bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sinus histiocytosis with massive lymphadenopathy: evidence for its relationship to macrophages and for a cytokine‐related disorder
Authors: Middel  , Hemmerlein  , Fayyazi  , Kaboth  , Radzun  
Published: March 2003

AimsSinus histiocytosis with massive lymphadenopathy (SHML) or Rosai–Dorfman disease is a rare histiocytic disorder of unknown origin. Immunophenotypically the histiocytes of SHML express intensively the S100 protein and in addition a panel of macrophage‐associated antigens. Their exact relationship to either monocytes/macrophages or immune accessory dendritic cells is, however, still controversial.Methods and resultsIn this report recurrent nodal and extranodal manifestations of SHML of a 70‐year‐old patient were analysed by differential phenotyping using a panel of monoclonal and polyclonal antibodies to macrophage and immune accessory dendritic cell related antigens and by applying nonradioactive in‐situ hybridization.ConclusionsWe conclude that stimulation of monocytes/macrophages via macrophage colony stimulating factor (M‐CSF) leading to immune suppressive macrophages represents a main mechanism for the pathogenesis of SHML. The study further provides evidence for the monocyte/macrophage but not dendritic cell differentiation of SHML histiocytes.
Morphological evidence for field effect as a mechanism for tumour spread in mammary Paget's disease
Authors: Mai  
Published: March 2003

AimsThe histogenesis of mammary Paget's disease is controversial. The purpose of this study was to investigate the mechanism of tumour spread in the nipple epidermis by examining 28 cases of mammary Paget's disease associated with underlying intraductal carcinoma.Methods and resultsThe atypical cells in the epidermis displayed a spectrum of cytological changes ranging from small‐sized atypical cells located in the basal cell layer to large‐sized atypical cells characteristic of Paget's cells in the upper layer of the epidermis. Serial sectioning revealed the presence of isolated, scattered and small atypical cells in the basal cell layer at the periphery of the epidermal lesion. The atypical cells, including those in the basal cell layer showed positive immunostaining for cytokeratin 7 and Her2/neu oncoprotein. Electron microscopy examination demonstrated the presence of intercellular junctions of desmosomal‐like or desmosomal types between tumour cells and adjacent squamous cells. Furthermore, examination of the intraductal carcinoma of the breast tissue in cases of Paget's disease as well as control cases of intraductal carcinoma also revealed areas of skip lesions of intraductal carcinoma.ConclusionsIn view of these changes, it is unlikely that tumour expansion or tumour cell motility are sufficient explanations to account for the pattern of tumour spread in both the epidermis and the duct epithelium with skip lesions. A ‘field effect’ in the duct system harbouring intraductal carcinoma and the adjacent epidermis may play an important role in the tumour cell spread in the epidermis as well as in the ductal epithelium.
HBME‐1, MOC‐31, WT1 and calretinin: an assessment of recently described markers for mesothelioma and adenocarcinoma
Authors: Oates  , Edwards  
Published: March 2003

AimsTo evaluate HBME‐1, WT1, calretinin and MOC‐31 in the differential diagnosis of pleural mesothelioma and adenocarcinoma of the lung.Methods and resultsParaffin‐embedded formalin‐fixed blocks from six reactive pleuras, 42 mesotheliomas and 40 adenocarcinomas were used. Sections were stained for Leu‐M1, HBME‐1, calretinin, WT1 and MOC‐31. Leu‐M1 was positive or equivocal in 34% of mesotheliomas and in 78% of adenocarcinomas; reactive pleuras were all negative. HBME‐1 was positive or equivocal in 76% of mesotheliomas and in 73% of adenocarcinomas; five reactive pleuras were positive. Calretinin was positive or equivocal in 92% of mesotheliomas and in 73% of adenocarcinomas; two reactive pleura were equivocal and four were positive. WT1 was positive or equivocal in 72% of mesotheliomas (excluding autopsy cases) and in 20% of adenocarcinomas; all reactive pleuras were positive. MOC‐31 was positive or equivocal in 5% of mesotheliomas and in 90% of adenocarcinomas; all reactive pleuras were negative. The reaction with Leu‐M1 was graded as equivocal in 25% of the adenocarcinomas. All 24 of the autopsy cases of mesothelioma were negative for WT1 and in many operative specimens only the periphery was stained.ConclusionsNeither calretinin nor HBME‐1 are sufficiently discriminatory to be of use, even as members of a panel of antibodies. WT1 shows some promise, but it cannot be used on autopsy material. The utility of MOC‐31 is confirmed, and outperforms Leu‐M1.
Monoclonal antibodies recognizing CD5, CD10 and CD23 in formalin‐fixed, paraffin‐embedded tissue: production and assessment of their value in the diagnosis of small B‐cell lymphoma
Authors: Watson  , Wood  , Lodge  , McIntosh  , Milton  , Piggott  , Proctor  , Taylor  , Smith  , Jack  , Bell  , Steward  , Anderson  , Horne  , Angus  
Published: March 2003

