A spindle cell predominant pancreatic solid-pseudopapillary tumor

A hitherto unrecognized variant of solid-pseudopapillary tumor (SPT) of the pancreas is reported. The tumor presented in the pancreatic tail of a 44-year-old female patient. It was a well-defined, solid nodule measuring 25 mm in diameter, with homogenous tan gray cut surface. Histologically, the neoplasm was mostly composed of sheets of spindle cells. No cellular atypia and mitosis was identified. The periphery of the tumor showed typical feature of SPT. Immunohistochemically, the tumor cells were positive for vimentin, CD10, CD56, beta-catenin, and alpha1-antichymotrypsin, but negative for cytokeratin, chromogranin, synaptophysin and S-100 protein. Ultrastructurally, the tumor showed a few acinar spaces with microvilli between tumor cells. This case is peculiar in that the tumor did not show gross cystic change and predominantly consists of spindle shaped tumor cells, so may cause difficult diagnostic problem.     

Expression of Wnt-signaling pathway proteins in intraductal papillary mucinous neoplasms of the pancreas: a tissue microarray analysis

Abrogation of the Wnt-signaling pathway is implicated in the carcinogenesis of several malignancies, especially colorectal cancer where up to 90% of cases are thought to have impaired Wnt signaling. It is less frequently involved in conventional ductal pancreatic adenocarcinoma. This pathway has not been explored in intraductal papillary mucinous neoplasms (IPMNs) of the pancreas previously and formed the basis of this study. A tissue microarray of 18 cases of IPMN was stained for proteins involved in the Wnt pathway: adenomatous polyposis coli (APC), pan-beta-catenin, axin 2, glycogen synthase 3alphabeta and 3beta, c-myc, E-cadherin, and cyclin D1. The IPMNs were classified as 8 adenomas, 3 borderline, and 7 cases with carcinoma in situ and/or invasive carcinoma, occurring in 13 females, and the overall age range was 45 to 73 years. Immunohistochemical analysis showed nuclear beta-catenin staining in 7 (39%) of the 18 cases. The cases with nuclear beta-catenin localization included 1 adenoma, 2 borderline IPMN, and 4 carcinomas in situ and/or invasive carcinomas. Seven cases showed absence of APC immunostaining and these included 4 cases with nuclear beta-catenin localization. Fourteen cases displayed marked diffuse up-regulation of c-myc protein, and 12 cases also showed diffuse cyclin D1 protein overexpression. E-cadherin expression was intense and membrane in location (comparable to normal tissue) in 6 of 8 adenomas (no tissue was available in 1 case). Decreased E-cadherin staining was noted in 8 cases where tissue was available for assessment. There was progressive decrease in membrane staining of E-cadherin in 2 of 3 borderline lesions, 1 of 2 carcinomas in situ, and 4 of 5 invasive carcinomas. All other immunostains were either normal in distribution or did not show any correlation with beta-catenin or clinicopathologic parameters. In conclusion, 7 (39%) of 18 cases of IPMN in this study demonstrated abnormal localization of beta-catenin, 4 of which also lacked APC expression. Of 5 carcinomas arising in IPMN, 4 displayed a decrease in E-cadherin expression. There was also a trend for the higher grades of IPMN to show nuclear localization of beta-catenin. These findings suggest that a proportion of cases of IPMN may show abnormalities in the Wnt-signaling pathway with consequent altered expression of downstream related proteins.     

Molecular characterization of pancreatic neoplasms

Molecular analyses of neoplasms of the pancreas, coupled with careful histopathologic examination has helped refine the classification of pancreatic neoplasia. A number of molecularly and histologically distinct subtypes of pancreatic neoplasms have been identified and, importantly, many of these subtypes have important clinical implications. For example, most of the solid-pseudopapillary neoplasms harbor mutations in the beta-catenin gene (CTNNB1), and, as a result, most solid-pseudopapillary neoplasms have an abnormal nuclear pattern of labeling with antibodies to the beta-catenin protein. Clinically, patients with a solid-pseudopapillary neoplasm have a much better prognosis than do patients with ductal adenocarcinoma of the pancreas. Therefore, the immunolabeling of a pancreatic biopsy for the beta-catenin protein can help identify patients with low-risk neoplasms. It is clear that the time is now ripe for a new modern classification of neoplasms of the pancreas; a classification that does not abandon gross and microscopic pathology, but which instead integrates molecular findings with gross, microscopic, and clinical findings.     

