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)

Although evidence suggests that extensive cortical beta-amyloid (Abeta) deposition is essential in Alzheimer disease (AD), it is also detected in nondemented elderly individuals with pathologic aging (PA). Given evidence that neutral endopeptidase (NEP) or neprilysin, a key enzyme for clearance of Abeta, is decreased in AD, the goal of the present study was to determine if NEP was also decreased in PA. We measured NEP immunoreactivity in frontal cortex of 12 AD and six PA cases and compared this with 10 normal (N) elderly individuals. None had any significant other pathology, and they were similar with respect to age, sex, and postmortem delay. In addition, Abeta1-40 and Abeta1-42 were measured by enzyme-linked immunosorbent assay (ELISA), whereas tau, synaptophysin, and alpha-synuclein were measured on Western blots. The AD cases had more neuritic plaques, neurofibrillary tangles, higher Braak stage, and more tau immunoreactivity in frontal cortex than both PA and N. In contrast, both PA and AD had more senile plaques and Abeta1-42 than N. NEP immunoreactivity was decreased in AD but not in PA. The decrease was unlikely the result of neuronal or synaptic loss because NEP immunoreactivity in frontotemporal degeneration with comparable degrees of synaptic loss as the AD cases was not different from control subjects. Although NEP enzyme activity was decreased in approximately half the AD cases, on average, it was not decreased compared with N or PA. The results add further evidence that PA is distinct from AD and indicate that decreased Abeta degradation by NEP is unlikely to contribute significantly to amyloid deposition in PA or, in many cases, of AD.
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PMID:Decreased neprilysin immunoreactivity in Alzheimer disease, but not in pathological aging. 1589 94

We report a case of a retiform Sertoli-Leydig cell tumor of intermediate differentiation presenting as a uterine intracavity polypoid mass in a 63-year-old woman. In contrast to sertoliform endometrioid carcinoma and to hitherto reported uterine tumors resembling ovarian sex cord tumors (UTROSCTs), which are primarily characterized by tubular glands and solid tubules, this tumor, which most likely represents a UTROSCT, showed a large spectrum of histologic features typical of a genuine retiform Sertoli-Leydig cell tumor. The diagnosis was confirmed by a battery of immunohistochemical stains, which also served as a tool for differential diagnosis with other neoplasms. The tumor cells were positive for broad spectrum keratin (CK) CK18, vimentin, calretinin, and progesterone receptor. Only a few isolated cells stained for inhibin. The tumor cells were negative for CK7, CK5/6, epithelial membrane antigen (EMA), carcinoembryonic antigen (CEA), carbohydrate antigen 125 (CA125), thrombomodulin, 013 (CD99), melan A, alpha-fetoprotein (AFP), placental alkaline phosphatase (PLAP), alpha-1-antitrypsin, estrogen receptor, S100, neurone specific enolase (NSE), chromogranin, synaptophysin, desmin, caldesmon, and CD10. Divergent differentiation of uterine cells seems to be the most likely pathogenetic mechanism. To the best of our knowledge, no UTROSCT showing such a variety of histologic features indicative of a true sex cord tumor has been reported before.
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PMID:Uterine retiform sertoli-leydig cell tumor: report of a case providing additional evidence that uterine tumors resembling ovarian sex cord tumors have a histologic and immunohistochemical phenotype of genuine sex cord tumors. 1617 78

We describe a rare case of a solid variant of a mammary adenoid cystic carcinoma with basaloid features (sbACC) and its coexistence with a "small cell" carcinoma (SCC), identified and confirmed by histological and immunohistochemical observations: the absence of glandular structures and PAS-positive globules, positivity for neuroendocrine markers (NSE, synaptophysin and chromogranin), and negativity for 34betaE12 and SMA actin were the aspects suggesting the presence of SCC. Furthermore, positivity for CD10 was found both in sbACC and in SCC, supporting the hypothesis that the two components share the same histogenetic myoepithelial origin and represent an example of dedifferentiation along neuroendocrine phenotype lines occurring in a multipotential neoplastic stem line, already committed towards a myoepithelial phenotype. To our knowledge, this is the first reported case of a solid basaloid adenoid cystic carcinoma merging with an SCC carcinoma. Furthermore, it is the first study in which CD10 was used to investigate the histogenesis of the two neoplastic components.
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PMID:Solid variant of mammary "adenoid cystic carcinoma with basaloid features" merging with "small cell carcinoma". 1632 13

