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D Hénin

Publications and source records attributed to D Hénin.

At least 37 records · Page 2Linked to original sources
PubMed1999

Report of a fatal case of dengue infection with hepatitis: demonstration of dengue antigens in hepatocytes and liver apoptosis.

A fatal case of dengue (DEN) infection associated with a spleen rupture and with hepatitis is reported here. Microscopic studies showed numerous areas of spleen rupture with hematomas and revealed necrotic foci in liver samples obtained at autopsy. Although hepatitis was reported in several cases of DEN fever, the mechanism of liver injury remains poorly understood. In this case, immunohistochemistry showed that DEN viral antigens were mostly detected in hepatocytes surrounding the necrotic foci. By in situ detection of DNA fragmentation, apoptotic hepatocytes were found to be colocated with DEN virus-infected hepatocytes. These findings suggest that hepatocytes are the major sites of DEN virus replication in the liver and that DEN virus induces apoptosis of hepatocytes in vivo.

Adult↗
PubMed1998

Primary central nervous system lymphomas in 72 immunocompetent patients: pathologic findings and clinical correlations. Groupe Ouest Est d'étude des Leucénies et Autres Maladies du Sang (GOELAMS)

We reviewed 72 primary central nervous system lymphomas occurring in immunocompetent patients. The cases were reviewed for clinical data, histology, immunophenotype, bcl-2 and p53 expression, and Epstein-Barr virus association. Follow-up was available for 40 patients included in the Groupe Ouest Est d'étude des Leucénies et Autres Maladies du Sang (GOELAMS) lymphomes cérébraux primitifs (LCP 88) trial. Each diagnosis, requiring a consensus among at least 3 pathologists, was performed according to the recent Revised European-American Lymphoma classification and equivalents in the updated Kiel classification. Tumors were predominantly classified as diffuse large B-cell lymphomas. There were 3 T-cell lymphomas and 1 Hodgkin lymphoma. The proteins bcl-2 and p53 were expressed in 35% and 16% of the tested cases, respectively. Epstein-Barr virus was not found by in situ hybridization except in the case classfied as a cerebral localization of Hodgkin disease. No significant association was found between subtypes, bcl-2 or p53 expression, and patient survival. From the standpoint of their biologic characteristics, primary central nervous system lymphomas are very similar to systemic diffuse large B-cell lymphomas. In contrast to AIDS-related primary central nervous system lymphomas, primary central nervous system lymphomas are rarely associated with Epstein-Barr virus and in immunocompetent patients they express bcl-2 at a relatively low rate.

Adult↗
PubMed1997

Prognostic influence of clinicopathologic features, DNA-ploidy, CD44H and p53 expression in a large series of resected hepatocellular carcinoma in France.

Factors affecting outcome after resection of hepatocellular carcinoma (HCC) in patients from Western countries are not clearly defined. Different clinicopathological factors, including DNA ploidy and expression of p53 and CD44H proteins were evaluated retrospectively in 113 patients undergoing curative resection; 11 clinical and 12 pathological factors were studied. Survival curves were calculated by the Kaplan-Meier method and multivariate analysis of outcome predictors for 103 HCC was assessed by Cox regression. By univariate analysis, survival was significantly better in patients with a high serum albumin level >4.0 g/dl, a normal serum alpha-fetoprotein level and an absence of microscopic vascular invasion by the tumor. In multivariate analysis, only high serum albumin level and absence of vascular invasion were found to be independent favorable predictive factors. CD44H expression was significantly correlated with vascular involvement. However, CD44H and p53 expression did not affect survival. The DNA ploidy pattern showed a bimodal distribution, but did not influence the survival rate. This study suggests that pre-operative level of albumin and microscopic vascular invasion can predict long-term survival in patients who have undergone curative resection for HCC. By contrast, the DNA-ploidy pattern and the immunohistochemical detection of p53 and CD44H expression are not predictors of outcome of patients with HCC.

Adolescent↗
PubMed1997

Chronic esophagitis dissecans: an unrecognized clinicopathologic entity?

BACKGROUND: We report the clinical and histologic features of a distinctive form of chronic esophagitis for which we propose the term chronic esophagitis dissecans. METHODS: The study group included five patients diagnosed at Hôpital Beaujon, Clichy, from 1988 to 1994. Clinical and endoscopic examinations were performed. Samples of esophageal biopsy specimens were analyzed by histologic and ultrastructural examinations and by immunohistochemistry with antibodies directed against cell adhesion molecules. RESULTS: All patients were elderly (mean age, 66 years). They presented the following combination of clinical and endoscopic features: (1) long-standing history of chronic dysphagia, without symptoms of reflux, (2) shedding of mucosal fragments, occurring spontaneously or after mechanical trauma, (3) existence of localized esophageal strictures, (4) lack of concurrent chronic cutaneomucous lesions. Two patients presented with thymoma. Histologic examination showed evidence of mucosal blistering, in the absence of significant inflammatory lesions. Altered cell-cell adhesion was suggested by the reduced number of desmosomes on ultrastructural examination and the decreased expression of immunoreactive intercellular adhesion molecule E-cadherin. CONCLUSION: Chronic esophagitis dissecans likely represents a hitherto unrecognized clinicopathologic entity and must be added to the causes of chronic dysphagia.

