Adenoid squamous cell carcinoma of the oral cavity

Because immunohistochemical features of adenoid squamous cell carcinoma (AdSCC) of the oral cavity is unclear, the author reports herein AdSCC in the gingival with an emphasis on immunohistochemical features. A 73-year-old woman presented with a left lower gingival tumor. The tumor was mildly elevated tumor measuring 1.5 x 1.5 x 0.5 cm. Dentist's diagnosis was granulation tissue, and a biopsy was taken. The biopsy showed proliferation of carcinoma cells arranged in cords, and squamous and tubular differentiations were noted in places. The biopsy diagnosis was adenosquamous carcinoma. Tumor excision with resection of mandibular bone was performed. The resected tissue showed a mixture and squamous cell carcinoma and tubular formation. Gradual merges between the two and acantholytic features of the squamous cell carcinoma element were seen. Both components were free from mucins. Both components were positive for pancytokeratins (AE1/3, CAM5.2) +++, cytokeratin (CK) 5/6 +, CK34βE12 ++, CK7 +, CK14 +++, CEA +, CA19-9 +, CA125 +, p53 +++, p63 +++, KIT + and MUC1 ++. Both components were negative for CK8, CK18, CK19, CK20, EMA, vimentin, TTF-1, desmin, myoglobin, S100 protein, melanosome, smooth muscle actin, CD34, CDX2, CD10, chromogranin, synaptophysin, NSE, CD56, lysozyme, CD68, MDM2, PDGFRA, MUC2, MUC5AC, and MUC6. Since both components were positive for squmaous cell carcinoma markers (CD5/6, CK34βE12, and p63) and adenocarcinoma markers (CEA, CA19-9, CA125, MUC1), this case of AdSCC appears an intermediate form between adenocarcinoma and squamous cell carcinoma. The margins were negative. No metastasis was found by imaging techniques. The patient is now free from tumor and is followed up carefully.     

An immunohistochemical study of metaplastic spindle cell carcinoma, phyllodes tumor and fibromatosis of the breast

The diagnosis of metaplastic (sarcomatoid) carcinoma (MSC) of breast often requires immunohistochemistry with a cytokeratin (CK) panel to distinguish them from phyllodes tumors (PT), primary sarcomas, and fibromatoses. CK staining may be heterogeneous in metaplastic carcinomas. The aim of the study was to investigate the theory that MSCs show evidence of myoepithelial differentiation and to evaluate immunohistochemical markers that may be helpful in distinguishing MSCs from PT and fibromatosis. We reviewed histology and performed immunohistochemistry for AE1/AE3, 34betaE12, CK5 and CK14, Cam5.2, CK7 and CK19, epithelial membrane antigen (EMA) (B55), smooth muscle actin (SMA), S100, desmin, vimentin, CD31, CD34, and bcl-2 on paraffin-embedded tissue from 18 MSCs, 26 PTs, and 8 fibromatoses. We assessed staining by using a semiquantitative method. Sarcomatous areas in MSCs were positive for 34betaE12 in 11 cases; for SMA in 10; for CK5 in 7; for CK14 in 6; for Cam5.2, AE1/AE3, and S100 in 5; and for CK7 and CK19 in 3. No CK expression was seen in stromal areas in PT or in fibromatoses. CD34 and bcl-2 were more frequently expressed in spindle cell areas in PTs (18 and 12 of 26, respectively) than in MSCs (0 and 2 of 18, respectively). MSCs show strong evidence of myoepithelial differentiation. CD34 and, to a lesser extent, bcl-2 positivity in PTs may be helpful in differentiating these two lesions from MSCs, particularly in small biopsies, because CK staining in MSCs may be heterogeneous. In our hands, 34betaE12 was the CK most frequently expressed in sarcomatoid areas in MSCs.     

