Both the tool and the carpenter are important

A 67-year-old woman with a history of a skin melanoma that was excised 7 years previously had a 6-month history of decreased vision in her right eye. A choroidal melanoma was diagnosed clinically, and the eye was enucleated. The results of a histopathological examination revealed a primary uveal melanoma. Slides of the skin melanoma were obtained, and the initial diagnosis was confirmed. In an attempt to illustrate a biological difference between the 2 melanomas, immunohistochemical studies were performed on sections of the 2 specimens using S-100 protein, HMB-45, and S-100-beta. Primary cutaneous and choroidal melanomas appearing in a patient with no predisposition are rare; this is believed to be only the fifth such case reported in the literature.     

Retinal thickness variation in the diabetic patient measured by the retinal thickness analyser

BACKGROUND: Acral melanomas are uncommon. Due to the thick overlying stratum corneum, accurate estimation of margins is difficult for minimally pigmented or amelanotic melanomas on the palm or sole. OBJECTIVE: To describe the use of Mohs micrographic surgery using frozen sections and HMB-45 immunostaining in the treatment of a multiply recurrent acral melanoma that had failed both standard surgery and Mohs surgery. METHODS: The melanoma was excised by Mohs technique, and the margins were checked by frozen section and HMB-45 immunostaining. RESULTS: The melanoma was completely excised in 11 stages, resulting in a defect that covered much of the plantar surfaces of the ball of the left foot, great, second, third, fourth, and fifth toes. No recurrence has been noted in 22 months of follow-up. CONCLUSIONS: HMB-45 immunostaining is a very valuable adjunct to examination of surgical margins for melanoma, particularly when combined with such histologic features as clustering of cells, melanocyte position within the epidermis, and cytologic atypia.     

Comparative immunoreactivity of CD-68 and HMB-45 in malignant melanoma, neural tumors and nevi

The monoclonal antibody CD 68 (KP 1) reacts with fibrohistiocytic and some epithelial neoplasms; its reactivity compared with that of HMB 45 in malignant melanoma (MM) and neural tumors needs further elucidation. Using a streptavidin-biotin-immunoperoxidase procedure, we examined the reactivity of 65 MM (46 conventional, 1 polypoid, 6 desmoplastic [DMM], and 12 metastatic), 21 neurofibromas, 1 neurofibrosarcoma, 10 schwannomas, 1 perineurioma, 2 neurothekeomas, and 14 blue and 26 other nevi for CD-68, HMB-45-defined antigen, S 100 and neurofilament protein. A positive staining for CD 68 was observed in 38 of 42 primary, 5 of 6 DMM, and 11 of 12 metastatic melanomas; 6 of 10 schwannomas; 5 of 10 nevi with junctional component and all 14 blue nevi. All 21 neurofibromas, 1 each neurofibrosarcoma and perineurioma, both neurothekeomas, and all 12 nevi with dermal component were CD 68-negative. HBM 45 was expressed by all 44 primary, none of 6 DMM, and 7 of 12 metastatic melanomas; by none of 10 schwannomas, 6 neurofibromas, 1 neurofibrosarcoma, 1 perineurioma and 2 neurothekeomas. Both junctional nevi, 8 of 10 nevi with junctional components, 1 of 10 dermal components of junctional nevi, and 11 of 13 blue nevi were also HMB 45 positive. Except for 1 perineurioma, S 100 decorated all tumors examined. NF was immunoreactive in 1 of 45 conventional melanomas, 2 of 21 neurofibromas, 2 of 10 schwannomas, and 3 of 10 blue nevi; it was non-reactive in all polypoid, desmoplastic and metastatic melanomas; neurofibrosarcoma, perineurioma, neurothekeoma and other nevi. We conclude that the CD-68-reactivity in primary melanomas, neurofibromas, neurofibrosarcomas, perineuriomas, and nevi was similar to that of HMB 45. The significantly higher CD 68-positivity than of HMB 45 in metastatic and desmoplastic melanomas and schwannomas may be of diagnostic value.     