AimsAssessment of the expression of antigens CD5, CD10 and CD23 can be of value in the differential diagnosis of small B‐cell lymphoma. Correct subclassification is important since optimal treatment regimes differ between the subtypes. The aim of this study was to generate monoclonal antibodies recognizing these antigens in paraffin‐embedded tissue and to assess their efficacy using a panel of cases of small B‐cell lymphoma of various subtypes.Methods and resultsFor each antibody synthetic recombinant protein and conventional murine hybridoma technology was employed. Monoclonal antibodies effective in formalin‐fixed, paraffin‐embedded tissue were successfully generated, designated NCL‐CD5‐4C7, NCL‐CD10‐270 and NCL‐CD23‐1B12, respectively. A series of 58 cases of small B‐cell lymphoma including examples of each subtype (lymphocytic, follicle centre cell, mantle cell, marginal zone and lymphoplasmacytoid) was assembled and immunostaining for the respective antigens carried out using the monoclonal antibodies produced. Our results indicate that the antibodies are specific for their respective antigens and give the predicted phenotypic profile in the small B‐cell lymphoma subtypes.ConclusionsThese novel monoclonal antibodies may be of value in routine diagnostic practice.
Chromosomal numerical aberrations are frequent in oesophageal and gastric adenocarcinomas: a study using in‐situ hybridization
Authors: Beuzen F , Dubois S , Fléjou J‐F 
Published: March 2003

Aims (i) To investigate and compare the numerical aberrations of chromosomes 7, 8, 11, 17 and Y in a series of 60 adenocarcinomas of the oesophagus, gastric cardia and gastric antrum; and (ii) to specify the sequence of chromosomal aberrations occurring during the neoplastic progression of Barrett's oesophagus. Methods and results: Chromosomal in‐situ hybridization was performed on deparaffinized tissue sections from 20 Barrett's adenocarcinomas, 20 adenocarcinomas of the cardia and 20 adenocarcinomas of the antrum, with centromeric alpha satellite DNA probes specific for chromosomes 7, 8, 11, 17 and Y, labelled with digoxigenin. Signals were detected by immunoperoxidase staining. The copy number for each chromosome was counted in 200 tumour cells nuclei and 100 lymphocytes as controls. In parallel, the DNA content of the nuclear suspensions was measured by flow cytometry. Numerical abnormalities of the five chromosomes (loss of the Y chromosome, monosomy, trisomy, and tetrasomy) were frequently observed in the three groups of adenocarcinomas (from 40% to 65% of the cases). Sixty per cent to 75% of oesophagus and gastric adenocarcinomas were DNA‐aneuploid. Chromosomal aberrations progressively increased with advancing degrees of dysplasia in Barrett's mucosa, with an increasing frequency of trisomy and loss of the Y chromosome from non‐dysplastic Barrett's mucosa to invasive adenocarcinoma, and with monosomy and tetrasomy present only in invasive cancers. Conclusions: Our study confirms the high frequency of chromosomal numerical aberrations in oesophageal and gastric adenocarcinomas, without differences between adenocarcinomas of the gastric cardia and antrum. We have shown that these alterations occur early during the neoplastic transformation of Barrett's mucosa.
Renal oncocytoma with prominent intracytoplasmic vacuoles of mitochondrial origin
Authors: Koller A , Kain R , Haitel A , Mazal P R , Asboth F , Susani M 
Published: March 2003

