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KIT (CD117) Expression in Benign and Malignant Sweat Gland Tumors
KIT (CD117, c-kit) is a receptor tyrosine kinase involved in the tumorigenesis of several neoplasms. KIT is expressed by the secretory cells of normal sweat glands. We studied the KIT expression and KIT mutational status in various benign and malignant tumors of eccrine and apocrine glands. We inclu...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The American Journal of Dermatopathology
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4894802/ https://www.ncbi.nlm.nih.gov/pubmed/25634571 http://dx.doi.org/10.1097/DAD.0000000000000301 |
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author | Nishida, Haruto Daa, Tsutomu Kashima, Kenji Arakane, Motoki Urabe, Shogo Yoshikawa, Yasuji Gamachi, Ayako Yokoyama, Shigeo |
author_facet | Nishida, Haruto Daa, Tsutomu Kashima, Kenji Arakane, Motoki Urabe, Shogo Yoshikawa, Yasuji Gamachi, Ayako Yokoyama, Shigeo |
author_sort | Nishida, Haruto |
collection | PubMed |
description | KIT (CD117, c-kit) is a receptor tyrosine kinase involved in the tumorigenesis of several neoplasms. KIT is expressed by the secretory cells of normal sweat glands. We studied the KIT expression and KIT mutational status in various benign and malignant tumors of eccrine and apocrine glands. We included a total of 108 cases comprising 10 benign and 6 malignant sweat gland tumors, and KIT expression was immunohistochemically detected (positive rate): 10 syringomas (0%), 8 poromas (25%), 20 mixed tumors (40%), 21 spiradenomas (43%), 1 cylindroma (0%), 5 hidradenomas (40%), 7 syringocystadenoma papilliferum cases (0%), 1 papillary hidradenoma (100%), 2 tubulopapillary hidradenomas (50%), 8 hidrocystomas (29%), 2 adenoid cystic carcinomas (100%), 5 porocarcinomas (20%), 6 apocrine carcinomas (33%), 10 extramammary Paget diseases (30%), 1 spiradenocarcinoma (100%), and 1 syringocystadenocarcinoma papilliferum (0%). Most KIT-positive cells were luminal cells, arising from glandular structures. We performed polymerase chain reaction–single-strand conformation polymorphism for detecting KIT mutational status. All cases showed no mutations at hot spots for KIT (exons 9, 11, 13, and 17). KIT mutation does not seem to be mechanism for KIT expression, but the expression may be from native sweat glands. |
format | Online Article Text |
id | pubmed-4894802 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | The American Journal of Dermatopathology |
record_format | MEDLINE/PubMed |
spelling | pubmed-48948022016-06-21 KIT (CD117) Expression in Benign and Malignant Sweat Gland Tumors Nishida, Haruto Daa, Tsutomu Kashima, Kenji Arakane, Motoki Urabe, Shogo Yoshikawa, Yasuji Gamachi, Ayako Yokoyama, Shigeo Am J Dermatopathol Original Study KIT (CD117, c-kit) is a receptor tyrosine kinase involved in the tumorigenesis of several neoplasms. KIT is expressed by the secretory cells of normal sweat glands. We studied the KIT expression and KIT mutational status in various benign and malignant tumors of eccrine and apocrine glands. We included a total of 108 cases comprising 10 benign and 6 malignant sweat gland tumors, and KIT expression was immunohistochemically detected (positive rate): 10 syringomas (0%), 8 poromas (25%), 20 mixed tumors (40%), 21 spiradenomas (43%), 1 cylindroma (0%), 5 hidradenomas (40%), 7 syringocystadenoma papilliferum cases (0%), 1 papillary hidradenoma (100%), 2 tubulopapillary hidradenomas (50%), 8 hidrocystomas (29%), 2 adenoid cystic carcinomas (100%), 5 porocarcinomas (20%), 6 apocrine carcinomas (33%), 10 extramammary Paget diseases (30%), 1 spiradenocarcinoma (100%), and 1 syringocystadenocarcinoma papilliferum (0%). Most KIT-positive cells were luminal cells, arising from glandular structures. We performed polymerase chain reaction–single-strand conformation polymorphism for detecting KIT mutational status. All cases showed no mutations at hot spots for KIT (exons 9, 11, 13, and 17). KIT mutation does not seem to be mechanism for KIT expression, but the expression may be from native sweat glands. The American Journal of Dermatopathology 2015-12 2015-11-20 /pmc/articles/PMC4894802/ /pubmed/25634571 http://dx.doi.org/10.1097/DAD.0000000000000301 Text en Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved. This is an open access article distributed under the terms of the Creative Commons Attribution-Noncommercial No Derivative 3.0 License, which permits downloading and sharing the work provided it is properly cited. The work cannot be changed in any way or used commercially. |
spellingShingle | Original Study Nishida, Haruto Daa, Tsutomu Kashima, Kenji Arakane, Motoki Urabe, Shogo Yoshikawa, Yasuji Gamachi, Ayako Yokoyama, Shigeo KIT (CD117) Expression in Benign and Malignant Sweat Gland Tumors |
title | KIT (CD117) Expression in Benign and Malignant Sweat Gland Tumors |
title_full | KIT (CD117) Expression in Benign and Malignant Sweat Gland Tumors |
title_fullStr | KIT (CD117) Expression in Benign and Malignant Sweat Gland Tumors |
title_full_unstemmed | KIT (CD117) Expression in Benign and Malignant Sweat Gland Tumors |
title_short | KIT (CD117) Expression in Benign and Malignant Sweat Gland Tumors |
title_sort | kit (cd117) expression in benign and malignant sweat gland tumors |
topic | Original Study |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4894802/ https://www.ncbi.nlm.nih.gov/pubmed/25634571 http://dx.doi.org/10.1097/DAD.0000000000000301 |
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