bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hepatosplenic γδ T‐cell lymphoma: relation to Epstein–Barr virus and activated cytotoxic molecules
Authors: Ohshima  , Haraoka  , Harada  , Kamimura  , Suzumiya  , Kanda  , Kawasaki  , Sugihara  , Kikuchi  
Published: March 2003

AimsHepatosplenic γδ T‐cell lymphoma (TCL) is a rare, aggressive subset of peripheral TCL that presents with hepatosplenomegaly and cytopenia. Epstein–Barr virus (EBV) infection and activated cytotoxic molecules (granzyme and perforin) are uncommon in hepatosplenic γδ CTL. EBV infection and activated cytotoxic molecules are occasionally detected in non‐hepatosplenic γδ TCL. We describe the clinicopathological features of three Japanese cases who were not immunodeficient.Methods and resultsAll cases showed γδ T‐cell type (CD2+, CD3+, T‐cell receptor (TCR)δ‐1+, βF1−). Two cases expressed natural killer (NK) cell‐associated antigens (CD8–, CD16+, CD56+; CD8−, CD16−, CD56+), and one expressed CD8 (CD8+, CD16−, CD56−). All cases expressed cytotoxicity‐associated molecules (perforin, granzyme B, TIA‐1 and Fas ligand). However, perforin and Fas ligand were not detected in one case. In‐situ hybridization analysis with EBER probes revealed strong nuclear positivity in all neoplastic cells. In addition, two cases showed clonal bands of the EBV terminal repeat (TR) gene. Cytologically, instead of the presence of monomorphic medium‐sized cells, our three cases showed pleomorphic medium‐sized and large cells.ConclusionsOur γδ TCL cases were clinicopathologically considered to be compatible with hepatosplenic γδ T‐cell lymphoma. However, with regard to EBV association, activated cytotoxic profile and cytological features they resembled non‐hepatosplenic γδ TCL. EBV may play a role in this disease by inducing cellular activation.
Overexpression of 27‐kDa heat shock protein relates to poor histological differentiation in human oesophageal squamous cell carcinoma
Authors: Lambot  , Peny  , Fayt  , Haot  , Noël  
Published: March 2003

AimsVarious stress conditions such as heat, chemical and mechanical stresses are known to play a major role in oesophageal squamous cell carcinoma development. Our goal was to evaluate whether changes in stress‐induced 27‐kDa heat shock protein (HSP27) expression could be demonstrated during oesophageal carcinogenesis.Methods and resultsHSP27 expression was studied using immunohistochemistry on formalin‐fixed, paraffin‐embedded tissue sections from 21 oesophageal squamous cell carcinomas occurring in smokers and/or alcohol abusers. Oesophagus from healthy patients (controls) (five), chemical (eight) and infectious oesophagitis (six) were also included in the study. In normal oesophagus, the protein is present only in the upper epithelial layers. In contrast, in chemical or infectious oesophagitis its expression is strong and occurs in all the epithelial layers including the basal layer. In non‐tumoral oesophageal mucosa from smoking and/or drinking patients adjacent to invasive carcinoma, the distribution of the protein is patchy and irregular. In malignant areas, HSP27 protein expression increases drastically from dysplastic lesions to invasive carcinoma, being highest in the less differentiated areas.ConclusionsIn human oesophagus, HSP27 expression is induced by various stresses but alcohol and tobacco generate focal perturbations in the stress response. Tumour immunoreactivity for this protein increases with the anaplasia of the tumour, as in some other tumours in which it is considered to play a role in drug resistance. To our knowledge, these data have not been previously described for oesophageal squamous cell carcinoma.
Expression of steroid hormone receptors, their regulated proteins, and bcl‐2 protein in myofibroblastoma of the breast
Authors: Magro G , Bisceglia M , Michal M 
Published: March 2003