Do patients with "pure" chronic fatigue syndrome (neurasthenia) have abnormal sleep?

We report the clinical and pathologic findings of a metaplastic carcinoma of the breast that exhibited melanocytic differentiation. The tumor possessed both in situ and invasive components. Lower grade regions of the infiltrating carcinoma had features of tubular, mucinous, and matrix-producing carcinomas. In the higher grade areas, conventional poorly differentiated ductal carcinoma merged with an anaplastic neoplasm that looked like malignant melanoma. The nonpigmented cells stained for keratin but lacked HMB-45 and S-100 proteins, whereas the cells containing melanin showed the opposite characteristics. Electron microscopic examination disclosed melanosomes in the neoplastic cells. We believe that these observations convincingly establish both the origin of the tumor from the mammary epithelium and the synthesis of melanin by the tumor cells. We propose the diagnosis of metaplastic carcinoma with melanocytic differentiation for this neoplasm and suggest that the phenomenon of melanocytic metaplasia might underlie the formation of primary melanomas of the breast.     

Malignant melanoma in the CNS, subtyping and immunocytochemistry

Paraffin-embedded specimens from 21 patients (mean age 49 years) with malignant melanocytic tumors of the central nervous system were studied. Extraneuronal primary tumors were situated at the trunk (38%), the lower (14%) or upper extremity (10%), and the head/neck region (5%). In 33% no extraneural primary tumor could be detected. The tumor location was frontal (19%), occipital (19%), parietal, spinal, multifocally (14%, respectively), or temporal (5%). Four subtypes were distinguished according to the predominant histological cell type: pleomorphic, epithelioid, spindle- and mixed-cell tumors. 29% contained no melanin, most of them belonging to the epithelioid subtype. The morphology and immunohistochemical reactivity for different antibodies (KL-1, EMA, VIM, HMB-45, NKI-C3, S-100, and MIB-1/Ki-67) were assessed. Positive staining was demonstrated for HMB-45 (in 86% of cases), NKI-C3 (100%), S-100 (95%), vimentin (75%), and KL-1 (33%). No expression of the cytokeratin EMA could be detected. The mean proliferation index measured by MIB-1 immunoreactivity was 21%. The 4 histological subtypes were found to express different antigen patterns. In the analysis of CNS tumors of unknown origin, the panel of antibodies used for diagnosis should include HMB-45 as the most specific marker for malignant melanoma.     

Fine needle aspiration biopsy of metastatic malignant melanoma with "rhabdoid" features. Frequency, cytologic features, pitfalls and ancillary studies

OBJECTIVE: To characterize the cytopathology of metastatic malignant melanoma (MM) with "rhabdoid" features, a recently described, rare morphologic variant of MM that can be incorrectly diagnosed in fine needle aspiration (FNA) biopsy. STUDY DESIGN: A retrospective review of all FNA biopsy material with the diagnosis of metastatic MM was performed at two institutions. Only cases with a predominant composition of cells that met criteria defined as "rhabdoid" morphology were selected for study. The cytomorphologic features, immunocytochemistry and clinical features of these cases were reviewed. RESULTS: Of 88 FNA cases previously diagnosed as metastatic MM, 4 (4.6%) had a predominance of cells with rhabdoid features. These cases consisted of scattered atypical cells having enlarged, eccentrically placed nuclei; prominent nucleoli; and a moderate amount of cytoplasm possessing round, globular inclusions in Papanicolaou- and Diff-Quik-stained smears. Immunochemistry showed strong S-100, HMB-45 and vimentin staining in two of four cases. CONCLUSIONS: Metastatic MM may present in FNA biopsy as a poorly differentiated malignancy with rhabdoid features, potentially leading to an incorrect cytologic diagnosis. MM must be considered when evaluating neoplasms with a rhabdoid phenotype. Correlation of the cytologic finding with the clinical history and immunohistochemical studies can help in diagnosing this morphologic variant.     