Expression of intercellular adhesion molecules in epithelioid sarcoma and malignant rhabdoid tumor

We clinicopathologically evaluated 31 cases of epithelioid sarcoma (ES; 25 'classical' type and six 'proximal variant' type) and six cases of malignant rhabdoid tumor (MRT; three extrarenal and three renal). We also did immunohistochemical studies on 12 classical and three proximal variant cases of ES, and six cases of MRT, to clarify the differences in biological behavior in these tumors. E-cadherin, beta-catenin and CD34 expression was evaluated. We also carried out mutational analysis of exon 3 of the beta-catenin gene by polymerase chain reaction-single-strand conformation polymorphism analysis. In ES, the 5- and 10-year survival rates were 71.1 and 55.3%, respectively. A high mitotic rate (>15/10 high-power fields) was significantly correlated with a poor overall survival rate in ES (P = 0.0248). E-cadherin expression was observed in nine cases (69.2%) of ES and in four cases (66.7%) of MRT. Most of these tumors showed aberrant E-cadherin expression. Seven cases (46.7%) of ES were positive for CD34, although none of the cases of MRT were CD34 positive. Eleven cases (73.3%) of ES were positive for beta-catenin, which was localized to the cellular membrane, whereas all of the cases of MRT were beta-catenin negative. Mutational analysis for the beta-catenin gene was done in nine cases of ES and six cases of MRT, however, genetic alteration was not found. From our results, we conclude that beta-catenin membranous expression could be a useful marker for distinguishing ES, including the proximal variant, from MRT.     

Endocrine cells in intraductal papillary-mucinous neoplasms of the pancreas

 The endocrine cells in intraductal papillary-mucinous neoplasms (IPN) of the pancreas have rarely been investigated. In the normal pancreatic ducts of normal pancreases (n=5) there were a few endocrine cells: argyrophil in 5 (100%), chromogranin A in (100%), pancreatic polypeptide (PP) in 3 (60%), and insulin in 7 (20%). These endocrine cells were scattered, and located in the basal portions of pancreatic ducts. In IPN of the pancreas (n=9), there were many endocrine cells: argyrophil in 7 (78%), argentaffin in 8 (89%), chromogranin A in 8 (89%), PP in 7 (78%), serotonin in 7 (78%), insulin in 4 (44%), and gastrin in 5 (56%). In invasive ductal adenocarcinoma of the pancreas (n=6), many endocrine cells were also detected: argyrophil cells in (67%), chromogranin A in 3 (50%), insulin in 3 (50%), glucagon in 4 (67%), and somatostatin in 3 (50%). In positive cases, endocrine cells were situated under or among the neoplastic cells and the proportion of endocrine cells in IPN was less than 5% of the total neoplastic cell population. These data show that normal pancreatic ducts contain endocrine cells and that IPN frequently contain argyrophil, argentaffin, chromogranin A, and hormone-containing endocrine cells. These data also suggest that endocrine differentiation occurs during neoplastic transformation and progression of IPN of the pancreas. Received: 3 December 1996 / Accepted: 25 February 1997     

The diagnostic utility of Merkel cell polyomavirus immunohistochemistry in a fine needle aspirate of metastatic Merkel cell carcinoma of unknown primary to the pancreas

Merkel cell carcinoma (MCC) is an aggressive skin tumor with a high tendency for metastases. We report a case of MCC initially presenting as axillary and pancreatic metastases. A 33‐year‐old HIV‐positive Hispanic male presented with a history of a rapidly growing axillary mass. A needle core biopsy demonstrated an epithelioid neoplasm composed of small to medium‐sized cells with high nuclear‐cytoplasmic ratio, nuclear molding, and frequent mitotic figures. A subsequent PET scan revealed a 1.5 cm FDG avid mass in the pancreas. Endoscopic ultrasound‐guided FNA of the pancreatic mass showed neoplastic cells with similar morphology to those of the axillary mass. The tumor cells were positive with pancytokeratin AE1/AE3, CK20, CD56, synatophysin, chromogranin, and Merkel cell polyomavirus (MCPyV). This case of MCC most likely originated from a resolved primary skin lesion drained by the involved axillary lymph node with subsequent metastases to the pancreas and distant lymph nodes.     

