Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.11 (CD10)
 9,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using serial frozen sections, monoclonal antibodies and an indirect immunoperoxidase method, 13 fibroadenomas (FA) and 3 cystosarcomas phyllodes (CSP) were analyzed for the expression of Egp34, HEA319-antigen, leucocyte differentiation antigens CD10, CD30, CD57, CD72, CDw75, and CD77, epidermal growth factor receptor (EGFR), estrogen (ER) and progesterone receptor (PR), and transferrin receptor (CD71). Egp34, CDw75, HEA319 antigen, CD10, and CD30 turned out to be consistently expressed in different cell types constituting FA and CSP and revealed that in malignant CSP the myoepithelial compartment acquires the ability to invade the stroma. Phenomenologically, the variable mode of expression of CD57 in myoepithelial cells, of CD77 in ductal epithelium, and of CD72 in both epithelial and stromal cells is suggestive for reflecting differences in their functional state but cannot be further interpreted at present. Expression of PR and ER was restricted to duct cells and was relatively independent, non-systematical. However, expression of ER and EGFR was inverse. This was also true for EGFR and CD71 in both duct cells and myoepithelial cells of FA. In contrast, stromal cells of FA were able to co-express EGFR and CD71 in the absence of PR and ER. This suggests a hormone-independent stimulation of the stromal cell compartment, possibly leading to local proliferation as the primary event in tumorigenesis of FA. In malignant CSP, however, the main proliferating cell is an abnormally mobile, HEA319 antigen-, CD10- and CD30-positive myoepithelial cell found to co-express ERFR and CD71 which is abnormal for this cell type but encountered in (myo-)fibroblasts of FA.
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PMID:Antigenic profile of mammary fibroadenoma and cystosarcoma phyllodes. A study using antibodies to estrogen- and progesterone receptors and to a panel of cell surface molecules. 217 50

The expression of EGF receptors has been studied on luminal and basal cells of human breast in vitro. Primary cultures of normal adult human breast epithelium were prepared as single cell suspensions containing a mixture of luminal and basal cells. The cells were simultaneously immunolabelled with antibodies recognising EMA (luminal epithelial cells), CALLA/CD10 (basal cells) and the epidermal growth factor receptor (EGFR). Flow cytometric analysis of these triple labelled cells detected low levels of EGFR on both cell types, with proportionally more EGFR on basal cells compared with luminal cells. Separated populations of basal and luminal cells were prepared from single cell suspensions by flow sorting or by immunomagnetic methods and cultured with and without EGF. Increased proliferation was detected in both cell types in the presence of EGF. To determine the localisation of the EGF receptor, purified cell populations were immunolabelled with anti-EGFR antibody and an FITC-labelled second antibody for fluorescence light microscopy and colloidal gold-labelled antibody for scanning electron microscopy (SEM). Low levels of EGFR were detected by indirect immunofluorescence on both cell types with higher levels on basal cells compared with luminal cells. The detailed subcellular distribution of the receptor was examined by SEM, with gold-labelling of EGFR detected using a field emission scanning electron microscope with a YAG crystal backscattered electron detector. Both luminal and basal cells expressed EGFR over the upper surface of individual cells when these were growing in isolation, but when cells formed part of a confluent island, levels of EGFR on the upper surface of cells were obviously reduced. Observations made by SEM on cells at the edges of such confluent islands showed that cultured basal cells expressed much higher levels of EGFR on their basal, as compared with their upper surfaces.
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PMID:Epidermal growth factor receptor expression on human breast luminal and basal cells in vitro. 868 18