Distinct subsets of CD1d-restricted T cells recognize self-antigens loaded in different cellular compartments

OBJECTIVE: To examine the immunohistochemical and ultrastructural features of the rare pleomorphic adenocarcinomas of the ciliary epithelium (CE). DESIGN: Retrospective case series. PARTICIPANTS: The study materials included 12 cases of adenocarcinoma of the ciliary epithelium: 9 cases of CE hyperplasia and 3 cases of CE adenomas. INTERVENTION: Histologic sections were stained with hematoxylin-eosin, alcian blue, periodic acid-Schiff, and occasionally with Masson trichrome. Additionally, the following immunohistochemical markers were used: Kermix (ae1/ae3 + ck1), cytokeratin 7 (CK7), cytokeratin 20 (CK20), epithelial membrane antigen, CAM 5.2, S-100 protein, neuron-specific enolase, glial fibrillary acid protein, smooth muscle actin, and vimentin. Five lesions were studied ultrastructurally. Clinical data were available in all cases, and follow-up was obtained in 9 of the 12 patients. RESULTS: Nine tumors occurred in phthisical eyes in adults. The tumor cells were arranged in tubular and solid patterns and surrounded by thick basement membrane (BM) material and fibrous stroma. Immunohistochemistry (IM) of adenocarcinomas showed positivity with kermix (8 of 12 lesions), CAM 5.2 (7 of 12), and CK7 (5 of 12). Ultrastructurally, the tumor cells were surrounded by a thick, homogeneous, and/or multilaminar BM and attached to each other by junctional complexes. CONCLUSIONS: Clinically, this intraocular neoplasm should be considered in adults with a longstanding blind eye with an epibulbar mass and/or proptosis of recent duration. Fatal cases only occurred in tumors with extraocular extension. Adenocarcinomas of CE should be differentiated from amelanotic melanoma and metastatic lesions by the presence of a thick BM material around the tumor cells and intraocular fibrosis. Immunohistochemistry is helpful in differentiating from melanomas but not helpful in cases of metastatic carcinomas.     

Molecular biologic markers and cancer risk assessment

BACKGROUND: Malignant melanoma is the second most common vulvar malignancy. The superficial inguinal lymph nodes are the main site of metastases. Endometrial metastasis of vulvar malignant melanoma has not been previously reported. CASE: Vulvar malignant melanoma was diagnosed in a 60-year-old, postmenopausal woman. Immunohistochemical stains were positive for vimentin and S-100 protein and negative for HMB-45. Six months following vulvectomy, right inguinal lymphadenectomy and immunotherapy, curettage was performed due to postmenopausal bleeding. Histologic and immunohistochemical examinations revealed metastatic malignant melanoma with the same staining reactivity as the primary vulvar neoplasm had. Hysterectomy and bilateral salpingo-oophorectomy was performed, disclosing invasion of the endometrium and the inner two thirds of the myometrium. CONCLUSION: Only 10 other cases of endometrial metastases from malignant melanoma have been previously reported. All those cases involved a primary tumor occurring in the trunk and extremities. This is presumably the first report on endometrial and myometrial metastases from vulvar malignant melanoma.     