Neuroendocrine breast carcinoma metastatic to renal cell carcinoma and ipsilateral adrenal gland

We report on a 60-year-old woman with neuroendocrine carcinoma of the left breast metastasizing to renal cell carcinoma (RCC) of the left kidney and to adrenal gland. A yellow, well-circumscribed tumor, 11 cm in largest diameter and limited to the kidney, was found. Histopathology revealed RCC with foci of neuroendocrine differentiation. Solid sheets of hyperchromatic epithelioid cells with high mitotic activity were found between typical clear cells of RCC. These cells were CAM5,2 and E-cadherin focally positive, synaptophysin and NSE weakly positive, CK19 moderately positive, and AE1-AE3 and EMA strongly positive. Chromogranin A, CD10, CK 14, CK 20, HER2 (score 1+), vimentin, and HMB45 were negative. The left adrenal gland contained multiple, separate foci of a tumor composed of neuroendocrine components. Because of the biphasic tumor in the kidney, extensive clinical examination and further analyses were recommended. Tumor in the left breast was revealed. Two months later, the patient underwent mastectomy with axillary lymph node dissection. The tumor was histologically and immunohistochemically similar to the neuroendocrine component within RCC. All axillary nodes were positive. To our knowledge, this is the first case of neuroendocrine breast carcinoma with metastasis to renal cell carcinoma and ipsilateral adrenal gland.     

Histopathological and immunohistochemical study of laterocervical lymph node metastases of unknown primary origin

In this study, we examined histopathologically and immunohistochemically 24 cases of laterocervical lymph node metastases with unknown primary origin. For immunohistochemical study, we used a large panel of antibodies represented by CK7, CK19, CK20, CKAE1/AE3, CK34betaE12, TTF1, HBME-1, CEA, MUC5AC and EBV. In the cases studied tumors accompanied by seemingly primitive adenopathies were located in the thyroid, lung, esophagus, stomach, rhinopharynx, hypopharynx, oropharynx and larynx.     

伴有神经内分泌分化的乳腺梭形细胞癌

目的探讨乳腺伴有神经内分泌分化的梭形细胞癌的病理形态学和免疫表型特点及鉴别诊断。方法复习2500例乳腺癌切片,找出以梭形细胞占主要优势（〉80％）的癌5例,其中2例梭形细胞型导管内癌和3例梭形细胞型浸润癌。采用HE、阿辛蓝（AB）／PAS和网织染色,以及用癌胚抗原（CEA）、上皮膜抗原（EMA）、细胞角蛋白（CK7、3413E12、AE1／AE3）、神经元特异性烯醇化酶（NSE）、突触素、嗜铬蛋白（cg）A、Lue-7、波形蛋白,S-100、平滑肌肌动蛋白（SMA）、calponin、雌激素受体（ER）、孕激素受体（PR）、c—erbB-2、E-钙黏素、Ki-67、p53抗体进行免疫组织化学观察。其中4例有随访信息。结果患者平均年龄在68岁。镜下：5例癌细胞形态主要为长梭形的上皮样细胞,3例有少数胞质内空泡状细胞,4例可见散在AB阳性细胞。免疫组织化学5例均表达AE1／AE3、EMA、CEA、E-钙黏素和突触素,CK7有4例表达,NSE阳性3例,CgA和Lue7阳性2例,ER阳性4例,PR阳性2例,1例表达c-erbB-2,1例有灶状波形蛋白阳性。免疫组织化学结果显示2例梭形细胞型导管内癌和1例梭形细胞型浸润性癌是梭形细胞型的神经内分泌癌,另外2例梭形细胞型浸润性癌是伴有神经内分泌分化的化生性癌。随访3例存活（24～58个月）,1例27个月内死亡。结论上皮样梭形细胞和细胞内黏液的出现是乳腺伴有神经内分泌分化癌的一个形态学特点。梭形细胞神经内分泌型导管内癌需要和普通导管增生及导管内乳头状瘤鉴别。梭形细胞型的神经内分泌癌和伴神经内分泌分化的梭形细胞浸润性癌需要与梭形细胞肌上皮肿瘤、恶性黑色素瘤及某些软组织肿瘤鉴别。     

