomorphology, Division of Pathology, University of Cagliari, via Ospedale, 54, 09124 Cagliari, Italy.

出版信息

Eur J Histochem. 2011 Jun 7;55(2):e20. doi: 10.4081/ejh.2011.e20.

DOI:10.4081/ejh.2011.e20
PMID:22193299
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3284155/
Abstract

C-Kit (CD117), the receptor for the stem cell factor, a growth factor for melanocyte migration and proliferation, has shown differential immunostaining in various benign and malignant melanocytic lesions. The purpose of this study is to compare c-Kit immunostaining in benign nevi and in primary and metastatic malignant melanomas, to determine whether c-Kit can aid in the differential diagnosis of these lesions. c-Kit immunostaining was performed in 60 cases of pigmented lesions, including 39 benign nevi (5 blue nevi, 5 intradermal nevi, 3 junctional nevi, 15 cases of primary compound nevus, 11 cases of Spitz nevus), 18 cases of primary malignant melanoma and 3 cases of metastatic melanoma. The vast majority of nevi and melanomas examined in this study were positive for c-Kit, with minimal differences between benign and malignant lesions. C-Kit cytoplasmatic immunoreactivity in the intraepidermal proliferating nevus cells, was detected in benign pigmented lesions as well as in malignant melanoma, increasing with the age of patients (P=0.007) in both groups. The patient's age at presentation appeared to be the variable able to cluster benign and malignant pigmented lesions. The percentage of c-Kit positive intraepidermal nevus cells was better associated with age despite other variables (P=0.014). The intensity and percentage of c-Kit positivity in the proliferating nevus cells in the dermis was significantly increased in malignant melanocytic lesions (P=0.015 and P=0.008) compared to benign lesions (compound melanocytic nevi, Spitz nevi, intradermal nevi, blue nevi). Immunostaning for c-Kit in metastatic melanomas was negative. Interestingly in two cases of melanoma occurring on a pre-existent nevus, the melanoma tumor cells showed strong cytoplasmatic and membranous positivity for c-kit, in contrast with the absence of any immunoreactivity in pre-existent intradermal nevus cells. C-Kit does not appear to be a strong immunohistochemical marker for distinguishing melanoma from melanocytic nevi, if we consider c-Kit expression in intraepidermal proliferating cells. The c-Kit expression in proliferating melanocytes in the dermis could help in the differential diagnosis between a superficial spreading melanoma (with dermis invasion) and a compound nevus or an intradermal nevus. Finally, c-Kit could be a good diagnostic tool for distinguishing benign compound nevi from malignant melanocytic lesions with dermis invasion and to differentiate metastatic melanoma from primary melanoma.

摘要

C-Kit(CD117)是干细胞因子的受体,是黑素细胞迁移和增殖的生长因子,在各种良性和恶性黑素细胞病变中显示出不同的免疫染色。本研究的目的是比较 C-Kit 在良性痣、原发性和转移性恶性黑色素瘤中的免疫染色,以确定 C-Kit 是否有助于这些病变的鉴别诊断。对 60 例色素病变进行了 C-Kit 免疫染色,包括 39 例良性痣(5 例蓝色痣、5 例真皮痣、3 例交界痣、15 例原发性复合痣、11 例 Spitz 痣)、18 例原发性恶性黑色素瘤和 3 例转移性黑色素瘤。本研究中检查的绝大多数痣和黑色素瘤均为 C-Kit 阳性,良性和恶性病变之间差异极小。在良性色素性病变和恶性黑色素瘤中均检测到表皮内增生痣细胞的 C-Kit 细胞质免疫反应性,且随患者年龄的增加而增加(两组均 P=0.007)。患者的发病年龄似乎是能够聚类良性和恶性色素性病变的变量。尽管存在其他变量,但 C-Kit 阳性表皮痣细胞的百分比与年龄的相关性更好(P=0.014)。与良性病变(复合黑素细胞痣、Spitz 痣、真皮痣、蓝色痣)相比,恶性黑素细胞病变中真皮内增生痣细胞的 C-Kit 阳性强度和百分比显著增加(P=0.015 和 P=0.008)。转移性黑色素瘤的 C-Kit 免疫染色为阴性。有趣的是,在 2 例发生在先前存在的痣上的黑色素瘤中,黑色素瘤肿瘤细胞显示出强烈的细胞质和膜 C-kit 阳性,而先前存在的真皮内痣细胞则没有任何免疫反应性。如果我们考虑表皮内增生细胞中的 C-Kit 表达,C-Kit 似乎不是区分黑色素瘤和黑素细胞痣的强免疫组织化学标志物。真皮内增生黑素细胞中的 C-Kit 表达有助于区分浅表扩散性黑色素瘤(伴有真皮浸润)和复合痣或真皮痣。最后,C-Kit 可能是一种很好的诊断工具,可用于区分具有真皮浸润的良性复合痣与恶性黑色素瘤病变,并区分转移性黑色素瘤与原发性黑色素瘤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ea/3284155/efbbaa6a7945/ejh-2011-2-e20-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ea/3284155/ae167148ba2d/ejh-2011-2-e20-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ea/3284155/c31b37f94693/ejh-2011-2-e20-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ea/3284155/f01d42af7db6/ejh-2011-2-e20-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ea/3284155/a700f31d631c/ejh-2011-2-e20-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ea/3284155/efbbaa6a7945/ejh-2011-2-e20-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ea/3284155/ae167148ba2d/ejh-2011-2-e20-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ea/3284155/c31b37f94693/ejh-2011-2-e20-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ea/3284155/f01d42af7db6/ejh-2011-2-e20-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ea/3284155/a700f31d631c/ejh-2011-2-e20-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ea/3284155/efbbaa6a7945/ejh-2011-2-e20-g005.jpg

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