Sarcomatoid carcinoma in the pelvic cavity

Sarcomatoid carcinoma in the pelvic cavity is very rare. A 58-year-old Japanese man was admitted to our hospital because of lower abdominal fullness. CT and MRI revealed a large mass in the left pelvic cavity. Transurethral bladder endoscopy showed tumor invasion, and large biopsies were obtained from the bladder lesion. Histologically, the tumor was composed of malignant round cells with hyperchromatic nuclei. Many intracytoplasmic vacuoles were present. No carcinomatous areas were seen. Immunohistochemically, the tumor cells were positive for cytokeratin (CK) 18, vimentin, p53 and Ki-67 (labeling 80%). The tumor cells were negative for panCK AE1/3, CD5/6, CK7, CK8, CK14, CK19, CK20, CK 34BE12, EMA, desmin, calretinin, WT-1, S100 protein, α-smooth muscle actin, CEA, CD34, CD45, CD20, factor VIII-related antigen, synaptophysin, p63, CDX2, and myoglobin. Because the CK18 was diffusely expressed, the pathological diagnosis was sarcomatoid carcinoma.     

Central granular cell odontogenic tumor: a histopathologic and immunohistochemical study

The central granular cell odontogenic tumor (CGCOT) is a rare lesion that usually affects the posterior region of the mandible of young adults. We present a case of CGCOT involving the mandible of a 20-year-old white woman, emphasizing the immunohistochemical characteristics using a large panel of antibodies. The lesion was removed surgically, and after 4 years of follow-up, there are no evidences of recurrences. The odontogenic epithelium (OE) showed positivity for cytokeratins (CKs) AE1/AE3, 34βE12, CK5, CK7, CK8, CK14, CK19, E-cadherin, β-catenin, CD138, and p63. The granular cells were positive for vimentin, CD68, lysozyme, muscle-specific actin, α-smooth muscle actin, calponin, neuron-specific enolase (NSE), CD138, and bcl-2. Dendritic-like cells surrounding the OE displayed positivity for vimentin, CD1a, S100, CD68, and bcl-2, but it was negative for factor XIIIa, supporting a Langerhans cell phenotype. Ki-67 labeling index was 1.8%, whereas p53 was negative. These data confirm the benign nature of CGCOT, the association of OE with Langerhans cells, and a variable phenotype of the granular cells.     

Intrahepatic bile duct adenoma (peribiliary gland hamartoma): a case report and review of literature

Bile duct adenoma (BDA) is a comparatively rare disease and there are relatively few reported cases in the English-language literature. Herein, we present a 63-year-old woman, who was incidentally found to have a liver-occupying lesion during a routine medical examination. Ultrasonography suggested “quick wash-in and wash-out” sign with an obvious nodular enhancement in the peripheral of the right intrahepatic nodular. Computed tomography revealed a 33 mm×25 mm×28 mm mass in the right hepatic segment. The patient underwent a liver tumor resection. Histological examination showed that the tumor was consisted of small heterogeneous tubular ducts with fibrous tissues and several inflammatory cells, without cell atypia and mitotic activity. Immunohistochemically, the tumor cells were positive for CK19, CK7, CD56 and CD10. The final histopathological diagnosis was intrahepatic BDA.     

Paratesticular cysts with benign epithelial proliferations of wolffian origin

Paratesticular cysts with benign epithelial proliferations (BEPs) are rare. Only 10 cases were found in a series of 431 paratesticular cysts and were classified as follows: cystadenoma, 5; papilloma, 2; and hamartoma, 3. Four cystadenomas showed multiple papillae lined by CD10+ epithelial cells with hyperchromatic nuclei. The remaining lesion showed areas with a microcystic, glandular, cribriform pattern, with small, benign glands without atypia. Urothelial papilloma presented BEPs with cytokeratin (CK) 7+ and CD10+ and CK20- umbrella-like cells. The mural papilloma was lined by proliferative cylindrical cells exhibiting strong CK7 and CD10 expression. The 3 Wolffian hamartomas were characterized by strongly CD10+ epithelium surrounded by smooth muscle cells. The consistent CD10 expression in BEPs of paratesticular cysts suggests a Wolffian origin. The differential diagnosis of paratesticular cysts with BEP vs metastatic prostatic and primary borderline or malignant tumors is discussed.     