Solid-pseudopapillary neoplasm of the pancreas: Three cases with a literature review.

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.     

Malignant intraductal oncocytic papillary neoplasm of the common bile duct

Recently, several cases of intraductal oncocytic papillary neoplasm (IOPN) of the liver and hepatic bile ducts have been reported. The author herein reports the first case of IOPN of the common bile duct (CBD). A 78-year-old man was admitted to our hospital because of jaundice. Imaging modalities including US, CT, MRI revealed an intraductal tumor of the middle CBD and biliary dilation distal to the tumor. A partial resection of the CBD was performed. Grossly, a papillary tumor measuring 20 × 15 mm was found within the CBD. Mucus is absent. Histologically, the papillary tumor was composed of atypical oncocytes. The atypia was enough to be diagnosed as adenocarcinoma. No invasive features were noted. Immunohistochemically, the tumor cells were positive for pancytokeratins (CK), CK 7, CK 18, CK19, EMA, CA19-9, CEA, mitochondria, p53 protein, C-erbB2, Ki-67 (labeling = 80%), MUC2, MUC5AC and MUC-6,. The tumor cells were negative for CK8, CK20, chromogranin, synaptophysin, neuron-specific enolase, S100 protein, CD56, MUC1, CD10 and CDX2. These immunohistochemical findings were compatible with IOPN. The patient died of other non-tumorous disease 7 year after the operation. In summary, the author presented the first case of IOPN of the CBD.     

Loss of expression of E-cadherin and beta-catenin is associated with progression of pulmonary adenocarcinoma

The aim of the present study was to determine the association of loss of membranous expression of epithelial (E)-cadherin and beta-catenin with the progression of pulmonary adenocarcinoma. The expression of E-cadherin and beta-catenin was examined in 154 cases of pulmonary adenocarcinoma, including 49 cases of atypical adenomatous hyperplasia (AAH), 40 cases of bronchioloalveolar carcinoma (BAC), 42 cases of BAC-dominant type of adenocarcinoma with mixed subtypes (early MX) and 23 cases of BAC-recessive type of adenocarcinoma with mixed subtypes (overt MX), by immunohistochemistry. E-cadherin expression was positive in all cases of AAH, in 37 cases (92.5%) of BAC and in 34 cases (81.0%) of early MX, while it was positive in three cases (13.0%) of overt MX. beta-Catenin expression was positive in 47 cases (95.9%) of AAH, in 28 cases (70%) of BAC, in 32 cases (76.2%) of early MX and in 11 cases (47.8%) of overt MX. The rates of expression of E-cadherin and beta-catenin among cases of AAH, BAC, early MX and overt MX were significantly reduced. Loss of expression of E-cadherin and beta-catenin may play an important role in the progression of pulmonary adenocarcinoma, and these events occur before structural destruction of the alveolar wall by invasion of carcinoma cell.     

Fine‐needle aspiration diagnosis of high grade adenoid cystic carcinoma metastatic to the pancreas

Pancreatic tumors are mostly primary tumors, with only rare metastatic tumors described in the literature. Here we report an unusual case of fine‐needle aspiration (FNA) diagnosis of high grade adenoid cystic carcinoma of the parotid gland metastatic to the pancreas. The aspirate smears were moderately cellular and revealed numerous basaloid neoplastic cells. The cytomorphologic differential diagnosis included primary pancreatic tumor with small cell morphology as well as metastatic tumors. By immunocytochemistry, the tumor cells were positive for cytokeratins (AE1/AE3, CAM5.2, and CK7), and CD117 (C‐KIT), and negative for CD45, WT1, synaptophysin, chromogranin, CD56, TTF‐1, and CK20. The cytomorphologic features and immunoprofile in our case were consistent with high‐grade carcinoma metastases from patient's known salivary gland primary. To the best of our knowledge, this case is the first reported encounter of FNA diagnosis of pancreatic metastasis with small cell morphology from a salivary gland neoplasm as primary site. Diagn. Cytopathol. 2015;43:117–120. © 2014 Wiley Periodicals, Inc.     

