Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.10.1 (ERK)
95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

All the preliminary observations on a lot of marker sets defining different stages in the tumor development are building a framework of work hypothesis which can be verified in characterising large pools of histological uniform rated paraffin probes. We developed a bootstrapping algorithm based on correlation measures to uncover regulatory patterns of immunohistochemical characterized tissue arrays with 550 invasive breast cancer cases. The algorithm is implemented in 'S' a computer language used to model mathematical solutions. Focussing on the Cytokeratins versus a set of prominent markers in breast cancer differentiation it will be obvious that markers which are known to appear in early (progenitor) forms conform to CK5/6 and CK14 while others associated with late stages conform to CK8/18 and CK19. Markers examined are among others EGFR, EMA, erb-B2, Vimentin, p53, ER and PR. The developed approach is an elegant and complete procedure to reveal the real regulatory patterns which are enclosed in a certain experimental design. The statistical significance of the results calculated by our algorithm is generally high and in the presented experimental design smaller than 0.6 * 10E-6.
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PMID:[Bootstrapping algorithm approach reveals inherent regulatory pattern in 550 invasive breast cancer cases: CK5/6/CK14 and CK8/18/CK19 builds an antagonistic set]. 1803 93

Non-Hodgkin lymphomas of the breast are rare, encompassing approximately 0.04-0.5% of all malignant breast tumors, and the vast majority are B-cell lymphomas. In contrast, lymphomas of T-cell phenotype have been rarely reported and some of these have been in close proximity to a breast implant. In our consultation practice, we have identified four patients with primary T-cell anaplastic large-cell lymphoma presenting adjacent to silicone or saline breast implants. All patients presented with seroma and neoplastic cells were identified in suspension in the serous fluid without solid tissue invasion. Three patients had no evidence of systemic disease (stage 1E), and one patient was not staged. The mean age of the patients was 46 years (range, 34-59 years). In all patients, the neoplastic cells had a T-cell phenotype, expressed CD30, cytotoxic granule-associated proteins, EMA and clusterin, and were anaplastic lymphoma kinase-1-negative. Clonal T-cell receptor gamma-chain gene rearrangements were identified in three patients. All patients underwent capsulectomy with removal of the implant. One patient subsequently received chemotherapy and radiation therapy, and another was treated with radiation alone. The third patient received no further therapy and the fourth patient has been recently diagnosed. After a mean time of 13 months (range, 9-20 months), all three patients with follow-up were alive and well without any recurrence or systemic disease. Although the follow-up time was relatively short, our series and other reported cases suggest that primary anaplastic large-cell lymphoma adjacent to breast implants is an indolent T-cell lymphoproliferative disorder.
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PMID:Seroma-associated primary anaplastic large-cell lymphoma adjacent to breast implants: an indolent T-cell lymphoproliferative disorder. 1822 53

Pagetoid dyskeratosis (PD) is considered a selective keratinocytic response in which a small part of the normal population of pale keratinocytes is induced to proliferate. PD has been found incidentally in the squamous epithelium of the skin and mucosas in various locations, but not in the nipple. In cases in which PD cells are conspicuous, there is the danger of overdiagnosis. In a retrospective study, we describe the location and incidence of PD and other pale cells in the nipple epidermis, in 288 mastectomy specimens from women operated on for breast carcinoma, in situ or infiltrating, selected consecutively from our histopathologic files. In addition to the conventional histologic methods an immunohistochemical study was performed in selected cases. PD was found in 184 (63.9%) cases and was a prominent finding in 37 (12.8%) cases. Toker cells (TCs) were identified by standard light microscopy in 24 (8.3%) nipples. Paget carcinoma cells (PCCs) were found in 12 (4.2%) cases, and in 9 (3.1%) they were an incidental finding. The immunohistochemical profile of each type of pale cells was as follows: PD cells, EMA-,LMWCK-,CK7-,HMWCK+, CEA-, HER2/neu protein-, HMB45-, HPV-; TCs, EMA+, LMWCK+, CK7+, HMWCK-, CEA-, HER2/neu protein-, HMB45-, HPV-; PCCs, EMA+, LMWCK+, CK7+, HMWCK-, CEA+, HER2/neu protein+, HMB45-, HPV-. In conclusion, friction may be the stimulus for the appearance of PD cells. PD cells must be distinguished from TCs, PCCs, clear cells of Bowen's disease, pagetoid melanoma cells, cells of clear cell papulosis, koilocytes, artifactual clear cells, and glycogen-rich squamous cells. A combination of immunohistochemical markers is useful for this distinction; however, routine histologic study is usually adequate for recognizing PD. Pathologists should be familiar with the histologic features of PD in the nipple epidermis to avoid misdiagnosis.
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PMID:Pagetoid dyskeratosis of the nipple epidermis: an incidental finding mimicking Paget's disease of the nipple. 1832 65