Bronchioloalveolar carcinoma of the lung

Iodine-123-iodobenzamide (IBZM) is a specific antagonist of dopamine D2 receptors and usually is used to study neuropsychiatric disorders. It also has a substantial affinity for malignant melanomas. This has been attributed to specific dopamine D2 receptor binding on melanoma cells because melanocytes and dopaminergic neurons share the same ectodermal origin and are both able to produce melanin. However, IBZM binding to melanoma metastases occurs predominantly 24 hr after injection, which is much later than maximal specific D2 receptor binding is expected. Furthermore, IBZM binding is not consistent in melanoma patients. This points to another mechanism of IBZM binding to melanoma cells. The aim of this study was to characterize IBZM-binding metastatic melanoma patients clinically and histologically to shed light on the nature of this mechanism. METHODS: Twenty-one patients with proven or suspected metastases of a malignant melanoma entered this prospective study after surgical removal of the primary tumor. Whole-body scans, planar scintigrams and SPECT scans were performed 2-5 hr and 1 day after intravenous injection of 185 MBq IBZM. RESULTS: The suspected diagnosis of metastatic cancer was later confirmed in 17 patients by histology, clinical follow-up, x-ray, CT or other radiologic methods. Four patients were free of tumor tissue at the time of investigation and remained stable for 2 yr thereafter. Twelve of the 17 patients had a melanotic and 5 had an amelanotic subtype of the tumor. Iodine-123-IBZM accumulation occurred in the metastases of 10 of the 12 patients with melanotic melanoma and in 0 of the 5 patients with the amelanotic tumor type (p < 0.01; chi-square test). Furthermore, IBZM accumulation occurred in 0 of the 11 amelanotic metastases but in 20 of the 25 melanotic metastases (p < 0.001). The sensitivity is, thus, 83% for the detection of melanotic melanoma metastases on a patient basis and 80% on a lesion basis. Iodine-123-IBZM scintigraphy demonstrated one previously unknown metastasis. Six initially suspected lesions were not due to melanoma metastases and were IBZM-negative. No false-positive IBZM accumulations occurred in our patients. CONCLUSION: Iodine-123-IBZM binds to melanotic malignant melanomas with high specificity and moderate sensitivity but not to amelanotic melanomas. Our data suggest that the tracer does not bind to membrane dopamine receptors of the tumor but is built in or closely bound to intracellular melanin.     

Expression and ultrastructural localization of HMB-45 antigen

HMB-45 is a monoclonal antibody specific for melanoma cells and premature developing melanocytes. We examined the expression and specific subcellular binding sites of HMB-45 in various types of melanocytes including epidermal melanocytes from fetuses and infants with or without tyrosinase-negative oculocutaneous albinism (type IA), melanin-producing and non-producing melanoma cell lines (G361 and MeWo), and in vivo melanoma cells (melanotic and amelanotic malignant melanoma). Subcellular HMB-45 binding was examined by using post-embedding immunogold electron microscopy with rapid freezing and freeze substitution fixation methods without the use of chemical fixatives to preserve the intracytoplasmic delicate antigen property of HMB-45. HMB-45 antigen was detected not only in in vivo melanoma cells and normal fetal melanocytes, but also in melanocytes in the other conditions. Post-embedding immunogold electron microscopy revealed that HMB-45 antigen was exclusively localized to stages I and II melanosomes in the cytoplasm of neoplastic melanocytes, but was detected mainly on stages II and III melanosomes in the melanocytes from fetuses and infants. In tyrosinase-negative oculocutaneous albinism, only stages I and II melanosomes were detected in the cytoplasm, but both stages of melanosomes were HMB-45 positive. We conclude that HMB-45 appears mainly on the immature melanosomes during melanogenesis in both neoplastic and non-neoplastic melanocytes regardless of their tyrosinase activity, but the intracytoplasmic localization of HMB-45 antigen is different by each condition of melanocytes.     

Activation of epidermal melanocytes is independent of epithelial proliferation and vascularization. Immunohistologic study using HMB-45 antibody with review of the literature

Antibodies against HMB-45 antigen are widely used in the immunohistochemical investigation of melanocytic tumours as a marker of activation. While malignant transformation is one explanation for HMB-45 expression, we searched for other factors by investigating 252 biopsies of non-melanocytic skin lesions with 21 different diagnoses for the presence of HMB-45, using both single and double staining techniques. Epidermal melanocytes in lesions with an increased epithelial proliferation-either neoplastic or reactive-and lesions with a prominent vasculature showed an enhanced expression of HMB-45. The results indicate that the presence of HMB-45 is not only influenced by primary melanocytic changes but also may be dependent on epithelial proliferation and vascular factors. These mechanisms should be considered when interpreting HMB-45 staining of melanocytic lesions.     