AimsTo investigate the possible role of steroid hormones in the pathogenesis of myofibroblastoma (MFB) of the breast, we analysed the immunohistochemical expression of oestrogen, progesterone, androgen receptors, their regulated proteins and bcl‐2 protein in a series of this rare tumour.Methods and resultsParaffin‐embedded sections from seven cases of MFB of the breast (five male; two female) were immunohistochemically tested for the expression of oestrogen receptor (ER), progesterone receptor (PR), androgen receptor (AR), oestrogen‐regulated pS2 protein, androgen‐regulated prostate‐specific antigen (PSA) and bcl‐2 protein. Rare cases of benign spindle cell tumours or tumour‐like lesions of the breast (primitive fibromatosis, inflammatory pseudotumour, muscular hamartoma) which enter into the differential diagnosis with MFB, were also investigated and compared with MFB. All cases of MFB showed a diffuse (70–90% of neoplastic cells) and strong nuclear labelling with ER and PR, whereas AR was expressed only in three cases (two men and one woman) in about 60–70% of cells. Conversely, no immunostaining was detected for the pS2 protein and PSA. bcl‐2 protein immunoreactivity was found in all cases of MFB, although with a variable degree of expression. No expression for steroid hormone receptors, their regulated‐proteins and bcl‐2 protein was observed in the rare benign spindle cell lesions of the breast included in this study.ConclusionThe in‐situ detection of ER, PR and AR suggests that steroid hormones and their receptors are implicated in the pathogenesis of breast MFB. The consistent demonstration of bcl‐2 protein, associated with a positive ER/PR status, provides evidence that bcl‐2 may be an oestrogen‐regulated protein also in MFB and that probably plays a role in the tumorigenesis. Finally, we postulate that the ER/PR and bcl‐2 positive immunoprofile of MFB of the breast, in contrast to the negative profile of other rare primitive benign spindle cell lesions of the breast herein studied, might be exploited as an ancillary diagnostic aid in differential diagnosis of doubtful cases.
CD44 isoform expression in synovial sarcoma correlates with epitheliogenesis but not prognosis
Authors: Sneath R J , Mangham D C 
Published: March 2003

Aims: We immunohistochemically determined the expression of CD44 standard and splice variant isoforms in a series of synovial sarcomas and sought correlations with histological subtype and clinical parameters including outcome. Methods  and results: From 39 patients, a total of 56 formalin‐fixed and paraffin‐embedded tumour samples (including initial, recurrent and metastatic tumours) were used to immunohistochemically evaluate the expression of epitopes encoded by CD44s and the CD44 splice variants CD44v3–v10. Significance of proposed prognostic indicators was evaluated in relation to the survival, time to local recurrence and time to metastases using log‐rank analysis. Sixty‐four percent of synovial sarcomas expressed CD44s and 46% expressed CD44v3–v10 (var). Synovial sarcomas with epithelial or epithelioid areas preferentially expressed CD44s in these areas when compared with the spindle cell element. There were no correlations with clinical parameters or outcome. Conclusions: The expression of CD44 was not found to correlate with survival, local recurrence or metastatic ability. In synovial sarcoma, CD44 and variant isoform expression appears to be associated with the degree of epithelial differentiation. CD44 expression in synovial sarcoma shows interesting similarities to CD44 expression in embryological epitheliogenesis.
Giant cell arteritis localized to the colon associated with Crohn's disease
Authors: Colombat M , Imbert A , Bruneval P , Chatelain D , Gontier M‐F 
Published: March 2003