Matrix metalloproteinase (MMP)-9 is an endopeptidase that digests basement membrane type IV collagen. Enhanced expression has been related to tumor progression both in vitro and in vivo. The control of MMP transcription is complex, but recently, epidermal growth factor receptor (EGFR) expression has been implicated in up-regulation of MMP-9 in tumor cells in vitro. Our objective was to evaluate the relationship between MMP-9 and EGFR expression in non-small cell lung cancer (NSCLC) and to assess the impact of expression on clinicopathological parameters and survival. This is a retrospective study of 169 patients who underwent resection for stage I-IIIa NSCLC with a postoperative survival >60 days. Minimum follow-up was 2 years. Standard avidin-biotin complex immunohistochemistry was performed on 4-microm paraffin-embedded sections from the tumor periphery using monoclonal antibodies to EGFR and MMP-9. MMP-9 was expressed in the tumor cells of 88 of 169 (52%) cases. EGFR expression was found in 94 of 169 (56%) cases [membranous, 55 of 169 (33%); cytoplasmic, 39 of 169 (23%)]. MMP-9 expression was associated with poor outcome in univariate (P = 0.0023) and multivariate (P = 0.027) analysis. Membranous, cytoplasmic, and overall EGFR expression were not associated with outcome (P = 0.13, 0.99, and 0.17, respectively). MMP-9 expression showed a strong correlation with EGFR expression (P < 0.0001) and EGFR membranous expression (P = 0.002) but not with cytoplasmic EGFR expression (P = 0.18). Co-expression of MMP-9 and EGFR (37%) conferred a worse prognosis (P = 0.0001). Subset analysis revealed only MMP-9 and membranous EGFR co-expression (22%) was associated with poor outcome (P = 0.0019). Our results show that a significant proportion of NSCLC tumors co-express MMP-9 and EGFR. The co-expression of these markers confers a poor prognosis. This finding suggests that EGFR signaling pathway may play an important role in the invasive behavior of NSCLC via specific up-regulation of MMP-9.
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PMID:Matrix metalloproteinase 9 and the epidermal growth factor signal pathway in operable non-small cell lung cancer. 1087 86

The present study was performed in four renal cell lines to evaluate their capability to: (1) produce and express transforming growth factor alpha (TGFalpha), its respective receptor, the epidermal growth factor receptor (EGFr) and the small G protein, RhoA, and (2) exhibit morphogenetic properties when grown on Matri-cell substrates. The cell lines were derived from normal (Madin-Darby canine kidney cells), embryonic (SK-NEP-1 and 293 cells), and cancerous (human renal adenocarcinoma cells) kidneys. TGFalpha messenger ribonucleic acid, evaluated by a nonradioactive in situ hybridization technique, was found to be expressed in all the cell lines. Large amounts of TGFalpha peptide were observed in all four cell lines, while EGFr was highly expressed only in cancerous ACHN and embryonic-tumor SK-NEP-1 cells. RhoA peptide was found in appreciable amounts in SK-NEP-1 and 293 cells (compared to the other two cell lines). The morphogenetic properties of the four cell lines were assessed, by culturing them on Matri-cell dishes: SK-NEP-1 cells alone were found to grow in three-dimensional structures forming clusters and worm-like cellular aggregates. This feature was displayed by SK-NEP-1 cells but not by the other three cell lines, and may be connected with the contemporary presence of RhoA, EGFr, and TGFalpha found in significant amounts only in the SK-NEP-1 cell line.
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PMID:Renal cell cultures for the study of growth factor interactions underlying kidney organogenesis. 1140 92

Multipotent neural stem cells (NSCs) present in the developing neural tube (E10.5, neuroepithelial cells; NEP) were examined for the expression of candidate stem cell markers, and the expression of these markers was compared with later appearing precursor cells (E14.5) that can be distinguished by the expression of embryonic neural cell adhesion molecule (E-NCAM) and A2B5. NEP cells possess gap junctions, express connexins, and appear to lack long cilia. Most candidate markers, including Nestin, Presenilin, Notch, and Numb, were expressed by both NEP cells as well as other cell populations. Fibroblast growth factor receptor 4 (FGFR4), Frizzled 9 (Fz9), and SRY box-containing gene 2 (Sox2) as assessed by immunocytochemistry and in situ hybridization are markers that appear to distinguish NSCs from other precursor cells. Neither Hoechst 33342 nor rhodamine-123 staining, telomerase (Tert) expression, telomerase activity, or breakpoint cluster region protein 1 (Bcrp1) transporter expression could be used to distinguish NEP stem cells from other dividing cells. NEP cells, however, lacked expression of several lineage markers that are expressed by later appearing cells. These included absence of expression of CD44, E-NCAM, A2B5, epidermal growth factor receptor (EGFR), and platelet-derived growth factor receptor-alpha (PDGFR alpha), suggesting that negative selection using cell surface epitopes could be used to isolate stem cell populations from mixed cultures of cells. Using mixed cultures of cells isolated from E14.5 stage embryos, we show that NEP cells can be enriched by depleting differentiating cells that express E-NCAM or A2B5 immunoreactivity. Overall, our results show that a spectrum of markers used in combination can reliably distinguish multipotent NSCs from other precursor cells as well as differentiated cells present in the CNS.
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PMID:Properties of a fetal multipotent neural stem cell (NEP cell). 1243 54