Epstein-Barr virus, beta-catenin, and E-cadherin in gastric carcinomas

Activated beta-catenin is suggested to inhibit NF-kappaB activation, and we previously demonstrated that NF-kappaB nuclear positivity was more frequent in Epstein-Barr virus (EBV)-infected gastric carcinomas. It is controversial that beta-catenin and E-cadherin are prognostic markers in gastric carcinomas. To define a relationship between beta-catenin and EBV, and the prognostic value of beta-catenin and E-cadherin, we analyzed in situ hybridization for EBV-encoded small RNAs, beta-catenin, and E-cadherin immunohistochemistry, and clinicopathological features in 111 gastric carcinomas. EBV infection was detected in seven carcinomas (6.3%); none of seven showed beta-catenin nuclear accumulation, and five out of seven revealed beta-catenin membranous loss or cytoplasmic expression. Eighty cases (72.1%) showed beta-catenin alteration; i.e., loss of membrane staining in 65 (58.6 %), cytoplasmic expression in 35 (31.5%), and nuclear accumulation in 15 (13.5%). E-cadherin alteration was observed in 34 cases (30.6%) and correlated with beta-catenin alteration. On multivariate analysis, the combined immunoexpression group of beta-catenin nuclear accumulation/ E-cadherin alteration and the advanced TNM cancer stage group showed poor patient's survival (p<0.05). In conclusion, beta-catenin activation through nuclear accumulation hardly occurred in EBV-infected gastric carcinomas. The combined immunoexpression pattern of beta-catenin and E-cadherin can be used as a prognostic marker in gastric carcinomas.     

Expression of CD44v6 but not E-cadherin or beta-catenin influences prognosis in primary pulmonary adenocarcinoma

Primary pulmonary adenocarcinoma was studied, looking for relationships between the expression of cell adhesion molecules (CAMs) E-cadherin, beta-catenin and CD44v6, and clinicopathological tumour parameters and patient post-operative survival. Formalin-fixed, paraffin-embedded tissue from 120 primary lung adenocarcinomas, including 23 poorly differentiated tumours, 17 of probable bronchial origin, and 29 with a prominent bronchioloalveolar pattern, together with nodal metastatic tumour from 34 of these patients was stained using monoclonal antibodies and immunohistochemistry. Sections were scored either high level (>10% cells positive) or low level (<10% positive). High level expression of CD44v6 was retained in 28.4% (34/120) of tumours, while high levels of E-cadherin (57.5%, 69/120) and beta-catenin (80. 8%, 97/120) were more frequent. For all CAMs, staining levels did not correlate with nodal status, stage or tumour type. The apical or basal staining seen in normal bronchial and alveolar epithelium was often seen in papillary, glandular, and bronchioloalveolar areas of tumour, while solid invasive tumour more often showed pericellular staining. When the staining for each CAM in 34 nodal metastases was compared with that in the corresponding primary tumour, a high degree of concordance was found, with no tendency for metastases to show less staining than the primary tumour. Expression of E-cadherin and beta-catenin in the primary tumour had no influence on post-operative survival, but patients whose tumours had low level CD44v6 expression had a poorer post-operative survival than those with high levels of CD44v6 (p=0.0014 for all patients, p=0.0012 for stage I patients only). In primary pulmonary adenocarcinoma, the levels of expression of E-cadherin, beta-catenin, and CD44v6 are not associated with lymph node metastases or tumour stage but the staining pattern is associated with tumour morphology. Low levels of CD44v6 expression predict a poor post-operative survival, independently of stage, while there is no such relationship with the expression of E-cadherin or beta-catenin.     

