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Shimizu Ku, Japan

Because there have been no reports on the incidence and expressions and mutations of KIT and PDGFRA in small cell neuroendocrine carcinoma (SCNEC) of the prostate, the author surveyed archival specimens of 2,642 prostatic specimens (biopsy, 1,503 cases; transurethral resection, 1,009 cases; prostatectomy, 130 cases). Of these, 706 cases were malignant tumors. In equivocal cases (n = 16) of Gleason 5 adenocarcinoma resembling SCNEC, several neuroendocrine markers were immunohistochemically examined. As the results, four cases of SCNEC were identified; therefore the incidence of SCNEC was 0.5% of all prostatic malignancies. All the four cases were biopsies. The remaining 686 cases were adenocarcinomas. In case 1 (50 years of age), the SCNEC tumor cells were positive for cytokeratin, P504S, synaptophysin, KIT, and PDGFRA, but negative for PSA, neuron specific enolase, CD56, and TTF-1. In case 2 (70 years of age), the tumor cells were positive for cytokeratin, PSA, P504S, chromogranin, and synaptophysin, but negative for neuron-specific enolase, CD56, TTF-1, KIT, and PDGFRA. In case 3 (72 years of age), the SCNEC tumor cells were positive for cytokeratin, PSA, P504S, synaptophysin, CD56, KIT, and PDGFRA, but negative for neuron-specific enolase, chromogranin, and TTF-1. In case 4 (81 years of age), the SCNEC tumor cell were positive for cytokeratin, PSA, P504S, chromogranin, synaptophysin, neuron-specific enolase, KIT, and PDGFRA, but negative for CD56 and TTF-1. A molecular genetic analysis using PCR-direct sequencing showed no mutations of KIT (exons 9, 11, 13, and 17) and PDGFRA (exons 12 and 18) genes in three informative cases of SCNEC. The present cases were the first of prostatic SCNEC with an examination of KIT and PDGFRA expression and KIT and PDFGRA gene mutations. © 2011 Wiley Periodicals, Inc. Source


Terada T.,Shizuoka City Shimizu Hospital
International Journal of Clinical and Experimental Pathology | Year: 2013

The author reviewed 910 cases of consecutive esophageal biopsies in the last 15 year in the pathology laboratory of our hospital. There were 693 normal mucosa and benign lesions (76.2%) and 217 malignant lesions (23.8%). No significant changes were recognized in the esophagus in 50 biopsies (5.5%). In benign lesions, the number and frequency (percentages) were as follows: 263 chronic esophagitis (28.9%), 98 heterotopic gastric mucosa (10.8%), 3 heterotopic colonic mucosa (0.3%), 71 glycogenic acanthosis (7.8%), 68 candidiasis (7.5%), 35 benign ulcer (3.8%), 41 squamous papilloma (4.5%), 4 granular cell tumor (0.4%), 1 tubular adenoma (0.1%), 2 cytomegalovirus esophagitis (0.2%), 3 leiomyoma (0.3%), 17 basal cell hyperplasia (1.9%), and 37 Barrett's epithelium (4%). In malignant lesions, the number and frequency (percentages) were as follows: 53 mild dysplasia (5.8%), 29 moderate dysplasia (3.2%), 31 severe dysplasia (3.4%), 13 carcinoma in situ (1.4%), 68 squamous cell carcinoma (7.5%), 7 primary adenocarcinoma (0.8%), 1 primary signet ring cell carcinoma (0.1%), 4 primary small cell carcinoma (0.4%), 2 primary amelanotic malignant melanoma (0.2%), 1 primary undifferentiated sarcoma (0.1%), 7 gastric cancer invasion (0.8%), and 1 primary adenoid cystic carcinoma (0.1%). In this article, the clinicopathologic features of these esophageal lesions were described. Source


The expression of NCAM (CD56), chromogranin A, synaptophysin, c-KIT (CD117) and PDGFRA in normal non-neoplastic skin and basal cell carcinoma (BCC) has rarely been investigated. The author immunohistochemically examined the expression of these molecules in 66 consecutive cases of BCC. In non-tumorous skin, NCAM chromogranin A, synaptophysin, c-KIT and PDGFRA expression was seen in the basal cell of the epidermis. NCAM, c-KIT and PDGFRA expression was also seen in the sweat glands and outer cells of hair follicles, but chromogranin and synaptophysin expression was not identified in these structures. In BCC, NCAM expression was seen in 95 % (63/66 cases). Its expression was membranous. Chromogranin A expression was recognized in 27 % (18/66 cases). Its expression was cytoplasmic. Synaptophysin expression was seen in 18 % (12/66 cases). Its expression was membranous and cytoplasmic. c-KIT expression was noted in 93 % (61/66 cases). Its expression was membranous and focally cytoplasmic. PDGFRA expression was seen in 65 % (43/66 cases). Its expression was membranous and cytoplasmic. The expression of these molecules in normal non-tumorous skin is a new finding. The expression of c-KIT and PDGFRA in BCC is also a new finding. In conclusion, the author described the normal (non-neoplastic) distribution of NCAM, chromogranin A, synaptophysin, c-KIT and PDGFRA. In addition, the author showed that, in cutaneous BCC, the expression of NCAM and c-KIT was high (95 and 93 % respectively), PDGFRA was intermediate (65 %), and chromogranin A and synaptophysin was relatively low (27 and 18 %, respectively). © 2013 Springer Science+Business Media New York. Source