兔股骨慢性骨髓炎模型的制作

背景：建立有效稳定的慢性骨髓炎动物模型是治疗慢性骨髓炎实验研究的基础。以往慢性骨髓炎模型常常建模成功率低,模型不稳定。 目的：探讨运用金黄色葡萄球菌制备兔股骨慢性骨髓炎动物模型的实验方法。 方法：健康成年新西兰兔40只,麻醉成功后在股骨大转子下2 cm剥离局部骨膜后用3.5 mm钻头的电钻,在该处钻2个纵向相连、部分重叠的骨洞,直达髓腔,孔洞用无菌骨蜡密封,实验组(20只)向髓腔内注射0.1 mL的5%鱼肝油酸钠,再向髓腔内注射0.5 mL的金黄色葡萄球菌液(1×106 cfu);对照组(20只)则向髓腔内注射0.1 mL的5%鱼肝油酸钠,再向髓腔内注射0.5 mL的生理盐水。4周后观察,兔感染部位大体观察、体质量、体温、X射线放射检查、细菌培养及改良Norden骨髓炎评价动物模型的制备情况。 结果与结论：实验组20只兔接种细菌1周后开始出现体温升高、食欲减退、跛行等症状,接种局部红肿;2周以后13只兔伤口局部出现渗液、流脓;4周后19只兔均有局部红肿、流脓和体温身高等症状;比对照组兔体温明显升高,体质量明显减轻;改良Norden骨髓炎评分也高于对照组;14只兔分泌物细菌培养试验阳性,结果显示均为金黄色葡萄球菌感染。造模成功率为95%。提示使用金黄色葡萄球菌和鱼肝油酸钠骨髓腔注入的方法,可稳定可靠地制备出兔股骨慢性骨髓炎动物模型,是慢性骨髓炎模型制作的可靠方法。  中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程     

Cycling CD34 expression in subpopulations of head and neck squamous cell carcinoma cell lines is involved in radioresistance and change in cytokeratin expression profile

The expression of the hair follicle stem cell marker CD34 was analyzed in five different head and neck squamous cell carcinoma (HNSCC) cell lines with different antibodies. All HNSCC cell lines expressed CD34 on their cell surface. After cell cycle synchronization via serum starvation, we observed cyclic CD34 expression in HNSCC cells dependent on cell cycle progression via immunofluorescent staining and flow cytometric analysis. Investigation of the CD34(+) and CD34(?) HNSCC populations revealed most of the cells in S-phase and G2/M-Phase in CD34(+) cells in contrast to CD34(?) cells. Knockdown of CD34 in HNSCC cells led to diminished clonal expansion in a colony forming assay after subjecting the cells to ionizing radiation. Furthermore, knockdown of CD34 after cell cycle synchronization induced high CK1, CK4, and CK5 gene expression and downregulation of CK10 gene expression as shown by Taqman^® quantitative PCR analysis. The expression levels of CK1 and CK10 were verified via western blot analysis. In summary, our study shows that CD34 plays a role during cell cycle progression of head and neck squamous cell carcinoma and additionally is involved in irradiation resistance and differentiation of malignant oral keratinocytes.     

Small cell carcinoma of the urinary bladder

Primary small cell carcinoma of the urinary bladder is very rare; only several studies have been reported in the English literature. A 62-year-old woman was admitted to our hospital because of hematuria and dysuria. Bladder endoscopy revealed a large polypoid tumor at the bladder base. Transurethral bladder tumorectomy (TUR-BT) was performed. Many TUR-BT specimens were obtained. Histologically, the bladder tumor was pure small cell carcinoma. Immunohistochemically, the tumor cells were positive for cytokeratin (CK) AE1/3, CK CAM5.2, CK8, CK18, neurone-specific enolase, chromogranin, NCAM (CD56), synaptophysin, Ki-67 (labeling=100%), p53, KIT (CD117), and platelet-derived growth factor receptor-α (PDGFRA). The tumor cells were negative for CK5/6, CK 34BE12, CK7, CK14, CK19, CK20, p63, CD45, 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. No metastases were found by various imaging techniques. The patient is now treated by cisplatin-based chemotherapy.     