Esophageal pleomorphic giant cell carcinoma combined with small cell carcinoma

Herein is presented the case of an esophageal pleomorphic giant cell carcinoma combined with small cell carcinoma (SCC). The patient, a 77-year-old man, initially presented with dysphagia and hoarseness, and endoscopy indicated a large esophageal tumor. Despite chemoradiation therapy, the patient died from widespread local extension of the tumor and distant metastases approximately 8 months after onset of the symptoms. Histologically, the primary tumor was composed of pleomorphic tumor components, SCC components, and a tiny focus of squamous cell carcinoma. The pleomorphic tumor cells, consisting of solid sheets of poorly cohesive epithelioid cells and numerous multinucleated giant cells with abundant eosinophilic cytoplasm, were immunohistochemically positive for vimentin and desmin, with scattered positivity for epithelial membrane antigen (EMA) and neuron-specific enolase (NSE), but negative for myoglobin. These findings were histopathologically compatible with pleomorphic giant cell carcinoma occurring at other sites such as the lung. SCC cells, morphologically similar to their pulmonary counterpart, were positive for EMA and some neuroendocrine markers such as chromogranin A and NSE, and occasionally positive for vimentin and desmin. Esophageal pleomorphic giant cell carcinoma can occur in close association with SCC, and should be included in the differential diagnosis of esophageal tumors showing pleomorphism.     

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.     

Squamous cell carcinoma originated from an epidermal cyst

Epidermal cyst (EC) of the skin is a very common condition. Squamous cell carcinoma (SCC) very infrequently arises from EC. A 76-year-old Japanese woman was admitted to our hospital because of multiple papules in the nose and nasal cavity. The clinical diagnosis was sebaceous hyperplasia. An excisional biopsy was obtained from one papule. Histologically, the papule showed an EC. The EC communicated with the epidermis. Islands of atypical cells with hyperchromatic nuclei and infrequent pearl formation were recognized around and adjacent to EC. No connections were seen between the atypical cell islands and epidermis. The atypical cells had hyperchromatic nuclei and nucleoli. Mitotic figures and keratinous pearls were scattered. The HE diagnosis was probable SCC probably arising from EC. Immunohistochemically, the atypical cells were positive for pancytokeratin AE1/3, cytokeratin (CK) 5/6, CK14, CK18, CK 34BE14, EMA, p53, Ki-67 (labeling 90%), and p63. They were negative for pancytokeratin CAM5.2, CK7, CK8, CK19, CK20, vimentin, S100 protein, HMB45, synaptophysin, and CD56. CD68 was positive in histiocytes and giant cells in the foreign body reaction. The EC showed the same immunoprofile as the SCC, except for negative p53 and low Ki-67 labeling in the EC. The histological and immunohistochemical diagnosis was definite SCC arising from EC.     

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.     

Immunohistochemical marker panels for distinguishing between epithelioid mesothelioma and lung adenocarcinoma

The distinction between epithelioid mesothelioma and lung adenocarcinoma remains an important diagnostic challenge for surgical pathologists. The aim of the present study was to select a limited and appropriate panel of antibodies that can differentiate between epithelioid mesothelioma and lung adenocarcinoma. Specimens of 90 epithelioid mesotheliomas and 51 lung adenocarcinomas obtained from Japanese cases were examined using calretinin, WT1, AE1/AE3, CAM5.2, cytokeratin (CK) 5/6, vimentin, epithelial membrane antigen (EMA), thrombomodulin, CEA, CA19-9, and CA125. Ninety-six percent of epithelioid mesotheliomas were positive for calretinin; 99% for WT1; 100% for AE1/AE; 97% for CAM5.2; 70% for CK 5/6; 91% for vimentin; 96% for EMA; 71% for thrombomodulin; 77% for mesothelin; 7% for CEA; 17% for CA19-9; and 85% for CA125. In contrast, 33% of lung adenocarcinomas were positive for calretinin; 16% for WT1; 100% for AE1/AE3, CAM5.2, and EMA; 41% for CK 5/6; 47% for vimentin; 20% for thrombomodulin; 69% for mesothelin; 98% for CEA; 73% for CA19-9; and 80% for CA125. For distinguishing between epithelioid mesothelioma and lung adenocarcinoma, the combination of CEA, calretinin and each WT1 or thrombomodulin was suggested to be the best panel of immunohistochemical markers.     