Terada T.,Shizuoka City Shimizu Hospital
International Journal of Clinical and Experimental Pathology | Year: 2013

In the current WHO blue book, combined hepatocellular-cholangiocarcinoma (C-HCC-CC) was classified into two types; classical type and type with stem cell features. The latter is extremely rare, and is subcategorized into the following three subtypes; typical subtype, intermediate cell subtype, and cholangiocellular subtype. Recently, intrahepatic cholangiocarcinoma (ICC) with features of ductal plate malformations (DPM) have been reported, and the ICC with DPM was proposed as a subtype of ICC. The author herein reports a case of C-HCC-CC with stem cell features. Characteristically, the CC element showed features of DPM. A 51-year-old man of HBV carrier was found to have high AFP. A laboratory test showed an elevated AFP (395 ng/ml, normal 9-10) and hepatitis B virus-related antigens and antibodies. Liver and ductal enzymes and PIVKAII were within normal ranges. Imaging modalities including CT identified a small liver tumor. Hepatocellular carcinoma (HCC) was suspected, and the resection of the hepatic tumor was performed. Grossly, the liver tumor is well-defined white solid tumor measuring 22x16x23 mm. Microscopically, the tumor was a C-HCC-CC, and was composed of following three elements: well differentiated HCC, well differentiated cholangiocarcinoma (CC), and intermediate tumor element. Characteristically, the CC cells formed tortuous markedly irregular tubules with intraluminal cell projections, bridge formations, intraluminal tumor biliary cells; such features very resembled the ductal plate (DP) and DPM. Immunohistochemically, the cells of CC element were positive for stem cell antigens (KIT (CD117), CD56, EMA, CD34), HepPar1, EpCAM, cytokeratin (CK) CAM5.2, AE1/3, CK34BE12 (focal), CK7, CK8, CK18, CK19, CA19-9, p53, MUC1, MUC2, MUC5AC, MUC6, and Ki-67 (labeling=25%). They were negative for CEA, CK5/6, CK20, NSE, chromogranin, synaptophysin, and p63. No mucins were found by histochemically. The background liver showed chronic hepatitis B (a1, f3). Very interestingly, many DPMs were scattered in the non-tumorous parenchyma. This type of C-HCC-CC with DPM features has not been reported. The author herein proposes that this tumor should be included or added in the C-HCC-CC subtype as C-HCC-CC with stem cell features, DMP subtype. Source


Expression of MUC apomucins has rarely been investigated in the signet-ring cell carcinoma (SRCC) of the stomach and colorectum. The author examined immunohistochemically the expression status of MUC1, MUC2, MUC5AC, and MUC6 in 30 cases of gastric SRCC and 12 cases of colorectal SRCC. The normal distribution of these MUC apomucins was also examined in the non-tumorous parts of the stomach and colorectum. In normal tissues, the stomach epithelial cells consistently expressed MUC2, MUC5AC, MUC6, but consistently not MUC1. In colorectum, cryptal epithelial cells consistently expressed MUC2, but consistently not MUC1, MUC5AC, and MUC6. The expression pattern of the gastric SRCC was as follows: MUC1, 3/30 (10%); MUC2, 4/30 (13%); MUC5AC, 20/30 (67%), and MUC6 21/30 (70%). The expression pattern of the colorectal SRCC was as follows: MUC1, 5/12 (42%); MUC2, 11/12 (92%); MUC5AC, 4/12 (33%); and MUC6, 0/12 (0%). Significant differences (p<0.05) were found in the expression of MUC1 (stomach SRCC 10% vs colorectal SRCC 42%), MUC2 (13% vs 92%), MUC5AC (67% vs 33%), and MUC6 (70% vs 0%). Thus, there was a significant tendency that primary gastric SRCC express MUC5AC and MUC6 but not MUC1 and MUC2, while primary colorectal SRCC express MUC1, MUC2 and MUC5A, but not MUC6. These different expressions of these MUC apomucins in gastric and colorectal SRCC seem useful to determine the primary site of metastatic SRCC and for differential diagnosis of SRCC of other sites. In the gastric SRCC, the up-regulation of MUC1 and the down-regulation of MUC2, MUC5AC and MUC6 appear to be associated with carcinogenesis, malignant potential, progression, and clinical behaviors in gastric SRCC. In the colorectal SRCC, the up-regulation of MUC1 and MUC5AC may be associated with carcinogenesis, malignant potential, progression, and clinical behaviors in colorectal SRCC. A comparative review of the present SRCC and presently reported ordinary adenocarcinoma and SRCC cases of the stomach and colorectum was performed. Source

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