A solid-pseudopapillary tumor is an uncommon and "enigmatic" pancreatic neoplasm, and the term encompasses the two most conspicuous histological features: solid and pseudopapillary areas. Grossly, it appears as a large solid, cystic or solid-cystic mass frequently having necrotic and hemorrhagic zones. Histologically, solid-pseudopapillary tumors are generally characterized by solid areas alternating with a pseudopapillary pattern, and cystic spaces which are the results of degenerative changes occurring in the solid neoplasm. Its immunohistochemical pattern is very distinctive and neoplastic cells are consistently vimentin-, CD10- and CD56-positive. Some cases express focal positivity for alpha-1-antitrypsin, alpha-1-antichymotrypsin, neuron-specific enolase and synaptophysin. Progesterone receptors are frequently present. Keratins are not expressed or are found only focally. Endocrine and pancreatic enzyme markers are absent; the origin of solid-pseudopapillary tumors has not yet been clarified. Many investigators favor the theory that solid-pseudopapillary tumors originate from multipotent primordial cells while others suggest an extra-pancreatic origin from genital ridge angle-related cells. Some controversy exists for both hypotheses. Solid-pseudopapillary tumors appear as a low malignancy tumor and only a small number of cases recur or develop metastases after resection. No pathological factors were found to correlate with the prognosis. Some histological features have recently been suggested to be associated with aggressive behavior.
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PMID:Solid-papillary tumors of the pancreas: histopathology. 1640 35

Solid pseudopapillary tumor is a rare but distinctive pancreatic neoplasm whose cell phenotype remains a mystery. We report 3 cases of a previously undescribed variant of solid pseudopapillary tumor of the pancreas composed almost entirely of multivacuolated clear cells (>90%). The cytoplasmic vacuoles did not contain glycogen, mucin, or lipid but seemed to be formed by dilatation of the endoplasmic reticulum and mitochondria. The tumors displayed prominent trabeculae and a solid growth pattern but lacked the characteristic pseudopapillary pattern of the classical solid pseudopapillary tumor. In contrast, the clinical features, gross characteristics, and immunoprofile were similar to those of classical solid pseudopapillary tumor. Two of the patients were young adult females with well-demarcated tumors involving the body and tail of the pancreas. Tumor cells showed immunoreactivity for vimentin, CD10, CD56, synaptophysin, and nuclear accumulation of beta catenin. In 2 patients, 1 male and 1 female, the tumors were discovered incidentally. Despite vascular invasion in one of the tumors all 3 patients are disease free after distal pancreatectomy. Clues to distinguish the clear cell variant of solid pseudopapillary tumor from endocrine pancreatic tumor composed of clear cells, clear and foamy cell variants of ductal carcinoma, metastatic renal cell carcinoma, serous cystadenoma and ectopic adrenocortical nodules are provided.
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PMID:The clear cell variant of solid pseudopapillary tumor of the pancreas: a previously unrecognized pancreatic neoplasm. 1700 Nov 53

Solid-pseudopapillary neoplasm of the pancreas is a very rare tumor. It most commonly occurs in young women and has unique pathologic features. Previous immunohistochemical studies demonstrated that most solid-pseudopapillary neoplasms were immunoreactive with antibodies directed against vimentin and neuron-specific enolase. Recently, expression of CD10 and CD56 in this tumor has been reported. In this report, we expanded the demographic profile, highlighting 3 cases of solid-pseudopapillary neoplasm of the pancreas that presented in an elderly woman, a young man, and a young woman and further characterized them histologically and immunophenotypically. Grossly, all 3 tumors were well circumscribed and had a variable degree of cystic formation, necrosis, and hemorrhage. Microscopically, these tumors were characterized by a pseudopapillary pattern of epithelioid cells arranged around a delicate fibrovascular core with sheets of bland epithelioid cells filling cystic spaces. Hyaline globules, cholesterol granulomas, and foamy cells were all seen to be common findings. Although these 3 tumors were strongly immunoreactive for vimentin, alpha-1-antitrypsin, alpha-1-antichymotrypsin, neuron-specific enolase, CD10, CD56, and progesterone receptor, they demonstrated only variable "positivity" for epithelial membrane antigen and broad-spectrum cytokeratin, but were being consistently nonreactive for synaptophysin, insulin, glucogon, chromogranin A, and estrogen receptor. Interestingly, 2 of the 3 tumors were S-100 protein and melanin A reactive but were nonreactive for HMB45.
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PMID:Solid-pseudopapillary neoplasm of the pancreas: Three cases with a literature review. 1712 44