Molecular markers of colorectal adrenocarcinoma progression

Colorectal adenocarcinoma and its lymph node metastases from 72 patients and 14 control samples were studied. Expression of adhesive molecules - E-cadherin and beta-catenin, antiadhesive molecule - tenascin C and tumor metastasis suppressor KAI-1 (CD82) were studied by immunohistochemistry. The expression of E-cadherin and beta-catenin, tenascin C and KAI-1 was significantly different in adenocarcinoma and control samples. The expression of E-cadherin, tenascin C and KAI-1 was diverse in primary tumor compared to lymph node metastases. The analysis of current data showed the association of E-cadherin expression with stage of disease and depth of invasion, such as the correlation of beta-catenin nuclear expression and tenascin C expression with depth of adenocarcinoma invasion. These data may be a useful indicator of disease progression.     

胰腺实体-假乳头状肿瘤32例临床病理分析及TFE3表达的诊断价值

目的 探讨胰腺实性-假乳头状肿瘤(solid-pseudopapillary neoplasms,SPN)的临床病理特征及转录因子E3(transcrip-tion factor E3,TFE3)表达在诊断中的价值.方法 采用免疫组化法检测32例胰腺SPN中TFE3、β-catenin、CD10、CK、vimen-ti...     

Mixed carcinoid and adenocarcinoma of the appendix: report of 4 cases with immunohistochemical studies and a review of the literature.

Four cases of mixed carcinoid and adenocarcinoma of the appendix were reported. All cases presented with a dominant cecal-appendiceal tumor mass and local metastasis. Two patients had multiple peritoneal implants mimicking primary peritoneal serous adenocarcinoma or carcinomatosis. Histopathologic features of the tumors are similar, with infiltrating microglandular and cribriform patterns of tumor nests, and variable numbers of goblet cells. A literature review of "goblet cell carcinoid" that included nonlocalized cases revealed a significant percentage (>14%) of tumor-associated death, in contrast to the classic carcinoid tumor. Immunohistochemical stains were helpful to separate these tumors from carcinoid tumors and primary peritoneal serous adenocarcinoma. Mixed carcinoid and adenocarcinomas were cytokeratin (CK)-20 positive, and negative or weakly positive for chromogranin A and synaptophysin. Carcinoid tumors were CK20 negative and diffusely positive for chromogranin A and synaptophysin. Peritoneal serous adenocarcinomas were CK20 negative. These cases were clinically aggressive, and 1 patient had multiple recurrences and responded partially to chemotherapy.     

A resected case of neuroendocrine carcinoma of the stomach with unusual lymph node metastasis

Gastric endocrine cell carcinoma is a relatively rare tumor. We experienced a case of early gastric cancer in which an endocrine cell carcinoma was identified within a differentiated adenocarcinoma, and a component of this endocrine cell carcinoma had metastasized to lymph nodes of the stomach. In its 2010 revision regarding digestive system tumors, WHO classified cancer cells with characteristics of both glandular system cells and neuroendocrine cells as mixed adeno neuroendocrine carcinoma (MANEC) under the neuroendocrine carcinoma (NEC) category. In this case, we observed an endocrine cell carcinoma continuous with an intramucosal differentiated adenocarcinoma, and cancer cells with an irregular gland duct structure were observed in the proliferative portion of the submucosal tissue. In addition, there was a 35 mm size lymph node metastasis in the lesser curvature of the stomach consisting entirely of poorly differentiated cancer cells with polymorphic, highly atypical nuclei and scant cytoplasm. Immunohistological analysis showed that the endocrine carcinoma in the gastric mucosa was chromogranin A positive and the infiltrated area of the submucosal tissue was also chromogranin A positive. The lymph node metastasis was positive not only for chromogranin A, but also for Synaptophysin and CD56. Furthermore, the Ki67 labeling index was high at approximately 80 % for the gastric endocrine cell carcinoma and approximately 90 % for the lymph node metastases. Until now, there are no reports related to the patients with early gastric cancer accompanied with lymph node metastasis of MANEC. This case is very interested in considering the mechanism of lymph node metastasis of MANEC. The patient has shown no sign of recurrence for 1 year and 4 months after postoperative chemotherapy.     