Pure sarcomatoid carcinoma of maxillary sinus and nasal cavity simulating malignant fibrous histiocytoma

Although a few cases of sinonasal carcinoma with focal sarcomatous differentiation have been reported, pure sarcomatoid carcinoma has not been reported in the English literature. Imaging studies and gross inspection in a 60-year-old man with left-sided face pain revealed a mass in the left maxillary sinus and nasal cavity. A large incisional biopsy specimen from the nasal cavity revealed proliferation of malignant spindle and round cells with a malignant fibrous histiocytoma (MFH) pattern. Tumor giant cells were scattered, and there were areas of a vague storiform pattern. Mitotic figures were numerous. Carcinomatous component was not recognized. The histologic diagnosis was storiform-pleomorphic MFH. Tumor cells were positive for pancytokeratins AE1/3, KL-1, and CAM5.2 and cytokeratin (CK) 18, vimentin, CD68, p53, Ki-67 (labeling, 90%), α?-antitrypsin, and α?-antichymotrypsin and negative for pancytokeratin WSS, CK 34βE14, CK7, CK8, CK14, CK19, CK20, epithelial membrane antigen, S-100 protein, desmin, α-smooth muscle actin, CD34, HMB45, chromogranin, synaptophysin, myoglobin, CD45, CD30, and CD15. Because keratins were positive in tumor cells, a diagnosis of sarcomatoid carcinoma simulating MFH was made. The patient was treated with chemoradiation without significant effect and died 9 months after initial examination.     

Collision tumor of primary merkel cell carcinoma and chronic lymphocytic leukemia/small lymphocytic lymphoma,diagnosed on ultrasound‐guided fine‐needle aspiration biopsy: A unique case report and review of literature

We report an extremely rare case of skin collision tumor between primary Merkel cell carcinoma (MCC) and chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) first diagnosed on ultrasound‐guided fine‐needle aspiration biopsy (US‐FNA). A 95‐year‐old female with a history of CLL presented with a slow growing left malar mass was referred to our clinic for US‐FNA. US scan showed a well‐defined subcutaneous mass (2.78 cm) with complex echogenicity. On‐site assessment showed a cellular aspiration which was interpreted as small blue round cell tumor. On further examination, smears and cell block showed dimorphic populations of relatively larger cells with neuroendocrine features and smaller lymphoid cells. Immunocytochemical studies of cell block sections revealed that the larger cells were positive for CD56, Chromogranin, Synaptophysin, CK8/18, CK20 (dot‐like pattern); and the smaller cells were positive for CD45. Flow cytometric analysis showed a majority of CD16/CD56 positive cells, 17% of monoclonal B‐cells, and 14% of reactive T cells. The immunophenotype of the monoclonal B cells were of CLL/SLL. The diagnosis of a collision tumor composed of primary MCC and CLL/SLL was confirmed. Surgical resection of the mass one month later concurred with the FNA cytological diagnosis. The fact that surgical specimen displayed a solid tumor with both CLL/SLL and MCC components ruled out the possibility that the FNA merely had MCC with peripheral leukemic blood contaminant. No additional MCC lesion was found in the patient, which ruled out the possibility of metastatic MCC to a lymphomatous lymph node. Diagn. Cytopathol. 2015;43:66–71. © 2014 Wiley Periodicals, Inc.     

Myoepithelial carcinoma of pharynx expressing KIT and PDGFRA

KIT and PDGFRA expression has rarely been examined in myoepithelial carcinoma (MC) of the salivary glands. An 89-year-old Japanese woman presented with a pharyngeal mass. Gross and imaging examinations revealed an elevated mass in the middle pharynx next to the oral cavity. A biopsy revealed atypical cells, and tumorectomy was performed. The tumor was composed of atypical epithelioid cells arranged in solid nests, cords, and vague acinar patterns. Mitotic figures were recognized in 3 per 50 high power fields. Immunohistochemically, the tumor cells were positive for myoepithelial markers including cytokeratin (CK) 14, α-smooth muscle antigen, S100 protein, and p63. They were also positive for KIT, PDGFRA, pancytokeratin AE1/3, CK34βE12, CK5/6, vimentin, p53, and Ki-67 (labeling=28%). They were negative for neuron-specific enolase, CD45, CD34, CD56, chromogranin, synaptophysin, melanosome, desmin, epithelial membrane antigen, CK18, CK20, pancytokeratin (CAM5.2). A pathologic diagnosis of myoepithelial carcinoma arising from minor salivary glands was made. No metastatic lesions were found by various imaging techniques. The patient is now receiving palliative radiation therapy 2 months after the operation. The present case showed that MC can express KIT and PDGFRA.     