Aims: We observed two oncocytomas with prominent intracytoplasmatic vacuoles. To investigate if this previously undescribed finding is a diagnostic feature and compatible with the diagnosis of oncocytoma, we characterized these vacuoles by electron microscopy and immunohistochemistry.Methods and results: The tumours were analysed by transmission electron microscopy. Immunohistochemistry was performed with antimitochondrial antibody, anti‐Golgi‐zone antibody, anti‐lysozyme antibody and anti‐human‐trans‐Golgi‐network antibody. By electron microscopy, the vacuoles were found to be double‐membrane‐bounded, and some contained fragmented christae. Immunohistochemistry showed a positive reaction of the vacuoles with anti‐mitochondrial antibody. Staining with anti‐Golgi‐zone antibody, anti‐lysozyme antibody and anti‐human‐trans‐Golgi‐network antibody was negative.Conclusion: Both tumours are benign oncocytomas. The phenomena of cells with prominent intracytoplasmatic vacuoles is not inconsistent with the diagnosis of oncocytoma. The vacuoles are of mitochondrial origin and may develop, by balloon degeneration, as a mechanism of mitochondrial involution and elimination.
Central neurocytomas are genetically distinct from oligodendrogliomas and neuroblastomas
Authors: Tong C Y K , Ng H‐K , Pang J C S , Hu J , Hui A B Y , Poon W‐S 
Published: March 2003

AimsCentral neurocytoma is a rare central nervous system tumour typically found in the lateral ventricles and at the septum pellucidum. Histologically, it resembles oligodendrogliomas and yet ultrastructurally, it shows neuronal differentiation. Its molecular oncogenesis is not known. The aim of this study was to examine whether major genetic events found in oligodendrogliomas and neuronal tumours, namely allelic deletions of chromosomes 1p and 19q and N‐myc amplification, can be found in central neurocytomas. As there was one report describing gain of chromosome 7 in central neurocytomas, we also examined epidermal growth factor receptor (EGFR) amplification, as the EGFR gene is located at chromosome 7p.Methods and resultsNine central neurocytomas and matched blood samples were examined for loss of heterozygosity (LOH) of 1p and 19q13.2–13.4 with 23 finely mapped microsatellite markers. N‐myc amplification was studied by fluorescence in‐situ hybridization using paraffin‐embedded sections. EGFR amplification was tested for by differential PCR. Six of nine (67%) tumours showed LOH at one or more loci at 1p and 5/9 (56%) of cases showed LOH at 19q. However, common regions of deletion cannot be identified. The majority of informative markers are retained at 1p (84%) and 19q (86%). Only one tumour showed amplification of N‐myc and none of the cases showed amplification of EGFR.ConclusionCentral neurocytomas are genetically distinct from oligodendrogliomas, and chromosomes 1p and 19q probably do not play an important role in their pathogenesis. N‐myc and EGFR amplification are rare.
Lymphoepithelioma‐like carcinoma of the breast: lack of evidence of Epstein–Barr virus infection
Authors: Dadmanesh F , Peterse J L , Sapino A , Fonelli A , Eusebi V 
Published: March 2003

Six cases of lymphoepithelioma‐like carcinomas of the breast were studied in order to better define the morphology of this type of breast tumour and to see if these neoplastic lesions are related to Epstein–Barr virus (EBV) infection by analogy with histologically similar tumours located in other organs.The cases were studied with immunohistochemistry using several antibodies and with in‐situ hybridization method employing different types of nucleotides in four cases. The cases presented the distinctive morphology of the lymphoepithelioma‐like carcinomas as seen in other organs. Specifically Rigaud and Schminke's patterns of growth were observed. In addition, at the edge of the neoplastic lesions, a lymphoepithelial lobulitis was seen. In‐situ hybridization failed to reveal any positivity for EBV genome.Lymphoepithelioma‐like carcinoma is a specific type of breast tumour, but its relation to EBV has yet to be proven. The differential diagnosis with medullary carcinoma is discussed.
Proliferating trichilemmal tumour: p53 immunoreactivity in association with p27Kip1 over‐expression indicates a low‐grade carcinoma profile
Authors: Fernández‐Figueras M T , Casalots A , Puig L , Llatjós R , Ferrándiz C , Ariza A 
Published: March 2003