Differentiation of ovarian mucinous carcinoma and metastatic colorectal adenocarcinoma by immunostaining with beta-catenin

AIMS: To investigate whether localization of beta-catenin is helpful in differentiating primary ovarian mucinous carcinoma and colorectal adenocarcinoma metastatic to the ovary. Extra-ovarian cancers which metastasize to the ovaries, especially from colorectal adenocarcinoma, frequently mimic primary ovarian carcinomas, particularly endometrioid and mucinous types. Distinguishing primary ovarian carcinoma from metastatic colorectal carcinoma is important for both therapeutic and prognostic reasons. Even after thorough histological examination, metastatic colorectal adenocarcinomas are still often mistaken for primary ovarian adenocarcinomas. Although some tumour makers have been advocated and are helpful in most cases, sometimes the distinction between primary mucinous carcinoma and metastatic colorectal carcinoma remains a problem. Activation of Wnt signalling through mutations of APC or beta-catenin is a key event in the development of colorectal cancer. These mutations lead to nuclear localization of beta-catenin, which can be demonstrated immunohistochemically. METHODS AND RESULTS: Formalin-fixed paraffin-embedded specimens from 43 primary ovarian mucinous carcinomas and 23 metastatic colorectal adenocarcinomas were included in this study. Sections were immunostained with antibodies to beta-catenin, cytokeratin (CK)7, CK20 and carcinoembryonic antigen (CEA). Nuclear localization of beta-catenin was found in 83% (19/23) of metastatic colorectal cancers and 9% (4/43) of ovarian mucinous carcinomas. Ovarian mucinous carcinomas were usually positive for CK7 (34/43, 79%). For comparison, 40 non-mucinous carcinomas of the ovary and 42 metastatic adenocarcinomas from other organs were also immunostained with antibodies against beta-catenin. Although nuclear localization of beta-catenin was occasionally seen in non-mucinous carcinoma of the ovary and metastatic adenocarcinoma from other organs, such tumours were usually distinguishable by their clinicopathological picture and rarely raised diagnostic problems. CONCLUSIONS: Immunostaining of beta-catenin is a useful marker for differentiating between ovarian mucinous carcinoma and metastatic colorectal adenocarcinoma.     

Pathologic observations of the duodenum in 615 consecutive duodenal specimens in a single Japanese hospital: II. malignant lesions

The author investigated histopathology of 615 consecutive duodenal specimens in our pathology laboratory in Japan. A computer review of the duodenal specimens was done. In cases of malignancy, histological slides were reviewed. The duodenal specimens were composed of 567 benign lesions (92%) and 48 malignant lesions (8%). The 48 malignant lesions were composed of 20 cases (42%) of primary adenocarcinoma, 10 cases (21%) of primary adenocarcinoma of ampulla Vater, 4 cases (8%) of primary squamous cell carcinoma, 1 (2%) cases of primary spindle cell carcinoma, 4 (8%) cases of carcinoid tumors, 1 (2%) case of malignant lymphoma, and 8 cases (17%) of secondary carcinoma from the pancreatic carcinoma or bile duct carcinoma. The primary adenocarcinoma (n=20) was composed of well differentiated adenocarcinoma (n=9), papillary adenocarcinoma (n=1), moderately differentiated adenocarcinoma (n=6), and poorly differentiated adenocarcinoma (n=4). The primary adenocarcinoma of the ampulla of Vater (n=10) was composed of well differentiated adenocarcinoma (n=7) and moderately differentiated adenocarcinoma (n=3). The primary squamous cell carcinoma (n=4) showed proliferation of malignant squamous cells with keratinization and intercellular bridges. The spindle cell carcinoma (n=1) consisted of only malignant spindle cells immunohistochemistry positive for various cytokeratins and vimentin. The carcinoid tumor (n=4) was typical carcinoid and showed organoid, trabecular, and ribbon-like arrangements. The carcinoid tumor was immunohistochemically positive for neuroendocrine markers such as CD56, neuron-specific enolase and synaptophysin. The malignant lymphoma (n=1) was diffuse large B-cell lymphoma immunohistochemically positive for CD10, CD20, and CD79α. The secondary carcinoma (n=8) was adenocarcinoma invaded from the pancreatic adenocarcinoma (n=6) and extrahepatic bile duct adenocarcinoma (n=2).     

