ABSTRACT
A celiac disease update review and a case report are presented, especially concerning a Clinical Pathology Laboratory approach. Implemented basic research, case finding strategy and information technologies are the key tools for a better understanding of the multi-etiological features of this disease. By these tools it will be achieved appropriateness in diagnosing and monitoring of the related clinical pictures.
Subject(s)
Celiac Disease/diagnosis , Celiac Disease/etiology , Adult , Autoantibodies/analysis , Autoantigens/analysis , Biomarkers/analysis , Celiac Disease/enzymology , Celiac Disease/genetics , Celiac Disease/immunology , Child , Chromosomes, Human, Pair 6/genetics , Female , Gliadin/immunology , HLA-DQ Antigens/genetics , Humans , Immunoglobulin A/blood , Immunoglobulin G/blood , Intestinal Mucosa/immunology , Intestinal Mucosa/pathology , Male , Middle Aged , Retrospective Studies , Transglutaminases/analysisABSTRACT
The aim of this study was to examine the correlation between intratumoral microvessel density (iMVD) and the presence of cellular fibronectin isoforms, ED-A and ED-B, in order to identify those tumours with a prominent angiogenic phenotype. 91 cases of invasive ductal breast carcinoma were evaluated for TNM, histological grading, percentage of Ki-67+ cells and receptor hormonal status. iMVD was determined as a single microvessel count in a 200 x microscope field from the region of the tumour that appeared to be most densely vascular. When the mean values of iMVD of the various groups were compared, no significant difference was noted (Mann-Whitney test). When tumours were classified as high or low iMVD, based on a cut-off value (99 vessels/0.74 mm2), cases with high iMVD were significantly more numerous in poorly differentiated G3 tumours (P = 0.01, Chi-square test), and in tumours with lymph node metastasis (N0 versus N1 + N2; P = 0.002). The possibility that high iMVD was the expression of prominent vascular neoformation was explored using ED-A and ED-B isoforms of fibronectin as markers of neoformed vessels. ED-A + and/or ED-B + blood vessels were < 10% of total vessels, were detected in approximately 50% of cases independently of iMVD values, and were not more numerous in tumour areas with hot spot vascularisation. Our findings indicate that iMVD and expression of ED-A/ED-B reflect different aspects of tumour-associated angiogenesis.
Subject(s)
Breast Neoplasms/blood supply , Carcinoma, Ductal, Breast/blood supply , Fibronectins/metabolism , Biomarkers, Tumor/metabolism , Breast Neoplasms/chemistry , Carcinoma, Ductal, Breast/chemistry , Female , Humans , Microcirculation , Middle Aged , Neovascularization, Pathologic/metabolismABSTRACT
Met protein encoded by MET oncogene is the high affinity receptor for hepatocyte growth factor (HGF)/scatter factor (SF). HGF/SF has to be cleaved in its heterodimeric form by the urokinase-type plasminogen activator (uPA) to become active as a ligand for Met receptor. The expression of Met protein and of the high affinity receptor for uPA (uPA-R) was investigated in 39 samples of papillary carcinoma using immunohistochemistry. Reactivity for Met protein was present in 33 of 34 tumours, mostly with a diffuse pattern of staining. Reactivity for uPA-R was present in 78 per cent of papillary tumours and exhibited a pattern of staining similar to that of Met protein. Staining for uPA-R was present in 23 of 25 cases (92 per cent) of papillary carcinoma with prominent sclerosis, and in only 1 of 7 cases (14 per cent) without sclerosis. Peritumoural normal thyroid, follicular adenomas, and follicular carcinomas were negative for Met protein and for uPA-R. Hyperfunctioning tall thyroid cells showed weak membrane reactivity for uPA-R and for Met protein. The findings of immunohistochemistry were confirmed at the mRNA level using in situ hybridization, since the signal for uPA-R and Met RNAs was detected in most tumour cells of five cases of papillary carcinoma.
