الفهرس 
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Abstract
Papillary thyroid carcinoma (PTC) is the most common thyroid cancer representing 80% of all thyroid cancers. Diagnosis of PTC depends on papillary architecture, nuclear features as clear, oval shaped nuclei with hypodense chromatin,pseudoinclusions, nuclear overlapping and grooving. The identification of PTC nuclear features is to a great extent dependent on the tissue processing (thickness of sections, fixative and duration of fixation).
Frequent morphologic similarities can be seen in both benign and malignant lesions in the form of papillary or follicular architectures and nuclear irregularity. Moreover, severe chronic lymphocytic thyroiditis, Hashimoto’s thyroiditis, and reactive atypia attributed to inflammation causenuclear morphology resembling that of PTC, with nuclear enlargement, chromatin clearing and even nuclear grooving. In contrast, FVPTC and other variants may cause, if the nuclear features of PTC are not prominant, difficult problems in differentiation from FTC, FA, or even from dominant nodule of multi-nodular goiter. Emerin is an integral inner nuclear membrane protein, which has important interactions with the cytoskeleton and related proteins. It provides an enhanced view of the nuclear envelope and tracing the nuclear alterations highlighting nuclear membrane details in PTC allowing identification of grooves, pseudoinclusions and garland-like nuclei(circumferential nuclear membrane irregularities). CD56/NCAM is an adhesion molecule from the immunoglobulin (Ig) superfamily that is expressed normally on the surface of neurons, glia, skeletal muscle cells, and natural killer cells. CD56 is present on follicular epithelial cells of the normal thyroid and it shows diffuse
staining.Reduction of its expression was previously reported in PTC.
This study aimed at evaluation of diagnostic value ofemerin and
CD56 expressionboth singly and in combination fordifferentiating PTC
from other neoplastic and non- neoplastic thyroid lesions.
This retrospective study was conducted on 71 thyroid gland
specimens, retrieved from the archives of Pathology Department, Faculty
of Medicine, Menoufia University spanning the period between January
2015 and January 2017. They were selected, based on the
histopathologicaldiagnosis.The studied cases included; 50 PTC, 9 FA and
12 non-neoplastic cases (Hashimoto thyroiditis, multinodular goiter and
hyperplastic nodule).
The investigated cases were received as hemithyroidectomy and
total thyroidectomy specimens. The non-neoplastic suspicious group was
seleced based on the presence of some similar overlapping features with
PTC such as papillary architecture or nuclear features.
Histologic variants, focality of tumor, background (thyroiditis,
goiter)and stage (TNM staging system) were all assessed using
patients’medical records and in H&E stained sections in studied
malignant cases.
Papillary architecture, clear nuclei and grooving were significantly
in favor of PTC compared to its mimickers (P = 0.02; P = 0.03; P= 0.001
respectively) while pseudoinclusions and calcification didn’t show any
differences. The sensitivity and specificity for papillary architecture were
84% and 50%, for clear nucleiwere 100% and 16.7% and for grooving
were 96% and 83.3% respectively The method used for immunostaining was streptavidin-biotin amplified system. Two primary antibodies have been used: emerin and CD56/NCAM.
Emerin was positive in 41 cases out of 50 PTC (82%) while it was negative in most of non-malignant cases (positive in 2 out of 21) and their expression showed significant difference between PTC and non-malignant cases (P=0.001) with 82% sensitivity and 90% specificity. The percentage of emerin expression was significantly higher in PTC compared to non-malignant cases (P=0.001) with 80% sensitivity and 86% specificity using 50% as a cut-off point. Nuclear changes of PTC highlighted by emerin were significantly in favor of PTC rather than non-malignant cases (P=0.001) with 82% sensitivity and 95% specificity.
CD56 was negative in most of PTC cases studied (positive only in 8 out of 50 (16%) cases) while it showed positive expression in 19/21 cases (90.5%) of non-malignant cases with a statistical significant difference (P=0.001). Negative CD56 expression showed 84% sensitivity and 90% specificity.
Combined positive emerin and negative CD56 offered 72% sensitivity and 100% specificity towards the differentiation of PTC from the non-malignant cases.
There were no significant associations between emerin expression (positivity or percentage) and the studied clinicopathological parameters in PTC. However, there was a significant negative correlation between percentage of emerin and age of patient, (P= 0.01).
Positive expression of CD56 was significantly associated with advanced stage (P= 0.009) and large tumor size (p value = 0.01).