Multiple cytokeratin-negative malignant tumors composed only of rhabdoid cells in the renal pelvis: a sarcomatoid urothelial carcinoma?

The author presents a unique case of multiple cytokeratin-negative malignant tumors consisting only of rhabdoid cells in the renal pelvis. A 54-year-old man complained of hematuria. A transurethral endoscopic examination revealed multiple papillary tumors, and transurethral resection of the bladder tumors was performed. Pathologically, they were ordinary papillary urothelial transitional cell carcinomas. Imaging modalities revealed multiple tumors of the right renal pelvis, and nephrectomy was performed. Grossly, three polypoid tumors measuring 2-4 cm were present in the pelvis. Histologically, they were composed only of malignant cells with rhabdoid features. There were no elements of transitional cell carcinoma. Immunohistochemically, the pelvic tumors were positive for vimentin and Ki-67 antigen (labeling=40%). They were negative for pancytokeratins (AE1/3, CAM5.2, KL-1 and polyclonal wide), 34βE12, cytokeratin (CK) 5/6, CK7, CK8, CK14, CK18, CK19, CK20, melanosome, EMA, CEA, desmin, S100 protein, α-smooth muscle actin, myoglobin, myogenin, CD34, p53 protein, p63, CD3, CD20, CD30, CD45, CD45RO, chromograin, synaptophysin, CD56, CD68, and KIT. NSE and PDGFRA were focally present, but this appeared nonspecific. Namely, the pelvic tumors expressed only vimentin. The author speculates that the pelvic multiple malignant “rhabdoid” tumors are not sarcomas but urothelial “rhabdoid” carcinoma with complete loss of CKs.     

Malignant melanoma with a rhabdoid phenotype: histologic, immunohistochemical, and ultrastructural study of a case and review of the literature

Malignant melanoma is known to display tremendous histologic diversity. One rare variant is the rhabdoid phenotype, so called because of the appearance of cells resembling rhabdomyoblasts seen in malignant rhabdoid tumors of the kidney. We present the histologic, immunohistochemical, and ultrastructural features of a malignant melanoma composed entirely of rhabdoid cells. A 62-year-old man presented with a 6.5-cm lung mass. Although presumed to be a metastatic lesion, extensive workup failed to reveal a primary tumor site. Histologic sections showed a mass composed entirely of polygonal neoplastic cells with prominent nucleoli and large hyaline cytoplasmic inclusions. The tumor cells were strongly immunoreactive with S100 protein, vimentin, and CD56, and were focally reactive with Mart-1. Tumor cells were negative for Melan-A, tyrosinase, HMB-45, AE1/AE3, cytokeratin (CK) 7, CK8/ 18, CK20, CK903, CAM 5.2, epithelial membrane antigen, smooth muscle actin, desmin, leukocyte common antigen, Bcl-2, CD3, CD20, CD30, CD138, kappa and lambda light chains, CD68, CD34, factor VIII, synaptophysin, and glial fibrillary acidic protein. Electron microscopy showed cytoplasmic whorls of intermediate filaments containing entrapped rough endoplasmic reticulum, mitochondria, and lipid. Recognition of this rare variant of malignant melanoma is important in the evaluation of tumors with rhabdoid morphology.     