Malignant lymphoma presenting in the bladder has been classified in primary cases, as the first sign of disseminated disease and as a secondary infiltration. Most of the examples in the literature have been reported as single cases. Reported herein is the case of a 45-year-old man with an anaplastic large cell lymphoma (anaplastic lymphoma kinase (ALK) and granzyme B positive) that presented as a bladder neoplasm. The morphological differential diagnosis was complex because the EMA-positive immunophenotype, CD45 and CD3 negativity and the clinical manifestation simulated a transitional cell carcinoma. It is important to be aware of its existence because a poorly differentiated bladder carcinoma cannot be ruled out if CD30 and ALK immunostaining are not performed. T-cell receptor-gamma clonal rearrangement could be also helpful in these cases. Although bladder involvement by recurrent lymphoma is a sign of widely disseminated disease and it is associated with a very poor prognosis, it seems that chemotherapeutic regimens in this kind of ALK-positive lymphoma could be effective, given that the present patient had an impressive response to chemotherapy treatment.
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PMID:Anaplastic lymphoma kinase-positive anaplastic large cell lymphoma presenting as a bladder neoplasm. 1832 19

We report on a 60-year-old woman with neuroendocrine carcinoma of the left breast metastasizing to renal cell carcinoma (RCC) of the left kidney and to adrenal gland. A yellow, well-circumscribed tumor, 11 cm in largest diameter and limited to the kidney, was found. Histopathology revealed RCC with foci of neuroendocrine differentiation. Solid sheets of hyperchromatic epithelioid cells with high mitotic activity were found between typical clear cells of RCC. These cells were CAM5,2 and E-cadherin focally positive, synaptophysin and NSE weakly positive, CK19 moderately positive, and AE1-AE3 and EMA strongly positive. Chromogranin A, CD10, CK 14, CK 20, HER2 (score 1+), vimentin, and HMB45 were negative. The left adrenal gland contained multiple, separate foci of a tumor composed of neuroendocrine components. Because of the biphasic tumor in the kidney, extensive clinical examination and further analyses were recommended. Tumor in the left breast was revealed. Two months later, the patient underwent mastectomy with axillary lymph node dissection. The tumor was histologically and immunohistochemically similar to the neuroendocrine component within RCC. All axillary nodes were positive. To our knowledge, this is the first case of neuroendocrine breast carcinoma with metastasis to renal cell carcinoma and ipsilateral adrenal gland.
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PMID:Neuroendocrine breast carcinoma metastatic to renal cell carcinoma and ipsilateral adrenal gland. 1853 46

The stratified squamous epithelium of the nipple-areola complex may contain pale cells including: Paget's disease cells (PDCs), Toker cells (TCs), and so-called clear cells (CCs). PDCs are atypical, commonly concentrated along the basal layer. They stain for EMA, CAM5.2, cytokeratin 7, and HER2/neu oncoprotein. TCs are bland cells with roundish and scant-chromatin nuclei. TCs are reactive for EMA, CAM5.2, and cytokeratin 7, but show negativity for HER2/ neu oncoprotein. The majority of cells that have been called epidermal CCs fit the features of pagetoid dyskeratosis, reactive for high molecular weight cytokeratin. Other CCs showing signet-ring morphology correspond to a fixation artefact.
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PMID:[Clear and pale cells of the nipple epidermis: a critical study of their varieties]. 1859 14