The main neoplasms in the differential diagnosis for primary ovarian tumors with a tubule-rich pattern are pure Sertoli cell tumor, endometrioid tumors (including borderline tumor, well-differentiated carcinoma, and the sertoliform variant of endometrioid carcinoma), and carcinoid tumor. Because traditional immunohistochemical markers [pan-cytokeratin (pan-CK), low molecular weight cytokeratin (CK8/18), epithelial membrane antigen (EMA), inhibin, calretinin, CD99, chromogranin, and synaptophysin] can occasionally have diagnostic limitations, the goal of this study was to determine whether or not any alternative markers [cytokeratin 7 (CK7), estrogen receptor (ER), progesterone receptor (PR), CD10, and CD56] have better diagnostic utility when compared with traditional markers for this differential diagnosis. Immunohistochemical stains for alternative, as well as traditional, markers were performed on the following primary ovarian tumors: pure Sertoli cell tumor (n = 40), endometrioid borderline tumor (n = 38), sertoliform endometrioid carcinoma (n = 13), well-differentiated endometrioid carcinoma (n = 27), and carcinoid tumor (n = 42). Extent and intensity of immunostaining were semiquantitatively scored. In addition, immunohistochemical composite scores (ICSs) in positive cases were calculated on the basis of the combination of extent and intensity scores. Cytokeratin 7 (CK7) was positive in 97% of endometrioid tumors, 13% of Sertoli cell tumors, and 24% of carcinoid tumors. The differences in the mean ICSs for endometrioid tumors versus Sertoli cell tumor or carcinoid tumor were statistically significant (P values ranging from <0.001 to 0.018). ER and PR were positive in 87% and 86% of endometrioid tumors, 8% and 13% of Sertoli cell tumors, and 2% each of carcinoid tumors, respectively. The differences in the mean ICSs for endometrioid tumors versus Sertoli cell tumor were statistically significant (P values ranging from <0.001 to 0.012). Among the epithelial markers, EMA seemed to be the most discriminatory but only slightly better than CK7, ER, or PR. Pan-CK and CK8/18 were not helpful. CD10 showed overlapping patterns of expression in all categories of tumors. Among the sex cord markers, CD10 was markedly less useful than inhibin or calretinin; CD99 was not discriminatory. CD56 showed overlapping patterns of expression in all categories of tumors. Among the neuroendocrine markers, CD56 was less useful than chromogranin or synaptophysin. When traditional immunohistochemical markers are problematic for the differential diagnosis of ovarian Sertoli cell tumor versus endometrioid tumors versus carcinoid tumor, adding CK7, ER, and/or PR to a panel of markers can be helpful. Endometrioid tumors more frequently express CK7, ER, and PR and show a greater extent of immunostaining in contrast to Sertoli cell tumor and carcinoid tumor. Compared with traditional epithelial markers, CK7, ER, and PR are nearly as advantageous as EMA. Inhibin is the most discriminatory sex cord marker, and CD10 is not helpful in the differential diagnosis. Chromogranin and synaptophysin are excellent discriminatory markers for carcinoid tumor, and CD56 is neither sufficiently sensitive nor specific enough for this differential diagnosis to warrant its use in routine practice.
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PMID:Comparative analysis of alternative and traditional immunohistochemical markers for the distinction of ovarian sertoli cell tumor from endometrioid tumors and carcinoid tumor: A study of 160 cases. 1725 71