Intestinal vasculitis is uncommon and usually accompanies systemic vasculitis. Although intestinal vascular changes including vasculitis have been studied intensively, and are found regularly in Crohn's disease, giant cell arteritis is distinctly unusual. We describe a case of giant cell arteritis localized to the colon of an 18‐year‐old girl suffering from Crohn's disease.After three years of medical treatment, the patient underwent a proctocolectomy. The medium‐sized arteries of the mesocolon demonstrated striking changes characterized by intimal fibrous thickening and an inflammatory infiltrate with giant cells, most predominant at the intima–media junction. Epithelioid cells and sarcoid‐like granulomas were not observed. The internal elastic lamina was fragmented. Neither clinical symptoms nor laboratory findings showed evidence of systemic vasculitis. Neither the chest CT scan nor the echo‐Doppler of the temporal arteries, supra‐aortic and abdominal vessels revealed any abnormality.This case illustrates an extremely rare feature in the spectrum of vascular lesions in Crohn's disease which have to be differentiated from temporal and Takayasu's arteritis.
Follicular lymphoid hyperplasia of the hard palate and oral mucosa: report of three cases and a review of the literature
Authors: Menasce L P , Shanks J H , Banerjee S S , Harris M 
Published: March 2003

Follicular lymphoid hyperplasia of the hard palate and oral mucosa: report of three cases and a review of the literature Aims: To bring to wider attention this uncommon, poorly understood entity which may closely resemble, clinically and morphologically, follicular lymphoma. Methods and results: We report three cases of follicular lymphoid hyperplasia of the hard palate and oral mucosa which caused diagnostic difficulties for the referring pathologists. The clinicopathological features are described and integrated into a review of the 16 previously recorded cases. The condition most commonly presents as a slowly growing mass situated in the posterior hard palate but may present with multicentric oral lesions and lymphadenopathy. Morphologically, it is characterized by a dense follicular lymphoid infiltrate within the lamina propria which may show the classical features of benign reactive hyperplasia, but not uncommonly, indistinct germinal centres, ill‐defined mantles and a lack of tingible‐body macrophages are features which may lead to an erroneous diagnosis of follicular lymphoma. Conclusions: Follicular lymphoid hyperplasia of the palate is a poorly recognized entity which is frequently confused with follicular lymphoma. Awareness of the entity combined with the use of immunohistochemistry for immunoglobulin light chains and bcl‐2 protein allows a correct diagnosis to be made avoiding extensive investigation and aggressive treatment to the patient.
Primary endometrioid adenocarcinoma of the large intestine arising in colorectal endometriosis
Authors: Petersen V C , Underwood J C E , Wells M , Shepherd N A 
Published: March 2003

Primary eneometrioid adenocarcinoma of the large intestine arising in colorectal endometriosis Aims: Three cases of endometrioid adenocarcinoma arising in colorectal endometriosis are described with discussion of their macroscopic and microscopic pathology and diagnosis, using immunohistochemistry. Methods and results: Three middle‐aged women presented with symptoms and signs of colorectal mass effect. Two had a preceding history of gynaecological endometriosis and all three had either been on hormone replacement therapy or had functioning ovaries prior to presentation with colorectal disease. Each underwent resection of tumours of the distal large intestine. The definitive diagnosis was dependent on histological examination and immunohistochemistry, which was used to demonstrate an origin in endometriotic tissue. Conclusions: Endometrioid adenocarcinoma is a rare complication of colorectal endometriosis, this report contributing to a total of 25 cases in the literature. Definitive diagnosis, aided by immunohistochemical studies, is important to enable the identification of the optimal management for this uncommon condition.
Multifocal distribution of pulmonary capillary haemangiomatosis
Authors: Erbersdobler A , Niendorf A 
Published: March 2003

Multifocal distribution of pulmonary capillary haemangiomatosis Aims: We investigated a case of pulmonary capillary haemangiomatosis, a rare condition, to determine the extent of the pathological changes within the lungs. Systematic histological sampling has not previously been performed in this condition. Methods and results: A 52‐year‐old woman with a history of ischaemic cardiomyopathy suffered from repeated respiratory infections, which were attributed to chronic pulmonary congestion. She died suddenly of fulminant pulmonary thrombembolism. An autopsy was performed and lung tissue was sampled at multiple sites. Beside passive congestion, the lungs showed well‐circumscribed areas containing proliferations of small capillaries infiltrating the pulmonary septa and the walls of otherwise normal blood vessels and bronchi. The most severely affected areas were found to be in the periphery of both lower lobes. A diagnosis of pulmonary capillary haemangiomatosis was made. Conclusions: This is the first case of pulmonary capillary haemangiomatosis in which systematic histological sampling has been performed. Mapping of lesions disclosed the multifocal distribution of pulmonary capillary haemangiomatosis in this patient.
Salivary duct carcinoma: cytokeratin 14 as a marker of in‐situ intraductal growth
Authors: De Araújo V C , Loducca S V L , Sobral A P V , Kowalski L P , Soares F , De Araújo N S 
Published: March 2003