Proliferating trichilemmal tumour: p53 immunoreactivity in association with p27Kip1 over‐expression indicates a low‐grade carcinoma profile Aims: Alterations of cell‐cycle regulatory molecules in tumorigenesis may predict the biological behaviour of neoplasms and greatly contribute to their proper classification. Since the behaviour of proliferating trichilemmal tumour (PTT) is controversial, we decided to explore the possible significance of altered p53 and p27Kip1 immunohistochemical expression patterns in PTT. Methods and results: We evaluated the percentage and distribution of positive tumour cells and compared the results with those obtained from usual trichilemmal cysts (TC) and squamous cell carcinomas with trichilemmal differentiation (SCCT). PTT showed p53 immunoreactivity (50.4 ± 29.6, mean ± standard deviation) that was not statistically different from that seen in SCCT (75.2 ± 36.3). On the other hand, p53 immunostaining was virtually absent in TC cases (positivity for p53 was observed in only one instance in < 1% of cells). As for p27Kip1, the mean percentage of positive cells in PTT (82.7 ± 9.9) was slightly lower than in TC (90.6 ± 4.6) but significantly higher than in SCCT (53.4 ± 30). Conclusions: The similar p53 immunoreactivity in both PTT and SCCT favour the interpretation of the former as carcinoma, albeit one whose behaviour would be tempered by the well‐known regulatory effect exerted by p27Kip1 on the cell cycle.
Clinical implications of telomerase detection
Authors: Matthews P , Jones C J 
Published: March 2003

Clinical implications of telomerase detection In 1994 a sensitive method for the detection of telomerase was described. This assay, which was based on the polymerase chain reaction, suggested that telomerase activity was associated with immortal and cancer cells. Since then more than a thousand studies have documented the expression and activity of the enzyme in diseased tissues, primarily tumours. This review gives an overview of the biological significance of telomerase expression and methods for detecting its activity. This is followed by an organ system‐based discussion of expression in normal tissues and disease states. We finish with speculation as to the future role of telomerase detection in diagnostic histopathology.
Pleomorphic lobular carcinoma of the breast: its cell kinetics, expression of oncogenes and tumour suppressor genes compared with invasive ductal carcinomas and classical infiltrating lobular carcinomas
Authors: Frolik D , Caduff R , Varga Z 
Published: March 2003

Pleomorphic lobular carcinoma of the breast: its cell kinetics, expression of oncogenes and tumour suppressor genes compared with invasive ductal carcinomas and classical infiltrating lobular carcinomas Aims: The study addresses whether pleomorphic lobular breast carcinomas represent a distinct entity with respect to proliferation and apoptosis as well the expression of the p53, bcl‐2 and Her2 protein. Methods and results: The study included 30 cases of pleomorphic lobular carcinoma (PLC; G2 n=15, G3 n=15). Poorly differentiated invasive ductal carcinomas (IDC; n=15) and well‐differentiated infiltrating lobular carcinomas (ILC; n=15) were used as controls. Lymph node metastases were present equally in all groups. MIB‐1 labelling was counted as: PLC (G2) 8.36%; PLC (G3) 11.3%; IDC 44.26%; ILC 2.19% (P=0.0001, P=0.004, P=0.001). Apoptotic index was: PLC (G2) 0.82%; PLC (G3) 1.2%; IDC 2.09%; ILC 0.6% (P=0.009, P=0.001). Over‐expression of Her2 protein was detected in 53% of PLC (G3) tumours and was present only in scattered cases in the other groups. PLCs and ILCs were strongly positive for bcl‐2 and for hormone receptors, while p53+ cells were rare. IDCs exhibited a heterogeneous staining pattern for bcl‐2 and for hormone receptors, while p53+ cells occurred considerably more frequently. Stage could not be linked directly to proliferation or apoptosis. Conclusion: Our data suggest that more frequent over‐expression of Her2 among PLCs (G3) as well as the generally low apoptosis can contribute to their aggressive behaviour.
CD99/MIC‐2 surface protein expression in breast carcinomas
Authors: Milanezi F , Pereira E M , Ferreira F V , Leitão D , Schmitt F C 
Published: March 2003

CD99/MIC‐2 surface protein expression in breast carcinomas Aim: To evaluate the expression of CD99/MIC‐2 surface protein in invasive breast carcinomas and demonstrate whether or not there is a relationship with tumour phenotype. Methods and results: Thirty‐five invasive breast carcinomas, including five metaplastic carcinomas, were stained with CD99 primary antibodies using standard protocols based on streptavidin–biotin–peroxidase method. Four out of five metaplastic carcinomas expressed CD99/MIC‐2 protein, three of them were matrix‐producing carcinomas. From the other 30 cases, only an invasive apocrine carcinoma was positive. There was no statistical correlation between CD99 expression and the parameters analysed (histological typing and grading, proliferative index and nodal status). Conclusions: CD99/MIC‐2 is expressed in breast carcinomas, especially in the matrix‐producing variant of metaplastic carcinomas, which impairs its use as a marker to differentiate metaplastic carcinomas from primary and metastatic sarcomas of the breast. It seems to have no prognostic implications. However, phenotype similarities with other chondromyxoid tumours that also express the protein, like mesenchymal chondrosarcomas, suggest a relationship between MIC‐2 reactivity and morphological differentiation.
Lipoblastoma‐like tumour of the vulva: report of three cases of a distinctive mesenchymal neoplasm of adipocytic differentiation
Authors: Lae M E , Pereira P F , Keeney G L , Nascimento A G 
Published: March 2003