Polyvinylpyrrolidone storage disease presenting as pathologic fracture and anemia: report of a case with imprint cytology

Polyvinylpyrrolidone (PVP) storage disease can be caused by local injection and systemic parenteral administration of PVP-containing solutions. PVP has been used as plasma expander, a retardant in certain medicines, components of food additive, and hair care products. High-molecular-weight PVP polymers are prevented from renal excretion and are retained in the reticuloendothelial system. The clinical manifestations include skin lesions and hematologic and orthopedic complications because of bone marrow failure and bony destruction with infiltration of PVP storage histiocytes. Herein, we report a 65-year-old female patient with PVP storage disease presenting as femoral fracture and anemia. In our case, some gelatinous material was noted atthe fracture site, and the initial clinical impression was bony tumor or metastatic lesion. Imprint cytology showed some atypical cells exhibiting foamy cytoplasm and vacuoles. The biopsy specimen revealed that some blue-grayish, vacuolated cells infiltrate in the bone marrow spaces and regional soft tissue near fracture site. The unusual morphology caused a diagnostic dilemma, with the differential diagnosis, including metastatic carcinoma, chordoma, liposarcoma, and hereditary storage disease. The vacuolated cells were positive for CD68, mucicarmine, and Congo red stains, but negative for CK (AE1/AE3) and S-100 protein. Combing the patient's history with long-term intravenous supplement of PVP-containing blood solutions, PVP storage disease involving the bone and regional soft tissue was diagnosed.     

Spindle cell carcinoma progressed from transitional cell carcinoma of the urinary bladder

The author reports a very rare case of spindle cell carcinoma (SpCC) of the urinary bladder progressed from ordinary papillary transitional cell carcinoma (TCC). A 63-year-old man complained of hematuria. A transurethral endoscopic examination revealed a papillary tumor, and transuthetral resection of bladder tumor (TUR-BT) was performed and was diagnosed as ordinary papillary urothelial TCC. Since then, he was treated with TUR-BT eight times. Chemotherapy, radiation, radical cystectomy and lymph nodes dissection were performed 16 years after the first TUR-BT. However, he developed rectal mucosal metastasis. He is now alive 17 years after the first presentation. All the TUR-BT specimens were ordinary papillary TCCs without invasion (pTa). Immunohistochemically, the TUR-BT specimens were positive for pancytokeratin, high molecular weight cytokeratin (CK), CK 5/6, CK 7, CK 18, CK 19, CK 20, p53, p63, Ki-67 (10%), and negative for other antigens examined including vimentin. The cystectomy bladder specimens show broad ulcers and polypoid lesions, and malignant spindle cells (SpCC) invading into muscular layer were present. No TCC elements were recognized. The tumor cells were positive strongly for vimentin, and less strongly for pancytokeratin, high molecular weight cytokeratin, CK 5/6, CK 14, CK 18, p53, p63 and Ki-67 (95%), and negative for other antigens examined. The rectal metastatic lesion showed SpCC without TCC elements, and were strongly positive for vimentin, and weakly positive for pancytokeratin, S100 protein, p53, p63, Ki-67 (90%), neuron-specific enolase, CD56, KIT and PDGFRA. It was negative for other antigen examined. It is strongly suggested that the present SpCC were progressed from ordinary TCC.     

Primary small cell carcinoma of the maxillary sinus: a case report with immunohistochemical and molecular genetic study involving KIT and PDGFRA

Primary small cell carcinoma of the nose and paranasal sinuses is very rare; only a few reports are present in the English literature. The author herein reports a very rare case of primary small cell carcinoma of the maxillary sinus with an emphasis on immunohistochemistry and on KIT and PDGFRA. A 64-year-old man was admitted to our hospital because of left nasal obstruction. Endoscopy revealed three nasal polyps, and imaging modalities revealed an infiltrative tumor (45 x 45 mm) in the left maxillary sinus with invasion into nasal cavity. Multiple biopsies are taken from the nasal lesions. Histologically, the tumor consists of proliferation of malignant small epithelioid cells with hyperchromatic nuclei, fine chromatin, scant cytoplasm, molded nuclei, and absent nucleoli. Immunohistochemically, the malignant cells were positive for cytokeratin (CK) 18, synaptophysin, CD56, p53, Ki-67 (labeling=95%), bcl-2, KIT, and PDGFRA. However, they were negative for pancytokeratins, high molecular weight CK, CK5/6, CK7, CK 14, CK 19, CK20, vimentin, neuron-specific enolase, chromogranin, CD15, CD45, S100 protein, CEA, CA19-9, glial fibrillary acidic protein, neurofilaments, neuroblastoma, CD99, surfactant apoprotein A, melanosome, and TTF-1. The pathologic diagnosis was small cell carcinoma. A molecular genetic analysis using PCR-direct sequencing was performed using paraffin sections, and it showed no mutations of KIT (exons 9, 11, 13, and 17) and PDGFRA (exons 12 and 18) genes. Imaging modalities including CT, MRI and PET did not reveal any tumors, including the lung, other than the maxillary sinus tumor. The present case is the first of small cell carcinoma of the maxillary sinus with a comprehensive immunohistochemical examination and a gene analysis of KIT and PDGFRA.     