Aims:  The aim of this study was to determine the immunoprofile of salivary duct carcinoma and to differentiate intraductal growth from invasive growth.Methods and results:  We applied a panel of antibodies (cytokeratins 7, 8, 13, 14, 19, vimentin and α‐smooth muscle actin) in five cases of salivary duct carcinoma. This panel is currently used for identification of different components of salivary gland tumours in our laboratory. All tumour cells were positive for cytokeratins 7 and 8. Few neoplastic structures expressed cytokeratin 14 in cells surrounding tumour islands.Conclusion:  The finding of cytokeratin 14 was important to confirm the in‐situ intraductal growth, which probably characterizes this low‐grade neoplasm.
T‐cell/histiocyte‐rich large B‐cell lymphoma is a disseminated aggressive neoplasm: differential diagnosis from Hodgkin's lymphoma
Authors: Fraga M , García‐Rivero A , Sánchez‐Verde L , Forteza J , Piris M A 
Published: March 2003

Aims:  An accurate diagnosis of T‐cell/histiocyte‐rich large B‐cell lymphoma needs to take into consideration those forms of Hodgkin's lymphoma also characterized by a predominance of small lymphocytes and histiocytes, i.e. nodular lymphocyte predominance Hodgkin's lymphoma and lymphocyte‐rich classical Hodgkin's lymphoma. We have studied the clinical, phenotypic and genetic features of a series of 12 cases of T‐cell/histiocyte‐rich large B‐cell lymphoma along with 18 cases of Hodgkin's lymphoma for comparative purposes.Methods and results:  Of the Hodgkin's lymphoma cases, there were 11 lymphocyte predominance type and seven classic type. T‐cell/histiocyte‐rich large B‐cell lymphomas presented usually in advanced stages (III or IV in 11/12 cases), frequently with ‘B’ symptoms (6/9 cases), and followed a more aggressive course than Hodgkin's lymphoma (4/8 patients died due to the tumour in T‐cell/histiocyte‐rich large B‐cell lymphoma versus 0/15 in Hodgkin's lymphoma). T‐cell/histiocyte‐rich large B‐cell lymphoma cases showed diffuse effacement of the nodal architecture by a proliferation of scattered large atypical B‐cells obscured by a background of small T‐lymphocytes (more CD8+, TIA1+ than CD57+). Five cases showed also a prominent histiocytic component. The large B‐cells expressed CD45 and often EMA (6/10 cases). On the other hand, CD30, CD15 and latent infection by Epstein–Barr virus (EBV) were generally lacking. bcl6 and CD10 were, respectively, detected in 6/6 and 1/5 cases. Conventional polymerase chain reaction (PCR) showed monoclonal immunoglobulin heavy chain (IgH) gene rearrangements in all T‐cell/histiocyte‐rich large B‐cell lymphomas studied (5/5), but did not detect any case with t(14;18) involving the major breakpoint region (0/4).Conclusions:  The differential diagnosis of T‐cell/histiocyte‐rich large B‐cell lymphoma from Hodgkin's lymphoma is facilitated by the integration of different immunophenotypic, molecular and clinical findings. T‐cell/histiocyte‐rich large B‐cell lymphoma is a monoclonal neoplasm of bcl6+ B‐cells with a phenotypic profile similar to lymphocyte predominance Hodgkin's lymphoma, suggesting a germinal centre origin andapossible relation to this disease. Therefore, in order to distinguish it from lymphocyte predominance Hodgkin's lymphoma, characterization of the reactive background, IgH gene rearrangement studies by conventional PCR and clinical features are more useful. In contrast, T‐cell/histiocyte‐rich large B‐cell lymphomacan be distinguished from classical Hodgkin's lymphoma thanks to the presence of monoclonal IgH rearrangement and the CD30–CD15–CD45+EMA+ immunophenotypic profile of the neoplastic cells in T‐cell/histiocyte‐rich large B‐cell lymphoma.
Modulation of alloimmune response in vitro by an IgM‐enriched immunoglobulin preparation (Pentaglobin)
Authors: Nachbaur D. , Herold M. , Gächter A. , Niederwieser D. 
Published: March 2003

