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)

Inflammatory myofibroblastic tumor (IMT) is a controversial lesion composed of myofibroblasts, accompanied by varying numbers of inflammatory cells. Various pathogenetic factors have been proposed (ie, reactive, infectious, autoimmune, and neoplastic) but the etiology of most IMTs remains unknown. Here we review the literature of oral IMTs, detailing the demographic profile of these rare lesions. Moreover, we present an unusual case of IMT arising from the mandibular alveolar mucosa of an 82-year-old female. Microscopic examination revealed plump spindle cells set in a myxoid vascular stroma admixed with inflammatory cells. Numerous large ganglion cell-like cells were seen, some exhibiting emperipolesis of neutrophils. Ultrastructurally, prominent myofibroblasts with abundant rough endoplasmic reticulum were noted. Tumor cells were immunoreactive for vimentin, smooth muscle actin, and KP1 (CD68), and negative for desmin, S-100, and EBV-LMP. The lesion was excised without margins and the patient has manifested no evidence of disease at an 18-month recall. In an attempt to further delineate the potential neoplastic nature of this lesion, we assessed the immunohistochemical expression of various markers that have been linked to neoplastic transformation. The recorded positivity for ALK, p53, MDM2, CDK4, pRb, and Ki-67, despite the absence of bcl-2 reactivity, strongly favors the neoplastic origin of the studied tumor.
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PMID:Oral inflammatory myofibroblastic tumor demonstrating ALK, p53, MDM2, CDK4, pRb, and Ki-67 immunoreactivity in an elderly patient. 1589 59

Smooth muscle cells (SMCs) form the backbone of arteries and their proliferation hallmarks collateral vessel growth, a process termed arteriogenesis, as well as pathogenic responses such as restenosis. Since signaling pathways in SMCs are the main targets for therapeutic interventions, we aimed to determine how and to what extent the activation of the ubiquitous MEK-ERK signaling pathway correlates with important in vivo phenomena such as dedifferentiation, nuclear activation and proliferation of SMCs. Specificity of this pathway was monitored using MEK inhibitors UO126 and PD98059 in platelet derived growth factor-AB (PDGF-AB)- and fibroblast growth factor-2 (FGF-2)-stimulated SMCs. PDGF-AB induced a rapid MEK activation followed by phosphorylation of the MEK substrates ERK1/2 while FGF-2 showed a less pronounced and delayed activation. Both growth factors triggered a marked phosphorylation of c-Myc and expression of Egr1. Pretreatment with MEK inhibitors suppressed the activation of the ERK cascade, abolished the down-regulation of desmin and led to cell cycle arrest. However, the reversibility of p27Kip1 down-regulation by UO126 was mainly observed after PDGF-AB stimulation, indicating MEK independent p27Kip1 down-regulation by FGF-2. Surprisingly, treatment of SMCs with UO126 or PD98059 increased the level of MEK phosphorylation in a dose dependent manner at serine residues 217/221 in the presence as well as in the absence of both growth factors. Our results strongly imply that depending on the environmental context phosphorylation of serines 217/221 serves as an "on" as well as an "off " switch.
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PMID:MEK hyperphosphorylation coincides with cell cycle shut down of cultured smooth muscle cells. 1592 Jul 55

Three patients developed firm, mobile, nontender masses in their breasts. Two were discovered by the patients and one after mammography. Macroscopically, the nodules were firm, circumscribed, yellow on cut sections, and composed of interlacing cytologically bland spindle cells admixed with chronic inflammatory cells, the latter predominantly of lymphocytes and plasma cells. Immunohistochemistry yielded strong smooth-muscle actin reactivity within the spindle cells; 2 lesions were negative for pankeratin, 1 was focally and weakly positive. No lesions were positive for anaplastic lymphoma kinase-1, desmin, S-100, CD34, CD21, or CD35. In each case, a diagnosis of inflammatory myofibroblastic tumor was made (aka, inflammatory pseudotumor). After conservative excision with apparently negative margins, there have been no recurrences, except in one patient who developed a recurrence after 3 months. The latter recurrence was managed successfully with a second excision. We report these patients to emphasize the diagnostic features of inflammatory myofibroblastic tumor of the breast and discuss how they can be distinguished from other spindle-cell breast lesions with which they can be confused, especially spindle-cell carcinoma.
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PMID:Inflammatory myofibroblastic tumor of the breast. 1594 52

