Research Artilce Open Access
Journal of Molecular Biomarkers
& Diagnosis
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ISSN: 2155-9929
Abdallah and MF El Deeb, J Mol Biomark Diagn 2017, 8:4
DOI: 10.4172/2155-9929.1000342
Volume 8 • Issue 4 • 1000342 J Mol Biomark Diagn, an open access journal
ISSN:2155-9929
*Corresponding author: Dina M Abdallah, Assistant Professor of
Pathology, Alexandria Faculty of Medicine, Egypt, Tel: +2034862506; E-mail:
dinabdalla@yahoo.com
Received March 31, 2017; Accepted April 28, 2017; Published April 30, 2017
Citation: Abdallah DM, MF El Deeb N (2017) Comparative Immunohistochemical
Study of P63, SMA, CD10 and Calponin in Distinguishing In Situ from Invasive
Breast Carcinoma. J Mol Biomark Diagn 8: 342. doi: 10.4172/2155-9929.1000342
Copyright: © 2017 Abdallah DM, et al. This is an open-access article distributed
under the terms of the Creative Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any medium, provided the
original author and source are credited.
Comparative Immunohistochemical Study of P63, SMA, CD10 and
Calponin in Distinguishing In Situ from Invasive Breast Carcinoma
Dina M Abdallah*, and Nevine MF El Deeb
Department of Pathology, Alexandria Faculty of Medicine, Egypt
Abstract
Background: Loss of the outer myoepithelial layer is the hallmark of invasive carcinoma, and demonstration of
this loss can be documented by immunohistochemical techniques. The purpose of this study was to compare the
specifcity and sensitivity of four of the most commonly used- markers of myoepithelial cells: P63, SMA, CD10 and
Calponin in distinguishing in situ from invasive breast carcinoma.
Material and methods: Immunostaining using antibodies against P63, SMA, CD10 and Calponin was performed
on representative paraffn sections from 40 cases of breast masses examined at the Department of Pathology,
Alexandria Faculty of Medicine, and diagnosed as ductal carcinoma in situ ± an invasive ductal or lobular carcinoma.
Results: Calponin yielded a slightly higher sensitivity than each of P63, CD10 and SMA (65% vs 54%, 19%
and 17%, respectively). The results of both semiquantitative assessment and computerized image analysis of
immunohistochemically-stained sections were statistically correlated, statistically p63 showed the highest specifcity
for myoepithelium and the least expression in non-myoepithelial layer of all antibodies tested. In contrast, SMA
showed the least specifcity and highest non-myoepithelial expression especially in stromal myofbroblasts and in
vascular smooth muscle cells.
Conclusions: Calponin and P63 are more sensitive myoepithelial markers as compared to CD10 and SMA;
with Calponin slightly more sensitive than P63. SMA should not be used alone as a myoepithelial marker due to its
low specifcity.
Keywords: Breast carcinoma; Myoepithelial cells; Cytokeratins;
Mammary glands
Introduction
Myoepithelial cells (MEC) are contractile elements found in
salivary, sweat, and mammary glands that show a combined smooth
muscle and epithelial phenotype [1]. Normal breast glands and ducts
are composed of 3 cell types that express diferent subsets of proteins:
luminal, basal, and myoepithelial [1,2]. Te luminal and basal cell
types express diferent cytokeratins (CKs); myoepithelial cells (MECs)
express basal cell-type CKs and other more specifc markers, such as
smooth muscle actin, calponin, and p63. An intact MEC layer is seen
in both benign and in situ lesions, whereas loss of the MEC layer is
considered the gold standard for the diagnosis of invasive cancer [2].
Carcinoma in situ (CIS) is defned as a proliferation of malignant
epithelial cells confned by the basal lamina, whereas invasive
carcinoma penetrates and grows beyond the basement membrane of the
microanatomic structure in which it arises. Invasive ductal carcinoma,
even the smallest, is treated diferently from ductal carcinoma in situ
(DCIS). Ruling out foci of invasion is most problematic in cases of
extensive high-grade DCIS accompanied by prominent periductal
stromal fbrosis and infammation. Another diagnostic problem in
which immunohistochemistry (IHC) can be of help is distinguishing
ductal/lobular CIS- involving sclerosing adenosis or other complex
sclerosing lesions from invasive carcinoma [3].
Earlier investigators approaching this problem stained for basal
lamina components but found this could not reliably distinguish in
situ from invasive tumors because some invasive carcinomas produce
basement membrane components including laminin type IV collagen
and type VII collagen [4].
Because MEC are not always readily identifable on routine
haematoxylin and eosin stained sections, many immunohistochemical
methods have been used to highlight an intact MEC layer. Given the
mixed epithelial and smooth muscle phenotype of MEC, and the need
to distinguish the MEC layer from the epithelial cell layer, most of the
markers used are directed against smooth muscle related antigens.
Except in the rare cases of myoepithelial carcinoma usual ductal
carcinoma cells are negative for MEC markers [3].
SMA is a sensitive marker of myoepithelial diferentiation, but it
is not specifc, because any cell with substantial expression of actin is
positive for SMA. In the breast, myofbroblasts and blood vessels are
generally positive for SMA. Tis becomes problematic in lesions where
there are either myofbroblasts or blood vessels in close proximity to the
epithelial lesion in question. CD10, the common acute lymphoblastic
leukaemia antigen, was originally described as a leukaemia associated
antigen expressed in lymphoid precursors and germinal B cells [5,6].
Te expression of this marker has been demonstrated in a wide range
of non-haemopoietic tissues, including glomerular cells of the kidney,
epithelial cells of the prostate gland and small and large intestine,
endometrial stromal cells, [7] and MEC of the breast [7-9].
Te nuclear stain, p63, a member of the p53 gene family, shows
no cross-reactivity with myofbroblasts or vascular smooth muscle.