Primary signet-ring cell carcinoma of the lung: a case report with an immunohistochemical study

Primary signet-ring cell adenocarcinoma (SRCA) of the lung is very rare. A 78-year-old man consulted to our hospital because of loss of appetite. Physical examination showed lymphadenopathy of the cervical lymph nodes. Chest X-ray showed a tumor of the right upper lobe. Blood laboratory test showed an increase of LDH and CRP. Tumor markers (CYFRA, SCC, CEA, ProGRP) were within normal range. Clinical diagnosis was suspected malignant lymphoma of the lung. Transbronchial lung biopsies showed SRCA (70%) mixed with poorly differentiated adenocarcinoma (30%). The SRCA cells were positive for mucins. Immunohistochemically, the SRCA cells were positive for cytokeratin (CK) AE1/3, CK CAM5.2, CK7, CK18, EMA, p53, Ki-67 (labeling=60%), CEA, CA19-9, TTF-1, and MUC1. They were negative for CK34BE12, CK5/6, CK8, CK14, CK19, CK20, vimentin, chromogranin, synaptophysin, CD45, CD20, CD3, surfactant Apoprotein-A, CDX-2, MUC2, MUC5AC and MUC6. A pathological diagnosis of SRCA of the lung was made. The patient showed downhill course, and died of carcinomatosis 3 months after the first manifestation. In conclusion, a vary rare case of primary pulmonary SRCA was reported with an immunohistochemical study.     

Immunohistochemical profile of normal mesothelium and histiocytic/methothelial hyperplasia: a case report

Immunohistochemical profiles of normal mesothelium and histiocytic/mesothelial hyperplasia (HMH) are unknown. A 19-year-old man was treated by thoracoscopic resection of bullae of left lung. Histologically, there were cell proliferative foci composed of round cells without significant atypia (histiocyte, mesothelium and T-lymphocytes). The cell proliferative foci were patch-like, and no invasive features were seen. Because it is composed of histiocytes, mesothelium, and T-lymphocytes, the diagnosis was HMH. Immunohistochemically, cell components of HMH showed the following immunoreactions: calrenitin 3+, D2-40 3+, pancytokeratin AE1/3 3+, pancytokeratin CAM5.2 3+, cytokeratin (CK) 34βE12 1+, CK5/6 1+, CK7 1+, CK8 3+, CK 14 1+, CK18 2+, CK19 2+, p53 10%, Ki67 20%, CD68 3+, CD45 2+, CD45 RO 2+, vimentin 3+, Ber-EP4 -, CK20 -, EMA -, desmin -, CEA -, CA19-9 -, TTF-1 -, S100 protein -, αsmooth muscle actin -, CD34 -, CD20 -, chromogranin -, synaptophysin -, NSE -, CDX2 -, CD56 -, HER2 -, MUC1 -, MUC2 -, MUC5AC -, and MUC6 -. The normal mesothelium showed the following immunoprofile: calrenitin 3+, D2-40 3+, pancytokeratin AE1/3 3+, pancytokeratin CAM5.2 3+, CK34βE12 3+, CK5/6 2+, CK7 2+, CK8 3+, CK 14 -, CK18 3+, CK19 2+, vimentin 1+, p53 -, Ki67 1%, CD68 -, CD45 -, CD45 RO -, Ber-EP4 -, CK20 -, EMA -, desmin -, CEA -, CA19-9 -, TTF-1 -, S100 protein -, α-smooth muscle actin -, CD34 -, chromogranin -, synaptophysin -, NSE -, CDX2 -, CD56 -, HER2 -, MUC1 -, MUC2 -, MUC5AC -, and MUC6 -. These findings indicate that the immunoprolfile of mesothelium in HMH was immunohistochemically very similar to that of normal mesothelium except for CD68, p53 protein, Ki-67 labeling, CD45 and CD45 RO. These indicate that the HMH was reactive phenomenon and HMH is composed of hyperplastic mesothelium, histiocytes and T-lymphocytes. The immunoprofile of normal mesothelium provide basic knowledge of mesothelial pathology.     