Lipoblastoma‐like tumour of the vulva: report of three cases of a distinctive mesenchymal neoplasm of adipocytic differentiation Aims: We sought to delineate and describe three cases of a distinctive mesenchymal neoplasm of the vulva showing adipocytic differentiation and affecting young patients. Methods and results: In three patients between 13 and 38 years of age, the vulvar tumours had well‐circumscribed borders and ranged in size from 35 to 100 mm. Histologically, they were well circumscribed and lobulated. The lobules were separated by thin fibroconnective tissue septa and were composed of slender spindle cells showing slightly eosinophilic cytoplasm with indistinct boundaries, uniform nuclei with finely granular chromatin, and no nucleoli. The cells were embedded in a richly myxoid stroma. The background in all three tumours was a ‘chicken‐wire’, capillary vascular network resembling that seen in myxoid liposarcomas. Two tumours had scattered signet‐ring‐type lipoblasts and the third a large number of such lipoblasts. Clusters of mature adipocytes were entrapped in the tumours. None had mitotic figures, necrosis, or pleomorphism. The neoplastic cells stained positively for vimentin and were negative for other immunohistochemical markers. Treatment for all three tumours was enucleation alone. After follow‐up of 10 years, 7 years, and 1 year, all patients are well with no evidence of disease. Conclusions: The benign behaviour of these neoplasms militates against the diagnosis of liposarcoma. We believe these are benign lesions of adipocytic differentiation akin to infantile lipoblastomas.
Tumour‐associated tissue eosinophilia as a prognostic factor in oral squamous cell carcinomas
Authors: Dorta R G , Landman G , Kowalski L P , Lauris J R P , Latorre M R D O , Oliveira D T 
Published: March 2003

Tumour‐associated tissue eosinophilia as a prognostic factor in oral squamous cell carcinomasAims:  Tumour‐associated tissue eosinophilia has been described in many sites, including head and neck. The mechanism of eosinophil recruitment and its role in tumours has not yet been defined, and its presence has been related to a favourable as well as unfavourable prognosis. The aim of this study was to evaluate the influence of tumour‐associated tissue eosinophilia on the prognosis of 125 oral squamous cell carcinoma patients.Methods and results:  The number of eosinophils was obtained by morphometric analysis and ranged from 0 to 392 per mm2. Tumour‐associated tissue eosinophilia was classified according to intensity as mild, moderate, or intense and correlated statistically to the intensity of the mononuclear inflammatory infiltrate as well as to the location of the eosinophilic inflammatory infiltrate. The multivariate analysis demonstrated that intense tumour‐associated tissue eosinophilia is an independent favourable prognostic factor for oral squamous cell carcinomas.Conclusion:  These findings suggest an anti‐tumoral role of eosinophils not as yet well understood that should be better investigated.
Malignant neoplasms infiltrating pseudoangiomatous’ stromal hyperplasia of the breast: an unrecognized pathway of tumour spread
Authors: Damiani S , Peterse J L , Eusebi V 
Published: March 2003

Aims:  To describe five malignant tumours in the breast (two invasive carcinomas and three non‐Hodgkin's lymphomas) showing an unusual pattern of spread within anastomosing spaces consistent with those described in pseudoangiomatous stromal hyperplasia.Methods and results:  The histological and immunohistochemical features of the cases are presented. In all cases, the neoplasms consisted of non‐cohesive E‐cadherin‐negative cells located within anastomosing vascular‐like channels. These channels showed morphological and immunohistochemical features consistent with those seen in pseudoangiomatous stromal hyperplasia: they were lined by flattened cells that expressed CD34, bcl2 and smooth muscle actin, while CD31 was consistently negative.Conclusions:  The open channels of pseudoangiomatous stromal hyperplasia have been regarded as spaces due to loss of cohesiveness between stromal fibroblasts if not artefacts. The fact that neoplastic cells spread through these spaces suggests that the spaces are true open channels that may represent part of a complex network of stromal channels (pre‐lymphatics) connected to the main lymphatic system of the breast. This finding opens new insights into the routes of tumour spread.