The mechanism by which neurotensin (NT) promotes the growth of prostate cancer epithelial cells is not yet defined. Here, androgen-independent PC3 cells, which express high levels of the type 1 NT-receptor (NTR1), are used to examine the involvement of epidermal growth factor receptor (EGFR), mitogen-activated protein kinases (ERK, SAPK/JNK and p38), PI3 kinase and PKC in the mitogenic effect of NT. NT dose dependently (0.1-30 nM) enhanced phosphorylation of EGFR, ERK and Akt, reaching maximal levels within 3 min as measured by Western blotting. These effects were associated with an accumulation of EGF-like substance(s) in the medium (assayed by EGFR binding) and a 2-fold increase in DNA synthesis (assayed by [3H]thymidine incorporation). The DNA synthesis enhancement by NT was non-additive with that of EGF. The NT-induced stimulation of EGFR/ERK/Akt phosphorylation and DNA synthesis was inhibited by EGFR-tyrosine kinase inhibitors (AG1478, PD153035), metallo-endopeptidase inhibitor phosphoramidon and by heparin, but not by neutralizing anti-EGF antibody. Thus, transactivation of EGFR by NT involved heparin-binding EGF (HB-EGF or amphiregulin) rather than EGF. The effects of NT on EGFR/ERK/Akt activation and DNA synthesis were attenuated by PLC-inhibitor (U73122), PKC-inhibitors (bisindolylmaleimide, staurosporine, rottlerin), MEK inhibitor (U0126) and PI3 kinase inhibitors (wortmannin, LY 294002). We conclude that NT stimulated mitogenesis in PC3 cells by a PKC-dependent ligand-mediated transactivation of EGFR, which led to stimulation of the Raf-MEK-ERK pathway in a PI3 kinase-dependent manner.
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PMID:Involvement of MAP-kinase, PI3-kinase and EGF-receptor in the stimulatory effect of Neurotensin on DNA synthesis in PC3 cells. 1517 34

Phyllodes tumor is an uncommon biphasic breast tumor, with the ability to recur and metastasize, and it behaves biologically like a stromal neoplasm. Traditionally, phyllodes tumors are graded by the use of a set of histologic data into benign, borderline, and malignant. In most series, all phyllodes tumors may recur, but only the borderline and malignant phyllodes tumors metastasize. On the basis of histologic features, prediction of behavior is difficult. The expression of many biological markers, including p53, hormone receptors, proliferation markers, angiogenesis group of markers, c-kit, CD10 and epidermal growth factor receptor have been explored, and many have been shown to be variably expressed, depending on the grade of the tumor. These markers are, however, of limited value in predicting the behavior of the tumor. Recently investigators have reported a plethora of genetic changes in phyllodes tumors, the most consistent of which seems to be 1q gain by comparative genomic hybridization. Some candidate genes have been mapped to various sites, and preliminary data suggest that some of these changes may be related to recurrence. It is foreseeable that more exciting data will be generated to help us to understand the etiology and pathogenesis of phyllodes tumor.
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PMID:Phyllodes tumor of the breast: an update. 1943 72

The cDNA microarrays allows the classification of breast cancers into 6 groups: luminal A, luminal B, luminal C, normal breast-like, human epidermal growth factor receptor 2-positive, and basal-like. This latter is characterized by the expression of basal cytokeratins (CKs), and frequent negativity for hormone receptors and human epidermal growth factor receptor 2. There is a marked parallelism between triple negative breast carcinomas and basal-like carcinoma, but these are not equivalent terms. Estimated concordance is around 80%. CK5 seems to be the best marker for the identification of these tumors. Other good markers to identify these tumors are CK14, CK17, and epidermal growth factor receptor. A subset of triple negative breast carcinomas has myoepithelial differentiation, with positivities for smooth muscle actin, p63, S-100, and CD10 among others. Recent studies suggest that basal like carcinomas are originated from mammary stem cells.
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PMID:Triple negative breast carcinomas: similarities and differences with basal like carcinomas. 1962 Aug 42