Ber EP4 and epithelial membrane antigen aid distinction of basal cell, squamous cell and basosquamous carcinomas of the skin

AIMS: Seventy-five skin tumours were studied to investigate the value of immunohistochemistry in differentiating basal cell, squamous cell and basosquamous carcinomas of the skin. METHODS AND RESULTS: Archived paraffin-embedded tissue samples of basal cell carcinomas (n = 39), squamous cell carcinomas (n = 23) and basosquamous carcinomas (n = 13) were stained immunohistochemically using a panel of antibodies. All of the basal cell carcinomas stained positively for Ber EP4, in contrast to the group of squamous cell carcinomas, that showed no staining. Basosquamous carcinomas all showed at least some areas of Ber EP4 positivity. None of the basal cell carcinomas, but most of the squamous cell carcinomas (22 of 23) expressed epithelial membrane antigen (EMA). Only one of the basosquamous carcinomas expressed EMA positivity focally. CAM 5.2, carcinoembryonic antigen (CEA) and 34betaE12 antibodies lacked specificity in relation to the different tumour types. CONCLUSION: Distinction of basal and squamous cell carcinomas of the skin can be readily achieved with routine immunohistochemistry using Ber EP4 and EMA. Identification of basosquamous carcinoma is also facilitated with this method.     

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.     

Comparison of structural genetics of non-schistosoma-associated squamous cell carcinoma of the urinary bladder

Little is known about genetic changes in squamous differentiation of non-schistosomiasis-associated bladder cancer. Therefore, we investigated pure squamous cell carcinomas (SqCC), squamous parts of mixed urothelial carcinomas with squamous differentiation (MIX) and mere urothelial cancers (UC) for structural genetic differences. Tissue microarray slides (n = 29 SqCC, n = 35 MIX and n = 23 UC) were analyzed by ZytoLight SPEC p16/CEN3/7/17 Quadruple Color Probe fluorescence-in-situ-hybridization (FISH) and DNA was investigated by comparative genomic hybridization (CGH) (n = 35 SqCCs, n = 40 MIX and n = 36 UC). By FISH the mean number of polysomic cells was lowest in SqCC (CEN3 P = 0.0498, CEN17 P = 0.0009). A slight tendency of lower copy numbers of chromosomes 3, 7 and 17 and higher numbers of the p16-locus in SqCC (P = 0.45) indicated less aneuploid tumor cells in SqCC compared to MIX and UC. In CGH SqCC showed the lowest mean number of aberrations per tumor (SqCC 5.37 changes, MIX 6.75 and UC 7.64; P = 0.1754). Significant differences between the three groups were found for loss of chromosome 3p (P = 0.004), 6q (P = 0.028), 11p (P = 0.024) and gains of 5p (P = 0.020). Loss of 3p was more frequent in SqCC (51.4%) than in MIX (37.5%) or UC (13.9%). To conclude, SqCCs show less polysomy and genetic alterations than MIX and UC. Loss of 3p is more frequent in SqCC but there are no absolute specific alterations for each tumor group. Squamous parts of mixed tumors show similar alterations than UC and should be considered as further development of UC, while pure SqCC seem to be a separate tumor group.     

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.     

Small oncocytic papillary renal cell carcinoma in diabetic glomerulosclerosis

Histologic and immunohistochemical features of oncocytic papillary renal cell carcinoma (RCC) have not been fully elucidated. The author herein report a case of oncocytic papillary RCC (OPRCC). A 71-year-old man with diabetes mellitus and diabetic nephropathy was found to have a small right renal tumor by CT. He had been treated with hemodialysis for chronic renal failure for 10 years. A nephrectomy was performed. Grossly, a small (1.5cm) encapsulated yellow tumor was found in the kidney. Histologically, the tumor was completely encapsulated, and consisted entirely of atypical oncocytes arranged in a diffuse papillary structure with fibrovascular cores. The oncocytes showed grade 3 atypia and pseudostratification. A few mitotic figures were seen, and psammoma bodies, foamy macrophages, and hemosiderin were scattered. Histochemically, the tumor cells were positive for colloidal iron, and negative for mucins (Alcian blue/PAS). Immunohistochemical results of the tumor were as follows: α-methylacyl-coenzyme A rasemase (AMACR) +++, vimentin +++, cytokeratin (CK) 18 +++, CD10 +++, S-100 protein +, MUC1 ++, MUC2 ++, MUC5AC ++, MUC6 ++, panCK Cam5.2 +, CK7 +, CK8 +, CK14 +, CK19 +, CK20 +, p53 +, HepPar1 +, CD68 +, platelet-derived growth factor-α (PDGFRA) +, PanCK AE1/3 -, PanCK WSS -, PanCK MNF115 -, CK 35BE12 -, CK5/6 -, EMA -, desmin -, smooth muscle antigen -, α-fetoprotein -, CEA -, estrogen receptor -, progesterone receptor -, HER2 -, p63 -, and KIT -. Ki67 labeling was 6%. These results suggest that OPRCC can express colloidal iron, low molecular weight CKs, S100 protein, MUC1, MUC2, MUC5AC, MUC6, p53, PDGFRA, and HepPar1.     