The mode of action of intravenous immunoglobulins (IVIG) in autoimmune and immunoregulatory disorders is still poorly understood. In vitro, direct effects of IVIG on cytokine release and on cytokine receptors have been described, as well as naturally occurring, neutralizing anti‐cytokine antibodies. The aim of our study was to investigate whether the enrichment in IgM and IgA would have any impact on the in vitro immunomodilatory capacity of IVIG. The preparation tested (Pentaglobin) contains 76% IgG and 12% IgM and IgA, respectively. We could demonstrate a significant inhibition of alloantigen‐induced proliferation in the mixed lymphocyte reaction (MLR) even at a Pentaglobin concentration of 1·0 mg/ml. About 10‐fold higher concentrations of standard 7S IVIG containing only trace amounts of IgM and IgA were necessary to achieve equivalent suppression of the alloimmune response. Similarly, phytohaemagglutinin (PHA)‐induced lymphocyte proliferation was more effectively inhibited by Pentaglobin than by standard 7S IVIG. Cytokine analyses in culture supernatants of MLR provide evidence that Pentaglobin not only modulates interleukin‐2 (IL‐2), which has already been observed with standard 7S IVIG, but, moreover, modulates interferon‐γ production with a subsequent impact on monocyte‐derived tumour necrosis factor‐α and IL‐6 release. Based on these results we conclude that in vitro the IgM‐ and IgA‐enriched Pentaglobin has a more potent immunomodulatory capacity than conventionally used standard 7S IVIG.BMT, bone marrow transplantation, GVHD, graft‐versus‐host diseaseIFN, interferonIL, interleukinIVIG, intravenous immunoglobulinMLRmixed lymphocyte reactionPHA, phytohaemagglutininTNF, tumour necrosis factor.
Immunomodulatory effect of a plasmid expressing CD40 ligand on DNA vaccination against human immunodeficiency virus type‐1
Authors: Ihata A. , Watabe S. , Sasaki S. , Shirai A. , Fukushima J. , Hamajima K. , Inoue J. , Okuda K. 
Published: March 2003

SummaryCD40 ligand is a costimulatory molecule which acts a potent immunomodulator. We found the mice inoculated with human CD40 ligand expression plasmid (pMEhCD40L) combined with human immunodeficiency virus type‐1 (HIV‐1) DNA vaccine exhibited both humoral and cellular antigen‐specific immunological enhancement. The expression of hCD40L induced predominantly antigen‐specific immunoglobulin G (IgG) antibody response while it failed to induce mucosal IgA response. Delayed‐type hypersensitivity (DTH) and cytotoxic T lymphocyte (CTL) activity were induced in a dose‐dependent manner. Examination of the relative levels of the two IgG subclasses showed that co‐injection of pMEhCD40L enhanced IgG2a response without suppressing IgG1 response. Similarly, the expression of pMEhCD40L enhanced not only T helper 1 (Th1)‐ but also Th2‐type cytokine production. In conclusion, co‐inoculation of pMEhCD40L with DNA vaccine was shown to be a useful way to enhance CTL responses without suppressing the humoral immune response in acquired immune deficiency syndrome (AIDS) patients.
Granulocyte–macrophage colony‐stimulating factor modulates lipopolysaccharide (LPS)‐binding and LPS‐response of human macrophages: inverse regulation of tumour necrosis factor‐α and interleukin‐10
Authors: Kreutz M. , Hennemann B. , Ackermann U. , Grage‐griebenow E. , Krause S. W. , Andreesen R. 
Published: March 2003