CEA reactivity in amelanotic malignant melanoma of the anal canal

Amelanotic malignant melanoma can present a diagnostic problem in histopathology, especially when it presents in an extracutaneous location. In such cases electron microscopy and/or immunohistochemistry are invaluable for diagnosis. A 63-year-old women with rectal bleeding was found to have an amelanotic malignant melanoma of the anal canal, with compatible clinical and gross pathology and light and electron microscopic findings. Tumor cells showed positive staining with antibodies to vimentin, S 100 protein, and HMB-45 (melanoma-specific antibody), but also with polyclonal antibody to carcinoembryonic antigen (CEA). Tumor cells failed to stain with monoclonal antibody to CEA. The nature and significance of CEA reactivity in malignant melanoma are discussed.     

Comparative decreases in tyrosinase, TRP-1, TRP-2, and Pmel 17/silver antigenic proteins from melanotic to amelanotic stages of syngeneic mouse cutaneous melanomas and metastases

Malignant cutaneous melanomas and metastases were taken directly from in situ lesions of genetically identical (C57BL/6 strain) Tyr-SV40E transgenic mice, and samples were analyzed by Western immunoblotting with antisera specific for the COOH terminus of each of four melanocytic proteins. These were tyrosinase, TRP-1, TRP-2, and Pmel 17/silver. Of the 13 melanomas examined, there were 5 melanotic primary tumors, 5 amelanotic primary tumors, and 3 amelanotic metastases. The melanotic tumors expressed all of the markers to some extent. In contrast, the amelanotic tumors lacked detectable levels of one, two, or three of the proteins, except for an apparently amelanotic tumor sample in which all were expressed, but in which some melanotic cells were likely to have been present. Thus, despite some variability, there is clearly a downward trend in the presence of these proteins as the tumors become amelanotic, a pigmentary change associated with ongoing malignant progression. In the amelanotic tumors, tyrosinase was most often deficient, whereas TRP-2 was most often persistently expressed. These results, obtained from melanomas of syngeneic origin, indicate that tumors in the relatively early stages of malignancy might be more responsive than later-stage tumors to immunotherapy involving an ensemble of antigenic peptides of the tested gene products. Moreover, TRP-2 peptides may be especially useful for therapeutic intervention at the later stages.     

Expression of DNA topoisomerase I, DNA topoisomerase II-alpha, and p53 in metastatic malignant melanoma

New anticancer drugs that target DNA topoisomerase I (topo I) are showing activity against a wide variety of solid human neoplasms. These drugs work by a novel mechanism of action and cause topo I-mediated DNA breaks. These DNA breaks become lethal in cycling cells when they interact with the replication fork. Because of the challenges in treating metastatic malignant melanoma, we performed an immunohistochemical study of this group of neoplasms to search for the presence of molecular markers that might indicate tumor response to topo I active drugs. Using a new immunohistochemical stain for topo I, we found elevation of this protein in 10 of 24 cases (41.6%) of metastatic malignant melanoma. The metastatic tumors that showed increased expression of topo I (2+ or 3+) had statistically significant higher proliferation indices, measured by immunohistochemical staining for DNA topo II-alpha, than did metastatic lesions with no detectable topo I expression. The average topo II-alpha index of metastatic melanomas with 2+ topo I expression was 45.1 (SD = 17.9) and with 3+ topo I expression was 52.3 (SD = 32.5). These values were found to be statistically different (P = .05) than the average topo II-alpha index of 18.9 (SD = 17.7) found for metastatic melanomas without detectable topo I immunostaining. Immunohistochemical staining for p53 suggested abnormal p53 function in 6 of the 10 melanomas (60%), which showed elevations of topo I (2 to 3+ topo I immunostaining) but normal p53 function in all 14 metastatic lesions that showed normal topo I expression.     