Reported herein are two cases of medulloepithelioma (ME) occurring in very unusual locations. Case 1 involved a 44-year-old man who presented with leg pain and urinary incontinence. Spine magnetic resonance imaging (MRI) showed an enhancing epidural and intradural lumbosacral mass. He underwent L3-S2 laminectomy with partial tumor resection. Approximately 2 months following surgery, he developed leptomeningeal spread of the tumor, and died 2 months later. Case 2 involved a 22-month-old girl who presented with painless left proptosis. MRI demonstrated diffuse, fusiform, and contrast-enhancing enlargement of the left optic nerve. Following biopsy, she was treated with chemotherapy. Histologically, the tumors in both cases consisted of primitive pseudostratified neuroepithelial cells, arranged in papillary, tubular, or trabecular configurations. A PAS-stained external limiting membrane (ELM) of the neuroepithelia was present. In case 1 there were scattered cartilaginous nodules within the tumor, in keeping with the diagnosis of a teratoid ME. Immunohistochemically, the tumor cells were positive for synaptophysin, nestin, microtubule-associated protein-2, CD56, CD10, glial fibrillary acidic protein (focal), and S-100 protein (focal). The main differential diagnoses include an immature teratoma and an optic nerve glioma in cases 1 and 2, respectively. Histological demonstration of the ELM by PAS stain is a simple but useful technique.
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PMID:Medulloepithelioma: Two unusual locations. 1730 Jun 73

Solid-pseudopapillary neoplasm of the pancreas occurs preferentially in young women and has a favorable prognosis. Differentiation of solid-pseudopapillary neoplasm from pancreatic endocrine neoplasm or adenocarcinoma can be difficult in the small biopsy specimen because they share common morphological features and immunoprofiles. Alterations of adenomatous polyposis coli (APC)/beta-catenin pathway have been identified as a genetic event contributing to the development of solid-pseudopapillary neoplasm. In the present study, to establish the diagnostic utility of beta-catenin and E-cadherin as markers for solid-pseudopapillary neoplasm, we performed immunohistochemical staining in 4 core biopsy specimens diagnosed as solid-pseudopapillary neoplasm and in tissue microarray blocks that contained histologically confirmed samples of 302 cases of adenocarcinoma, 56 cases of pancreatic endocrine neoplasm, and 50 cases of solid-pseudopapillary neoplasm. We compared the immunohistochemical results for beta-catenin and E-cadherin with those for known markers. Of the solid-pseudopapillary neoplasm cases, 51 (94.4%) were positive for nuclear beta-catenin, 45 (83.3%) were positive for CD10, 30 (55.5%) were positive for CD56, 15 (27.8%) were positive for synaptophysin, 3 (5.6%) were positive for cytokeratin (CK), and none was positive for E-cadherin and chromogranin. Of the adenocarcinoma cases, all were positive for CK, 300 (99.3%) were positive for E-cadherin, 30 (9.9%) were positive for CD10, 2 (0.7%) were positive for synaptophysin, 1 (0.3%) was positive for CD56, and none was positive for chromogranin and nuclear expression of beta-catenin. Of the pancreatic endocrine neoplasm cases, 54 (96.4%) were positive for synaptophysin and E-cadherin, 50 (89.3%) were positive for chromogranin, 26 (46.4%) were positive for CK, 15 (26.8%) were positive for CD56, 6 (10.7%) were positive for CD10, and none was positive for nuclear expression of beta-catenin. In conclusion, nuclear expression of beta-catenin and loss of E-cadherin can be used in the definite diagnosis of solid-pseudopapillary neoplasm on small biopsy specimens. CD10 immunopositivity should be carefully interpreted in the diagnosis of solid-pseudopapillary neoplasm because pancreatic adenocarcinoma or pancreatic endocrine neoplasm can also stain for CD10.
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PMID:Loss of E-cadherin and cytoplasmic-nuclear expression of beta-catenin are the most useful immunoprofiles in the diagnosis of solid-pseudopapillary neoplasm of the pancreas. 1870 51

A 46-year-old woman with epigastric pain was found to have a cystic tumor in the pancreas head on radiological examinations. The tumor was hypervascular, and its multilocular appearance resembled the "honeycomb" pattern of serous cystic tumor (SCT). The patient underwent surgery. The cut surface of the tumor showed a thick fibrous capsule with multiple cystic components, which contained necrotic tissue and brownish serous fluid, indicating an episode of hemorrhage. The cut surface of the tumor resembled solid-pseudopapillary tumor (SPT) on gross appearance. On immunohistochemical staining, the tumor cells showed diffuse and strong staining for synaptophysin (SYN), chromogranin A (CGA), and grimelius, and no staining for alpha 1-antitrypsin or CD10. We finally made a diagnosis of pancreatic endocrine tumor (PET). As PET sometimes shows an atypical multicystic appearance, immunohistochemical staining is mandatory for its correct diagnosis.
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PMID:Cystic endocrine tumor of the pancreas with an atypical multilocular appearance. 1804 Jun 26


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