Benign peripheral nerve sheath tumors are uncommon in the gastrointestinal tract, and perineuriomas have not previously been reported to occur at this anatomic location. In this study, we analyzed the clinicopathologic and immunohistochemical features of 10 perineuriomas arising in the intestine. Eight patients were female and 2 male (median age, 51 years; range, 35-72 years). Eight of the lesions were intramucosal perineuriomas presenting as small sessile polyps detected during colonoscopy; 6 of these 8 patients were asymptomatic and undergoing colorectal cancer screening. The remaining 2 cases were submucosal masses, one each located in the colon and jejunum. Of the mucosal polyps, six were located in the rectosigmoid or sigmoid colon and one each was detected in the descending colon and transverse colon. The polyps ranged from 0.2 to 0.6 cm (median, 0.4 cm) in greatest dimension. The colonic and jejunal masses measured 3 cm and 4.5 cm, respectively. Histologically, the intramucosal perineuriomas were composed of uniform bland spindle cells having ovoid to elongated nuclei and pale indistinct cytoplasm, with no cytologic atypia, pleomorphism, or mitotic activity. The lesions had a fine collagenous stroma, demonstrated irregular borders with the adjacent lamina propria, and entrapped colonic crypts. Five cases exhibited hyperplastic changes in the adjacent or entrapped epithelium. The colonic submucosal tumor was microscopically well circumscribed, whereas the jejunal perineurioma showed focal infiltration through the muscularis propria into the subserosa. The stroma was collagenous in the colonic tumor and predominantly myxoid in the jejunal tumor. The spindle cells in the submucosal perineuriomas demonstrated tapered nuclei and elongated bipolar cytoplasmic processes. All tumors except one were positive for epithelial membrane antigen (EMA); 4 of 10 expressed claudin-1 and 2 of 10 expressed CD34. All tumors were negative for S-100 protein, glial fibrillary acidic protein, neurofilament protein, smooth muscle actin, desmin, caldesmon, KIT, and pan-keratin. Electron microscopy was performed on the tumor lacking EMA expression, revealing typical features of perineurioma, namely, spindle cells with long bipolar cytoplasmic processes and prominent pinocytotic vesicles, surrounded by discontinuous basal lamina. Clinical follow-up was available for 4 patients (median, 34 months; range, 8-53 months). No tumor recurred. In summary, perineuriomas may arise in the intestine, most often as intramucosal lesions detected as colorectal polyps with distinctive histologic features including entrapment of colonic crypts. Distinguishing perineuriomas from other spindle cell neoplasms of the gastrointestinal tract can be facilitated by immunostaining for EMA and claudin-1.
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PMID:Intestinal perineuriomas: clinicopathologic definition of a new anatomic subset in a series of 10 cases. 1700 Nov 68

Calcifications within primary gastrointestinal tumors are rare. Gastrointestinal stromal tumor (GIST) is an unusual nonepithelial tumor that develops in the gastrointestinal tract. In this paper we describe a case of spurt bleeding from a calcificated GIST in the stomach successfully treated by partial gastric resection. A 77-year-old man was admitted for chest discomfort and loss of consciousness. Endoscopic examination revealed spurt bleeding from the top of the submucosal tumor. No other lesions or points of bleeding were found in the stomach. Emergency partial gastrectomy was performed, and the stomach was closed. The cut surface of the tumor had a firm, solid, whitish-gray parenchyma with patchy calcification. Microscopic observation revealed a profusion of spindle-shaped tumor cells with calcification growing from the gastric muscular propria to the submucosa. The cells exhibited low mitotic activity and no prominent signs of nuclear atypia. Immunohistochemical staining of the tumor demonstrated positive reactivity for CD34, KIT, and vimentin, but negative reactivity for alpha-smooth muscle actin, desmin, and S-100 protein. Tumor cells positive for Mib-1 were rare. The diagnosis of the tumor was established as GIST.
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PMID:Spurt bleeding from a calcificated gastrointestinal stromal tumor in the stomach. 1624 32

Gastrointestinal stromal tumors (GISTs) constitute the largest category of primary nonepithelial neoplasms of the gastrointestinal tract. It is extremely rare that this tumor occurs in the bile tract, and only a few cases have been reported. Immunohistochemically, the tumor cells revealed a phenotype similar to Cajal cells, occasionally with differentiation to smooth muscle cells or neural cells. We present a case of malignant stromal tumor similar to GISTs with rhabdomyomatous differentiation of the gallbladder in a 68-year-old woman. The resected tumor was predominantly composed of spindle cells with rhabdomyomatous differentiation. Immunohistochemical study revealed diffuse staining of tumor cells using vimentin despite negative staining for desmin or S-100. This indicated a mesenchymal origin of the cells without smooth muscle or neuronal differentiation. Myoglobin-positive cells, in which phosphotungstic acid hematoxylin staining revealed cross striations of the cytoplasm, suggested rhabdomyomatous differentiation. Diffuse positivity for KIT in the cells suggested that the pathogenesis of this tumor may resemble that of GIST. The tumor may have derived from a mesenchymal stem cell that had undergone partial rhabdomyomatous differentiation.
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PMID:Malignant stromal tumor, so called "gastrointestinal stromal tumor", with rhabdomyomatous differentiation occurring in the gallbladder. 1625 16