Utility of high molecular weight cytokeratins, but not p63, in the differential diagnosis of neuroendocrine and basaloid carcinomas of the head and neck

High-grade neuroendocrine carcinomas of the head and neck overlap significantly in morphology with both basaloid squamous and solid-type adenoid cystic carcinomas. High-grade neuroendocrine carcinomas have sheets of small cells with scant cytoplasm, granular chromatin, and inconspicuous nucleoli. Basaloid squamous and adenoid cystic carcinomas are aggressive variants of their respective tumor types which both have nests of basaloid tumor cells with round nuclei, little cytoplasm, and inconspicuous nucleoli. As the management and prognosis of these tumors are very different, it is important to differentiate them. We performed high molecular weight cytokeratin (CK) and p63 immunohistochemistry on 19 neuroendocrine carcinomas, 18 basaloid squamous carcinomas, and 11 solid-type adenoid cystic carcinomas. All tumors were immunostained for p63, CK 34betaE12, CK 5/6, synaptophysin, chromogranin-A, S-100, and smooth muscle actin. All basaloid squamous and adenoid cystic carcinomas were positive for CK 5/6 and 34betaE12. Only 4 and 5 of the 19 neuroendocrine carcinomas, respectively, were positive for these markers. Staining was focal in the neuroendocrine cases when positive, whereas almost all basaloid squamous and adenoid cystic carcinomas showed strong staining. Almost all tumors of each type were positive for p63, including neuroendocrine carcinomas, but with different staining patterns. Basaloid squamous carcinomas were diffusely positive, neuroendocrine carcinomas were diffusely positive, but with weak staining, and adenoid cystic carcinomas showed a distinct pattern with staining at the periphery of the cell nests only. We conclude that high molecular weight cytokeratin immunostaining is helpful in distinguishing high-grade neuroendocrine carcinomas from similar tumor types.     

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.     

Pigmented adenoid cystic carcinoma of the ear skin arising from the epidermis: a case report with immunohistochemical studies

Adenoid cystic carcinoma (ACC) in the skin is very rare; only about 60 cases have been reported. Herein presented is a case of pigmented ACC arising from epidermis of the ear skin. An 85-year-old man presented black tumor of the right ear. Dermatologists' diagnosis was basal cell carcinoma (BCC). Large biopsy was obtained. The biopsy showed proliferation of atypical basaloid cells arranged in a cribriform pattern. The tumor cells were continuous with epidermis, as if it arose from the epidermis. Focal areas show melanin deposition in the tumor cells. Mucin stains showed that the tumor cells and tubular lumens contained acidic mucin. Immunohistochemically, the tumor cells were positive for cytokeratin (CK) AE1/3, CK34BE12, CK5/6, CK7, CK14, p63, alpha-smooth muscle actin (ASMA), S100 protein, p53, Ki-67 (labeling 85%), KIT, PDGFRA and CD56. The tumor cells were negative for CK CAM5.2, CK8, CK18, CK19, CK20, EMA, desmin, CEA, HMB45, CD10, CD34, neuron-specific enolase, chromogranin, synaptophysin, CDX2, MUC1, MUC2, MUC5AC and MUC6. HMB-positive and S100-positive melanocytes were seen in a very few areas. Since characteristic cribriform pattern was recognized in the tumor and the tumor showed epithelial markers, myoepithelial markers (CD14, p63, ASMA, S100 protein) and KIT, the pathological diagnosis of ACC was made. No distant and lymph node metastasis is now seen. The patient will be treated by complete resection. The present cutaneous ACC was unique in that the ACC arose from the epidermis, had melanin pigment, and occurred in ear skin.