Limitations of imaging choroidal tumors in vivo by optical coherence tomography

AIM: To study the immunohistochemical expression of the Thomsen-Friedenreich antigen (T) and its precursor, Tn, in the skin in various cancers. METHODS: T and Tn antigens were studied with monoclonal antibodies in 91 primary premalignant and malignant lesions, 13 cases of Paget's disease, and 26 carcinomas metastatic to the skin. The material had been collected over a 10 year period, formalin fixed, and paraffin embedded. Diagnoses had been made after examination of standard histological sections, supplemented when needed by appropriate immunohistochemical staining. RESULTS: 21% and 29% of the primary cutaneous premalignant and malignant epithelial tumours expressed the Tn and T antigens, respectively. By contrast, 81% of metastatic carcinomas to the skin were Tn positive, while only 23% of them expressed the T antigen. All cases of Paget's disease were Tn positive but only 15% of them expressed the T antigen. The 21 nonepithelial tumours (including melanomas) were as a rule unreactive. CONCLUSIONS: The accumulation of the precursor (Tn) antigen in tumours metastasising to the skin highlights the incomplete glycosylation of carbohydrate antigens occurring in these tumours. The predominant Tn versus T antigen expression appears to be a useful immunohistochemical feature which may aid in the differentiation of primary cutaneous carcinomas from metastatic tumours.     

Inhibin A is a sensitive and specific marker for testicular sex cord-stromal tumors

We compared the expression of inhibin A, chromogranin, synaptophysin, S-100 protein, cytokeratins AE1/AE3, 7, and 20, and estrogen and progesterone receptors in testicular sex cord-stromal tumors: 11 Sertoli cell tumors, 3 Sertoli cell adenomas (nodules), 26 benign Leydig cell tumors, 7 malignant Leydig cell tumors (defined clinically by metastatic behavior), and a variety of germ cell tumors. Inhibin was the most sensitive marker, expressed in 91% of the Sertoli cell tumors and 100% of the Sertoli cell adenomas and Leydig cell tumors. The non-neoplastic Sertoli and Leydig cells invariably stained for inhibin. Conversely, no germ cell tumors were immunoreactive. One testicular tumor of the adrenogenital syndrome was immunoreactive. Neuroendocrine marker immunoreactivity was variable. Chromogranin was expressed in the non-neoplastic Sertoli and Leydig cells, 82% of the Sertoli cell tumors, 92% of the benign Leydig cell tumors, and 43% of the malignant Leydig cell tumors. Synaptophysin was expressed in the non-neoplastic Sertoli and Leydig cells, 45% of the Sertoll cell tumors, and 70% of the Leydig cell tumors, in approximately similar proportions between the benign and malignant Leydig cell tumors. S-100 protein was expressed in 64% of the Sertoli cell tumors, 8% of the benign Leydig cell tumors, and none of the malignant Leydig cell tumors. Cytokeratins AE1/AE3 were expressed in 64% of the Sertoli cell tumors and 42% of the Leydig cell tumors, with similar proportions in the benign and malignant cases. Estrogen and progesterone receptor expression were identified in 24 and 39% of benign and malignant Leydig cell tumors, respectively. We conclude that inhibin is a characteristic marker for Sertoli and Leydig cells and that it serves to differentiate testicular sex cord-stromal tumors from germ cell tumors.     

The mechanism of positive scintigraphy with 99mTc-pertechnetate in adenolymphomas of the parotid grand

Inhibin is a peptide hormone produced by ovarian granulosa cells and testicular Sertoli cells. Ovarian granulosa cell and other sex cord-stromal tumors usually exhibit positive immunohistochemical staining with antiinhibin antibodies, and this may be valuable in differentiating these neoplasms from histologic mimics. In the present study, we investigated the immunohistochemical staining of testicular sex cord-stromal tumors using antiinhibin. Immunostaining with CAM5.2, vimentin, S-100 protein, desmin, epithelial membrane antigen (EMA), carcinoembryonic antigen (CEA), and placental alkaline phosphatase (PLAP) also was performed because few studies have investigated in detail the immunophenotype of testicular sex cord-stromal tumors. Fifteen of 16 Leydig cell tumors exhibited strong positive staining with antiinhibin. A proportion of Leydig cell tumors also stained positively with CAM5.2 (7 of 16), vimentin (14 of 16), S-100 protein (10 of 16), desmin (2 of 16) and epithelial membrane antigen (4 of 16). Four of six testicular sex cord-stromal tumors with varying degrees of Sertoli or granulosa cell differentiation were positive with antiinhibin, as were two of three sex cord-stromal tumors that were unclassified. Some of these tumors were positive with CAM 5.2, vimentin, S-100 protein, desmin, and epithelial membrane antigen. All tumors were negative with carcinoembryonic antigen and placental alkaline phosphatase. The immunohistochemical findings show that, analogous to their ovarian counterparts, most testicular sex cord-stromal tumors are immunoreactive with antiinhibin. Immunohistochemistry using this antibody as part of a panel may be valuable in confirming a diagnosis of testicular sex cord-stromal tumor and in differentiating these neoplasms from others that may mimic them.     