Paraffin-section detection of CD10 in 505 nonhematopoietic neoplasms. Frequent expression in renal cell carcinoma and endometrial stromal sarcoma

We tested 505 cases of nonhematopoietic neoplasms by immunohistochemistry using a newly characterized monoclonal antibody (clone 56C6) against the CD10 antigen. CD10 was expressed widely in neoplasms of the genitourinary tract, including 41 (89%) of 46 cases of renal cell carcinoma, 13 (54%) of 24 cases of transitional cell carcinoma, and 11 (61%) of 18 cases of prostatic adenocarcinoma. In addition, 5 (100%) of 5 endometrial stromal sarcomas, 3 (60%) of 5 rhabdomyosarcomas, 7 (50%) of 14 pancreatic adenocarcinomas, 5 (45%) of 11 cases of schwannoma, and 12 (40%) of 30 cases of malignant melanoma also were positive for CD10. Similar to normal tissue, CD10 positivity was restricted to the apical surface of malignant glandular cells of well-differentiated colonic, pancreatic, and prostatic adenocarcinoma, whereas in poorly differentiated adenocarcinoma and other tumors, such as melanoma, transitional cell carcinoma, renal cell carcinoma, and endometrial stromal sarcoma, the CD10 positivity showed diffuse cytoplasmic or membranous/Golgi patterns. The monoclonal antibody clone 56C6 is a reliable marker for CD10 in paraffin immunohistochemistry after heat-induced epitope retrieval. CD10 expression in renal cell carcinoma and endometrial stromal sarcoma may be a useful marker in the differential diagnoses of these tumors because both tumors otherwise lack specific markers.     

Role of cd56 and e-cadherin expression in the differential diagnosis of papillary thyroid carcinoma and suspected follicular-patterned lesions of the thyroid: the prognostic importance of e-cadherin

Introduction: The pathological diagnosis of papillary thyroid carcinoma (PTC) is generally easy on routine sections stained with hematoxylin and eosin (H&E). However, the differentiation of the follicular variant of PTC (FVPTC) from other suspected follicular-patterned lesions of the thyroid is highly difficult. Among these, the lesions for which FVPTC cannot be excluded are classified as well-differentiated tumors of uncertain malignant potential (WDT-UMP). The most common immunohistochemical (IHC) markers used in the differential diagnosis include HBME-1, galectin-3, and CK19. However, none of these markers provide a 100% differential diagnosis. Objective: The present study compared the diagnostic value of CD56 and E-cadherin for the differentiation of FVPTC from the other benign follicular-patterned lesions, with HBME-1, galectin-3, and CK19. Using these markers, the controversial cases within the WDT-UMP group were reclassified. Additionally, the relationship between the reductions in E-cadherin expression with poor prognostic factors was investigated. Materials and methods: The IHC expressions of CD56, E-cadherin, HBME-1, galectin-3, and CK19 were evaluated in 181 thyroid lesions, including 101 PTCs (45 classical variant PTCs and 56 FVPTCs), 20 WDT-UMPs, 20 follicular adenomas (FAs), 20 hyperplastic nodules (HN), and 20 hyperplastic foci of lymphocytic thyroiditis. The results were statistically compared via SPSS. Results: The expressions of all of the markers were statistically significantly different in PTC and follicular-patterned lesions (P<0.05). It was found that the only marker with both sensitivity and specificity above 90% was CD56 negativity (sensitivity 91.1%, specificity 91.7%). The most sensitive and also the most specific double panel was CD56 negativity and galectin-3 positivity (sensitivity 96%, specificity 85%), and the most sensitive and specific triple panel was CD56 negativity, HBME-1 positivity, and galectin-3 positivity (97% and 70%, respectively).