Myoepithelial carcinoma (MEC) is a rare type of breast cancer composed purely of myoepithelial cells. Most often it presents with a spindle cell morphology that can mimic several benign and malignant lesions and may be misdiagnosed by the pathologist. We report 15 cases of MEC, which were sent to our consultation practice: Five of them were initially diagnosed as benign. The patients, all female, ranged from 45 to 86 years in age (mean 69.5) and-with one exception-presented with a breast mass. The tumor size measured between 1 and 4.8 cm (mean 2.6 cm). Microscopically, the tumors had infiltrative growth pattern most frequently with thin anastomosing cords of tumor cells associated with an intimately admixed reactive spindle cell stroma. The neoplastic myoepithelial cells were emanating from the myoepithelial cell layer of entrapped ductules in every case. The nuclei showed mild to moderate pleomorphism, and the mitotic activity ranged from 0 to 9/10 high power field. Immunohistochemical stains for p63, CD10, CK903, and CK5/6 reacted strongly and diffusely with the tumor cells, and mainly the reactive stroma had weak positivity for calponin, S-100, and smooth muscle actin. Estrogen receptor, progesteron receptor, and Her2 immunostains were negative, but strong epidermal growth factor receptor expression was observed. Follow-up was available for seven patients: All of them were alive at last contact; one patient had local recurrence, and one developed pulmonary metastases. MEC is a potentially aggressive malignant neoplasm sharing many features with metaplastic carcinomas. Morphologically, it is often difficult to distinguish it from benign spindle cell proliferations.
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PMID:Myoepithelial carcinoma of the breast: a clinicopathological and immunohistochemical study of 15 diagnostically challenging cases. 2065 49

Adult granulosa cell tumors are usually diagnosed at an early stage. However, most patients with advanced or recurrent disease will die of the disease due to limited treatment options. Data on the immunohistochemical characteristics of recurrent granulosa cell tumors are limited. The aim of this study was to compare the immunohistochemical profile of primary and recurrent adult granulosa cell tumors. Special emphasis is given to epidermal growth factor receptor expression because it represents a potential marker for targeted therapy with monoclonal antibodies.Inhouse granulosa cell tumor cases accessioned between 1999 and 2008 were retrieved and reviewed according to the WHO classification. Cases were studied by immunohistochemistry using a panel of 11 antibodies. Immunostaining was semiquantitatively recorded.We have studied 20 cases of primary and 20 cases of recurrent adult granulosa cell tumors from 31 patients. Immunohistochemistry showed that primary tumors were positive for inhibin in 100%, calretinin 100%, CD56 90%, CD99 40%, D2-40 35% and low molecular weight keratin 30%. Recurrences were positive for inhibin 90%, calretinin 85%, CD56 95%, CD99 65%, D2-40 55% and low molecular weight keratin 10%. Recurrences were positive for inhibin 90%, calretinin 85%, CD56 95%, CD99 65%, D2-40 55%, and low molecular weight keratin 10%. All primary and recurrent tumors were negative for melan-A, CD10, and epithelial membrane antigen. Epidermal growth factor receptor was positive in 65% of primary tumors and 85% of recurrences. Ki67 index was higher in recurrence specimens. The immunoprofile of primary and recurrent adult granulosa cell tumors is highly concordant. Similar to primary tumors, almost all recurrent cases exhibited evidence of sex cord lineage. The lack of specific markers emphasizes the need for evaluation using a panel of antibodies. Special attention should be paid when low molecular-weight keratin is used as part of a panel differentiating granulosa cell tumors from carcinomas, as a significant proportion of the former are positive. Although targeted therapies directed against epidermal growth factor receptor have not been tested yet in the setting of advanced or recurrent granulosa cell tumors, the high level of epidermal growth factor receptor expression is important as we step to an era of advanced biolabeled imaging techniques.
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PMID:Immunohistochemical characterization of primary and recurrent adult granulosa cell tumors. 2301 18


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