Malignant myoepithelioma of the breast

Malignant myoepithelioma of the breast is rare. A 50-year-old Japanese woman was admitted to our hospital because of a right breast tumor (11 × 10 × 5.5 cm). Core needle biopsy revealed malignant spindle cells. A mastectomy was performed. The tumor consisted of malignant spindle, round, pleomorphic and giant cells with many mitotic figures and necrotic areas. Tumor and osteoclast-like giant cells were scattered. Much lymphovascular permeation was seen. In a few areas, particularly on the tumor periphery, there were merges between the tumor cells and myoepithelial cells of the non-tumorous ducts, as if the tumor emanated from the duct myoepithelium. The tumor was invasive into the skin and pectoral muscle. Immunohistochemically, the tumor cells were diffusely positive for vimentin, CD10, α-smooth muscle antigen, and Ki-67 (labeling = 95%). The significant areas of the tumor were positive for S100 protein, p63, p53, CD68, caldesmon, desmin and TGFβ1. A few areas were positive for pancytokeratin (AE1/3), cytokeratin (CK) 5/6, and CK 34βE12. In contrast, the tumor cells were negative for pancytokeratins (WSS, CAM5.2), CK7, CK8, CK14, CK18, CK19, CK20, EMA, CEA, bcl-2, myoglobin, CD34, CD56, CD45, HMB45, GFAP, α-1-antitrypsin, synaptophysin, estrogen receptor, progesterone receptor, HER2/neu, MUC1, MUC2, MUC5AC and MUC6. The author diagnosed the tumor as malignant myoepithelioma, as myoepithelial markers (C10, p63, S100 protein, α-smooth muscle actin, caldesmon) were positive, and also because there was a transition between the tumor cells and myoepithelium of non-tumorous ducts. The grade of the tumor was high. The patient was treated with chemoradiation and was free of disease 5 months after the operation.     

Protein kinase 2 (CK2) controls CD4+ T cell effector function in the pathogenesis of colitis

Crohn's disease (CD), one of the major forms of inflammatory bowel disease (IBD), is characterized by chronic inflammation of the gastrointestinal tract and associated with aberrant CD4⁺ T-helper type 1 (Th1) and Th17 responses. Protein kinase 2 (CK2) is a conserved serine–threonine kinase involved in signal transduction pathways, which regulate immune responses. CK2 promotes Th17 cell differentiation and suppresses the generation of Foxp3⁺ regulatory T cells. The function of CK2 in CD4⁺ T cells during the pathogenesis of CD is unknown. We utilized the T cell-induced colitis model, transferring CD45RB^hi-naive CD4⁺ T cells from CK2α^fl/fl controls and CK2α^fl/fldLck-Cre mice into Rag1^−/− mice. CD4⁺ T cells from CK2α^fl/fldLck-Cre mice failed to induce wasting disease and significant intestinal inflammation, which was associated with decreased interleukin-17A-positive (IL-17A⁺), interferon-γ-positive (IFN-γ⁺), and double-positive IL-17A⁺IFN-γ⁺ CD4⁺ T cells in the spleen and colon. We determined that CK2α regulates CD4⁺ T cell proliferation through a cell-intrinsic manner. CK2α is also important in controlling CD4⁺ T cell responses by regulating NFAT2, which is vital for T cell activation and proliferation. Our findings indicate that CK2α contributes to the pathogenesis of colitis by promoting CD4⁺ T cell proliferation and Th1 and Th17 responses, and that targeting CK2 may be a novel therapeutic treatment for patients with CD.     

