Please cite this article in press as: Kolude B, et al. Strong immunohistochemical expression of C-kit may characterize adenoid cystic
carcinoma of the salivary gland. J Oral Maxillofac Surg Med Pathol (2014), http://dx.doi.org/10.1016/j.ajoms.2013.11.008
ARTICLE IN PRESS
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JOMSMP-246; No. of Pages 5
Journal of Oral and Maxillofacial Surgery, Medicine, and Pathology xxx (2014) xxx–xxx
Contents lists available at ScienceDirect
Journal of Oral and Maxillofacial Surgery,
Medicine, and Pathology
j o ur nal ho me pa ge: www.elsevier.com/locate/jomsmp
Original Research
Strong immunohistochemical expression of C-kit may characterize
adenoid cystic carcinoma of the salivary gland
Bamidele Kolude, Akinyele Olumuyiwa Adisa, Ahmed Oluwatoyin Lawal
∗
,
Bukola Folasade Adeyemi
University of Ibadan, Nigeria
a r t i c l e i n f o
Article history:
Received 16 August 2013
Received in revised form
22 November 2013
Accepted 29 November 2013
Available online xxx
Keywords:
C-kit
Adenoid cystic carcinoma
Salivary gland tumors
a b s t r a c t
C-kit is a trans-membrane tyrosine kinase receptor detected in some malignant tumors but its expres-
sion in salivary gland tumors (SGTs) is rather controversial, although affinity for adenoid cystic carcinoma
(ACC) has been reported. Since C-kit is a target for the tyrosine kinase inhibitors, its use in treating malig-
nant SGTs is needed as other therapeutic modalities have poor outcome. This study therefore investigated
C-kit expression among subtypes of ACC and other SGTs.
FFPE SGT sections were processed with antibody to C-kit using the specifications of the manufacturer
(Polyclonal PA1-37375, Thermo-Scientific). Two investigators scored intensity of staining from negative
to strongly positive. Data analysis was done using version 20 of SPSS. Qualitative data were compared
using chi-squared statistics. Quantitative data were summarized using mean, standard deviation and
compared using Student’s t-test and/or one-way analysis of variance. The level of significance was set at
p < 0.05.
Only ACC showed strong C-kit expression (38.5%) when compared to other C-kit positive SGTs and this
was statistically significant (p = 0.03, Mann–Whitney U). There were however no significant differences
in C-kit expression between the variants of ACC (p = 0.52, Mann–Whitney U). There was also a signif-
icant difference in positive C-kit expression between the major and minor glands in MSGTs (p = 0.04,
Mann–Whitney U).
Strong expression of C-kit among MSGTs was exclusive in ACC and therefore may prove useful in
resolving diagnostic challenges and for therapeutic intervention.
© 2013 Asian AOMS, ASOMP, JSOP, JSOMS, JSOM, and JAMI. Published by Elsevier Ltd. All rights
reserved.
1. Introduction
C-kit (CD117) is a trans-membrane tyrosine kinase receptor that
is required for normal hematopoiesis, melanogenesis and gameto-
genesis. Expectedly, C-kit expression has been detected in chronic
myelogenous leukemia (CML), malignant melanomas and semi-
nomas but it has also been expressed in gastrointestinal stromal
tumors (GISTs) and salivary gland tumors (SGTs) especially ade-
noid cystic carcinoma (ACC) [1–4]. The gain of functional mutation
is the basis of C-kit overexpression in GIST and seminomas, how-
ever, among SGTs this is rarely reported and highly controversial
AsianAOMS: Asian Association of Oral and Maxillofacial Surgeons; ASOMP: Asian
Society of Oral and Maxillofacial Pathology; JSOP: Japanese Society of Oral Pathol-
ogy; JSOMS: Japanese Society of Oral and Maxillofacial Surgeons; JSOM: Japanese
Society of Oral Medicine; JAMI: Japanese Academy of Maxillofacial Implants.
∗
Corresponding author at: Department of Oral Pathology, University of Ibadan,
Nigeria. Tel.: +234 8055133964; fax: +234 22411768.
E-mail addresses: lawaloluwatoyin@gmail.com, toytoy219@yahoo.com
(A.O. Lawal).
[5]. C-kit is a target for the tyrosine kinase inhibitor imatinib mesy-
late (Gleevec) that has had significant therapeutic responses in CML
and advanced C-kit positive GIST [6,7].
Targeted molecular therapy is also desirable for malignant sali-
vary gland tumors (MSGTs) as the existing combination of surgery,
radiotherapy and chemotherapy has resulted in poor success rates
of 15–50% for recurrent and advanced cases [8,9]. ACC and polymor-
phous low-grade adenocarcinoma (PLGA) have similar precursor
cells and histomorphology [10,11]. Hence, histological differen-
tiation may pose a significant challenge, especially with small
biopsies. It is necessary to distinguish between these two lesions
because ACC is more aggressive and infiltrative than PLGA [12,13].
Previous studies on the expression of C-kit among SGTs were
focused mostly on the expression of C-kit among the subtypes of
ACC or the role of C-kit in distinguishing between ACC, PLGA and
other types of SGTs [12,14,15].
The level of expression among the subtypes of ACC is highly
conflicting with some authors reporting higher expression among
the well differentiated cribriform and tubular subtypes while oth-
ers reported higher expression among the poorly differentiated
2212-5558/$ – see front matter © 2013 Asian AOMS, ASOMP, JSOP, JSOMS, JSOM, and JAMI. Published by Elsevier Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.ajoms.2013.11.008