Primary cutaneous anaplastic large-cell lymphoma (ALCL) ordinarily is distinguished from systemic ALCL by clinical presentation, absence of anaplastic lymphoma kinase (ALK) expression, and immunophenotype (CLA+, EMA/MUC1-). We present an exceptional case of an elderly man with primary cutaneous ALCL and no systemic disease for a 13-year period. Recurrent skin tumors in this patient were characterized by anaplastic, often multinucleated, cells infiltrating the lymphatics and associated with pseudoepitheliomatous hyperplasia. Cutaneous lymphocyte antigen was absent and EMA/MUC1, typical of systemic ALCL, was strongly expressed by the tumor cells. Remarkably, the tumor cells expressed a cytoplasmic-only variant of ALK protein, as reported in 3 previous cases of primary cutaneous ALCL. Fluorescence in situ hybridization revealed lack of rearrangements of the chromosome 2 ALK gene locus usually involved by translocation t(2;5) or other chromosomal rearrangements that generate nucleophosmin-ALK or the variant ALK fusions that occur in systemic ALCL. Nonetheless, the cytoplasmic ALK protein in the patient's tumor cells was shown to be phosphorylated/activated, suggesting a novel mechanism of ALK activation. Primary cutaneous ALCL of this novel subtype should be distinguished from systemic ALCL to ensure proper clinical management.
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PMID:Primary cutaneous ALCL with phosphorylated/activated cytoplasmic ALK and novel phenotype: EMA/MUC1+, cutaneous lymphocyte antigen negative. 1867 Mar 45

A 13 year old boy presented with a huge mass on his right arm of 6 months duration. Histopathological examination revealed sheets of malignant small round blue cells with immunopositivity for LCA, CD43, CD45Ro, CD30, EMA, ALK-1 and CD99, and negativity for CD20, TdT, myogenin, myoD1, NSE, bcl-6, bcl-2 and CD10. Fluorescent In-Situ Hybridization (FISH) testing excluded the diagnosis of Ewing's sarcoma/PNET. Pathologists need to be aware of the diagnosis of a small cell variant of ALCL, as well as of the fact that CD99 expression commonly occurs in cases of ALK-positive ALCL, in order to distinguish this entity from Ewing's sarcoma/PNET.
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PMID:Small cell variant of anaplastic large cell lymphoma with positive immunoreactivity for CD99. 1894 5

A case of CD30-positive microvillous lymphoma (MVL) in an 87-year-old man who was encountered generalised lymphadenopathy is presented. Histopathologically, the tumour showed a morphological mimic of anaplastic large cell lymphoma (ALCL) with sinusoidal growth pattern. Immunohistochemically (IHC), the tumour cells were CD30(+), CD20(+), CD45(+), BCL-2(+), BCL-6(+), MUM1(+), Ki-67(+), CD45RO(-), CD3(-), CD10(-), CD15(-), CD56(-), EMA(-), TIA-1(-) and ALK(-). Flow cytometry confirmed the IHC. In situ hybridisation for Epstein-Barr virus RNA was negative. Electron microscopically, the tumour cells were similar to large transformed lymphocytes and had circumferentially profuse microvillous projections resembling those of epithelial mesothelioma cells. In conclusion, CD30-positive MVLs are indistinguishable from ALCLs that have ultrastructural microvillous projections by morphology alone. However, the lack of EMA, TIA-1 and ALK expression in this MVL case facilitated a definite distinction from ALCLs. The results of a panel of three markers (CD10(-), Bcl-6(+) and MUM1(+)) suggested that the present case of CD30-positive MVLs has an activated non-germinal centre B-cell origin.
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PMID:CD30-positive diffuse large B-cell lymphoma with microvillous features: so-called microvillous lymphoma. 1912 65

The stratified squamous epithelium of the nipple-areola complex may contain pale or clear cells including: Paget's disease cells (PDCs), Toker cells (TCs), and so-called clear cells (CCs). Paget's disease is an uncommon presentation of breast carcinoma. PDCs are large, atypical, have abundant, pale-staining cytoplasm that may contain mucin secretion vacuoles and bulky heterochromatic nuclei. They are commonly concentrated along the basal layer and stain for EMA, CAM5.2, cytokeratin 7, and HER2/neu oncoprotein. TCs are bland cells with roundish and scant chromatin nuclei. They are found incidentally and are reactive for EMA, CAM5.2, and cytokeratin 7, but show negativity for HER2/neu oncoprotein. So-called CCs show varied morphology, are found incidentally, and have been variably interpreted by different authors. The majority of cells that have been called epidermal CCs fit the features of pagetoid dyskeratosis. These cells are reactive for high molecular weight cytokeratin. Other CCs showing signet-ring morphology present negativity for mucins and correspond to a fixation artefact.
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PMID:An overview of the pale and clear cells of the nipple epidermis. 1913 Apr 6


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