Small cell carcinoma of the oral cavity (cheek mucosa): a case report with an immunohistochemical and molecular genetic analysis

Small cell carcinoma (SCC) of the oral cavity is extremely rare; only one case has been reported in the English Literature. The author herein reports the second case of SCC of the oral cavity. A 59-year-old man presented with oral tumor (5 cm) in the right cheek mucosa. A biopsy was taken. The HE histology was typical SCC consisting of small epithelial cells with hyperchromatic nuclei, molded nuclei, scant nucleocytoplasmic ratio, and negative nucleoli. Immunohistochemically, the tumor cells are positive for pancytokeratin (PCK) WSS, PCK MNF-116, cytokeratin (CK) 34BE12, CK5/6, CK14, vimentin, KIT (CD117), CD56, synaptophysin, p53 protein, and Ki67 antigen (Ki-67 labeling = 70%). The tumor cells are negative for PCK AE1/3, PSK CAM5.2, CK7, CK8, CK18, CK19, CK20, EMA, NSE, chromogranin, platelet-derived growth factor-α (PDGFRA), CD45, CD45RO, CD3, CD20, CD30, CD79a, and bcl-2. A retrospective genetic analysis using PCR-direct sequencing method in paraffin sections identified no mutations of KIT (exons 9, 11, 13 and 17) and PDGFRA (exons 12 and 18) genes. Various imaging modalities including CT and MRI and upper and lower gastrointestinal endoscopy did not identified no tumors other than the oral tumor. Thus, the oral tumor was thought primary. The oral tumor rapidly enlarged, and distant metastases to cervical lymph nodes, ribs and iliac bones emerged. The patient is now treated by cisplatin-based chemotherapy 16 months after the first manifestation.     

Monstrous epithelial cell clusters in the seminal vesicle

A 60-year-old man presented with dysuria and elevated PSA (6.95 ng/ml). Needle biopsies of the prostate revealed well differentiated adenocarcinoma of Gleason's score 6. Prostatectomy and bilateral seminal vesiculotomy were performed. The material was totally cut into 16 preparations. The prostate showed well differentiated adenocarcinoma. The left seminal vesicle showed intraluminal monstrous large epithelial cells with acidophilic cytoplasm and hyperchromatic nuclei, simulating carcinoma cells. Lipochrome pigment was present in the monstrous cells, and some monstrous cells showed large bizarre nuclei. Such monstrous cells were also present in the mucosal seminal vesicle epithelium, and gradual merge between the intraluminal and mucosal monstorous epithelium. Immunohistochemically, the monstrous epithelial cells showed the following reactions: pancytokeratin (AE1/3, CAM5.2) +, cytokeratin (CK) 5/6 +, CK34βE12 -, CK7 +, CK8 -, CK14 -, CK18 +, CK19+, CK20 -, Ki-67 0%, p53 -, P63 -, NSE -, CEA -, EMA -, CA19-9 -, ER -, PgR -, HER2 -, HepPar1 -, CD34 -, CD10 +, PSA -, AMACR -, Desmin -, ASMA -, CD68 -, S100 -, CD45 -, synaptopysin -, TTF-1 -, CDX-2 -, MUC1 -, MUC2 -, MUC5AC - MUC6 +, CD56 -, PAS -, dPAS -, and alcian blue +. The immunoprofile of normal seminal vesicle epithelium was as follows: pancytokeratin (AE1/3, CAM5.2) +++, cy-tokeratin (CK) 5/6 +++, CK34βE12 -, CK7 +++, CK8 +, CK14 -, CK18 +++, CK19, +++, CK20 -, KI-67 1%, p53 -, P63 +++, NSE -, CEA - EMA -, CA19-9 -, ER -, PgR -, HER2 +, HepPar1 -, CD34 -, CD10 +, PSA -, AMACR -, Desmin -, ASMA -, CD68 -, S100 - , CD45 -, synaptopysin -, TTF-1 -, CDX-2 -, MUC1 -, MUC2 -, MUC5AC -, MUC6 +++, CD56 -, PAS -, dPAS -, and alcian blue +. That is, the immunophenotype was very similar but much weaker in monstrous cells than in normal seminal vesicle epithelium. These findings suggest that the monstrous seminal vesicle epithelial cells are degenerative changes. The monstrous epithelial cells should not be mistaken for carcinoma.