Signet-ring cell melanoma mimicking adenocarcinoma. A case report

The fine needle aspiration findings in a lymph node involved by signet-ring cell melanoma, a very rare variant of malignant melanoma, are reported. The patient had a history of superficial spreading melanoma of the right foot, treated 10 years earlier by below-the-knee amputation. He presented with a right groin mass. Fine needle aspiration of the mass yielded poorly cohesive, large cells with eccentric nuclei and abundant, eosinophilic cytoplasm; many of them exhibited a signet-ring appearance. Melanin pigments were identified in a small proportion of tumor cells, and a diagnosis of metastatic melanoma was made. The subsequent lymph node excision revealed a metastatic tumor composed of polygonal and signet-ring cells that were positive for S-100 protein and HMB-45 but not cytokeratin. Nearly all reported cases of signet-ring cell melanoma occurred as metastatic or recurrent disease. It is important not to mistake signet-ring cell melanoma for adenocarcinoma in aspiration cytology, and a constellation of clinical features and of histochemical and immunohistochemical findings enables a correct diagnosis to be reached.     

Comparison of several mouse and rat monoclonal antibodies against human fibrinogen

A rare case of desmoplastic melanoma arising from the maxillary gingiva of a 66-year-old woman is reported. This tumour metastasised to the submandibular lymph node 5 years after extirpation, and local recurrence was observed 2 years later. The gingival tumour showed the histopathological characteristics of desmoplastic melanoma and the metastasised tumour cells were immunohistochemically positive for S-100 protein, neuron specific enolase, HMB-45 highly specific for conventional melanoma, and Fontana-Masson staining. The gingival tumour, originally regarded as benign clinically, was actually a desmoplastic melanoma.     

Allergic eye disease mechanisms

The histologic distinction between epithelial peritoneal mesothelioma and papillary serous carcinoma diffusely involving the peritoneum may be difficult. Although some investigators have indicated that immunohistochemistry can facilitate this differential diagnosis. only a few studies using a limited number of markers have been published. In this study, the immunoreactivity of keratin 5/6, vimentin, epithelial membrane antigen, thrombomodulin, calretinin, MOC-31, Ber-EP4, carcinoembryonic antigen, TAG-72 (B72.3), CD15 (Leu-M1), placental alkaline phosphatase, CA19-9, CA-125, HBME-1, 44-3A6, and S-100 protein was investigated in 35 epithelial peritoneal mesotheliomas, and 45 papillary serous carcinomas [30 ovarian (10 primary and 20 metastatic to the peritoneum) and 15 papillary serous carcinomas of the peritoneum]. After analyzing the results, it is concluded that calretinin, thrombomodulin, and keratin 5/6 are the best positive markers for differentiating epithelial malignant mesotheliomas from papillary serous carcinomas diffusely involving the peritoneum. The best diagnostic discriminators among the antibodies considered to be negative markers for mesothelioma are MOC-31, B72.3, Ber-EP4, CA19-9, and Leu-M1. Immunostaining for carcinoembryonic antigen, placental alkaline phosphatase, epithelial membrane antigen, vimentin, HBME-1, 44-3A6, CA-125, or S-100 have little or no diagnostic utility in establishing the differential diagnosis between these conditions. The results of this study also confirm previous observations indicating that both papillary serous carcinomas of the peritoneum and serous carcinomas of the ovary have a similar phenotype and, therefore, immunohistochemical studies are not useful in separating these entities.