Most mesenchymal neoplasms of the gastrointestinal tract belong to the category of gastrointestinal stromal tumors (GISTs) and are characterized by the immunohistochemical expression of KIT receptor. In cases without detectable KIT receptor expression several differential diagnoses have to be taken into consideration. Here, we report a case of a 41-year-old man with a tumor of the small bowel composed of large epithelioid tumor cells arranged in solid and alveolar sheets including scattered osteoclast-like multinucleated giant cells. Immunohistochemically, the tumor cells expressed strongly S-100 protein, vimentin, and to a lesser extent, bcl-2. HMB-45, melan-A, KIT receptor, desmin, smooth-muscle actin, and CD-34 were not detectable. Ki-67 index was 20%. The diagnosis was established by 2 different FISH strategies demostrating the presence of a t(12;22)(q13;q12) translocation, the diagnostic hallmark of clear cell sarcoma of soft parts. Our results provide further evidence for the existence of a new tumor entity designated gastrointestinal clear cell sarcoma with osteoclast-like giant cells. The diagnosis of this entity should be considered in the presence of S-100-positive tumors of the gastrointestinal tract containing multinucleated giant cells and can be established by FISH analysis.
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PMID:Clear cell sarcoma-like tumor with osteoclast-like giant cells in the small bowel: further evidence for a new tumor entity. 1627 85

Metastatic gastrointestinal stromal tumors (GIST) have an extremely poor prognosis; however, their immunohistochemical and genetic features have not been assessed satisfactorily and the mechanisms responsible for their high malignant potential remain unclear. We examined the immunohistochemical differences between gastric GIST and metastatic lesions in the liver of four patients who had undergone a postgastrectomy hepatectomy for metachronous liver metastases. We also carried out genetic analysis of the tumors in three of the four cases. In all cases, the immunoreactivity profiles, including KIT (CD117), CD34, smooth muscle actin (SMA), desmin, S-100 and vimentin, were similar between the gastric and metastatic tumors, but the Ki67 labeling index in the metastatic GIST was higher than that of the primary GIST. Interestingly, in the case who had received neoadjuvant imatinib therapy before gastrectomy, its therapeutic effect was observed in most of the primary lesion, with the exception of a specific small area with high cellularity. Genetic analysis revealed no acquired mutations in the c-kit or PDGFRA genes in the metastatic lesions in any of the patients, but loss of heterozygosity (LOH) of the c-kit gene was observed mainly in the metastatic tumors in two of the three cases. Furthermore, in the case of neoadjuvant imatinib therapy, LOH of the c-kit gene was shown in the high cellularity area in the primary lesion and metastatic liver GIST. It is suggested that LOH of the c-kit gene is an important event that leads to imatinib resistance and metastatic progression of GIST. In conclusion, both gastric and metastatic GIST had almost the same immunohistochemical features, except for their proliferative activity, and LOH of the c-kit gene played an important role in the process of liver metastasis.
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PMID:Immunohistochemical and genetic features of gastric and metastatic liver gastrointestinal stromal tumors: sequential analyses. 1644 23

Inflammatory myofibroblastic tumor (IMT) of the genitourinary tract is rare and has been classified into separate groups based on their anatomical site and postulated aetiology. Herein, we present a case of IMT of the renal pelvis. A 44-year-old man presented with gross hematuria. Abdominal computed tomography (CT) and magnetic resonance imaging (MRI) revealed a tumor of the left renal pelvis. Under the diagnosis of left renal pelvic tumor, he underwent left nephrectomy and ureterectomy. Microscopic examination revealed fascicular spindle cell proliferation in an oedematous myxoid background with an infiltrate of plasma cells. The spindle cells were strongly positive for smooth muscle actin (SMA) and vimentin, and negative for desmin and anaplastic lymphoma kinase (ALK). Diagnosis of the lesion was IMT of the renal pelvis.
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PMID:[Inflammatory myofibroblastic tumor of the renal pelvis]. 1647 87

We report a case of gastrointestinal stromal tumor (GIST) that developed in a male F344 rat at week 101 of an experiment in a carcinogenicity study. Macroscopically, the primary tumor, which measured 1 cm in diameter, involved the submucosal tissue of the forestomach at the lesser curvature extending to the glandular stomach and esophagus. Histopathologically, the tumor was composed of neoplastic cells with small- to medium-sized spindle-shaped single nuclei and fibrillary cytoplasm lacking distinct cell borders. It invaded extensively into the tunica muscularis and subserosa, further extending to the lamina propria mucosa and serosal surface. A few densely proliferating portions showed a tendency to storiform pattern. Metastatic tumor nodules were found in the liver, spleen, and femur bone marrow, with multiple nodules, up to 1 cm in diameter, apparent in the liver. Immunohistochemically, diffuse, but weak cytoplasmic immunoreactivity for KIT was evident, and most neoplastic cells also exhibited strong immunoreactivity for a -smooth muscle actin and vimentin. Sparse nuclear S-100-immunoreactive cells were further observed, but none of neoplastic cells were immunoreactive for CD34, caldesmon, desmin, cytokeratin, or synaptophysin. Collectively, these features meet the criteria for a GIST, with limited potential for differentiation to smooth muscle and neural cells.
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PMID:A case report of a spontaneous gastrointestinal stromal tumor (GIST) occurring in a F344 rat. 1653 95


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