SummaryGranulocyte–macrophage colony‐stimulating factor (GM‐CSF) is a well‐known stimulus for the activation, differentiation and survival of monocytes (MO). Up to now most investigations focused on the short‐term effects of GM‐CSF. In this study we investigated the effects of GM‐CSF on the long‐term differentiation of human MO in the presence of serum. We found that MO‐derived macrophages (Mφ) cultured with serum plus GM‐CSF (GM‐Mφ) were different from control Mφ (SER‐Mφ) in terms of lipopolysaccharide (LPS)‐stimulated cytokine release: GM‐Mφ showed an increased tumour necrosis factor‐α (TNF‐α) and interleukin‐6 (IL‐6) production, especially at lower LPS concentrations, but the secretion of IL‐10 was diminished. In addition, GM‐Mφ secreted TNF‐α but not IL‐6 and IL‐10, spontaneously. The spontaneous TNF‐α production was not due to LPS contamination as it could not be blocked by anti‐CD14 antibody. Flow cytometry revealed, however, that the receptor for LPS, CD14, was up‐regulated on GM‐Mφ and those Mφ released twice as much soluble CD14 into the supernatant as compared with SER‐Mφ. The higher CD14 expression also resulted in an enhanced LPS‐binding capacity of GM‐Mφ. Furthermore, the LPS‐response of GM‐Mφ could only be blocked by about fourfold higher concentration of anti‐CD14 antibody compared with SER‐Mφ. In summary, GM‐CSF promotes the generation of a pro‐inflammatory type of Mφ in two different ways: first, the down‐regulation of autocrine IL‐10 production increases the release of cytokines such as IL‐6 and TNF‐α and second, the up‐regulation of membrane and soluble CD14 expression leads to a higher sensitivity towards LPS‐stimulation.
Transcriptional and post‐transcriptional regulation of monocyte chemoattractant protein‐3 gene expression in human endothelial cells by phorbol ester andcAMP signalling
Authors: Kondo A. , Isaji S. , Nishimura Y. , Tanaka T. 
Published: March 2003

SummaryMonocyte chemoattractant protein‐3 (MCP‐3) is one of the most broadly active chemokines, potentially inducing chemotaxis of all leucocytic cells. In the present study, we examined the regulation of MCP‐3 mRNA and protein production in endothelial cells by protein kinase C (PKC) activator, phorbol 12‐myristate 13‐acetate (PMA) and cAMP signalling. On stimulation of endothelial cells with 10 n m PMA, MCP‐3 mRNA increased to 300‐fold the basal level at 3 hr and rapidly declined to 0·2‐fold the basal level at 24 hr. PMA‐induced MCP‐3 mRNA and protein production of human endothelial cells were partially inhibited by pretreatment with the adenylate cyclase activator, forskolin, or membrane‐permeable cAMP derivative. The PMA‐induced MCP‐3 mRNA increase was almost abrogated when cells were pretreated with cycloheximide (CHX). Forskolin inhibited the transcription of PMA‐induced MCP‐3 gene expression. Following PMA stimulation for 3 hr, subsequent addition of actinomycin D suppressed the rapid decay of PMA‐induced MCP‐3 mRNA. These results suggest that PMA induces the transcriptional activation of the MCP‐3 gene through de novo protein synthesis and the rapid decay of PMA‐induced MCP‐3 mRNA through de novo synthesis of adenosine/uridine (AU)‐rich element binding proteins and cAMP signalling inhibits the PMA‐induced transcriptional activation of the MCP‐3 gene expression.