Aged↗
PubMed1997

Interphase cytogenetic analysis reveals numerical chromosome aberrations in large liver cell dysplasia.

BACKGROUND/AIMS: Little is known about genetic alterations in large or small liver cell dysplasia. The aim of this study was to determine whether these lesions present numerical chromosome aberrations. METHODS: Eight patients with hepatocellular carcinoma on cirrhosis, five with large liver cell dysplasia and three with small liver cell dysplasia, were analysed by in situ hybridization with different centromeric nucleic acid probes specific respectively for chromosomes 1, 7, 17 and 18. In each case results were compared between dysplastic, tumoral and non-dysplastic cirrhotic cells. Four normal livers were also studied with the same method and served as cytogenetic controls. RESULTS: All cases of large liver cell dysplasia dysplayed a polysomic population for each investigated chromosome. A high variability of numerical chromosome aberrations was observed with a copy number of chromosomes which ranged from two to more than six. By contrast, only one case of small liver cell dysplasia showed chromosomal anomalies. Numerical aberrations of at least one chromosome were observed in six of the eight hepatocellular carcinoma while the non-dysplastic cirrhosis and normal liver always showed a diploid pattern. CONCLUSIONS: These results demonstrate that cellular modifications in large liver cell dysplasia coexist with an early acquisition of genomic alterations, supporting the view that these phenotypic changes are preneoplastic.

Adult↗
PubMed1997

Expression of cell adhesion molecules by microvascular endothelial cells in the cortical and subcortical regions of the normal human brain: an immunohistochemical analysis.

We studied the repertoire of junctional, cell-matrix and leucocyte-endothelial adhesion molecules normally expressed by cortical and subcortical brain microvessels, as compared with large intracranial vessels. An indirect immunoperoxidase method was applied to acetone-fixed cryostat sections of normal brain tissue obtained from 10 adult patients during surgical resections for intracranial aneurysms or at autopsy. Like large intracranial vessels, brain microvessels expressed the two endothelial-specific junctional cell adhesion molecules VE-cadherin and platelet-cell adhesion molecule-1. We verified that they also expressed the molecular components of adherens-type junctions, including catenins, plakoglobin, vinculin and alpha-actinin. Brain microvessels expressed a large repertoire of integrin molecules of the beta 1, beta 3 and beta 4 subfamilies. However, they displayed apparently lower levels of alpha 2, alpha 5, alpha V and beta 3 integrin chains than large intracranial vessels. Brain microvessels constitutively expressed large amounts of the leucocyte-endothelial adhesion molecules, intercellular adhesion molecule (ICAM)-2 and CD34 and very low amounts of ICAM-1 and lymphocyte function-associated antigen-3. In contrast to large intracranial vessels, brain microvessels presented no constitutive expression of P-selectin. Our study shows that, in contrast to their highly specific structural and functional characteristics, brain microvascular endothelial cells present a repertoire of cell adhesion molecules very similar to that of most other capillary vessels in the body.

Adult↗
PubMed1996

p53 protein expression and DNA ploidy in cystic tumors of the pancreas.

Cystic tumors of the pancreas form a heterogeneous group, with benign, premalignant, and malignant tumors. The molecular events that underlie their neoplastic transformation process are poorly understood. Our purpose was to study DNA ploidy by flow cytometry and p53 protein expression by immunohistochemistry in a large series of cystic tumors of the pancreas. The series of 51 surgical specimens included 18 serous cystadenomas, 20 mucinous cystic tumors (benign, n = 14; borderline, n = 1; malignant, n = 5), 10 intraductal papillary-mucinous tumors (benign, n = 4; borderline, n = 1; malignant, n = 5), and 3 papillary and cystic tumors. The p53 protein immunohistochemical study was done in all cases on deparaffinized sections stained with the monoclonal antibody DO7. DNA flow cytometry was performed in 31 cases on formalin-fixed and paraffinembedded material. Neither p53 protein immunoreactivity nor DNA aneuploidy was observed in any case of serous cystadenoma. p53 protein overexpression was present in four of five malignant mucinous cystic tumors but was absent in benign and borderline cases. Only one case of malignant mucinous cystic tumor was DNA aneuploid. All benign and borderline intraductal papillary-mucinous tumors were p53 negative, and two of five malignant cases were p53 positive. There was no DNA aneuploidy in any case of intraductal papillary-mucinous tumors. The three cases of papillary-cystic tumors showed neither p53 protein immunoreactivity nor DNA aneuploidy. In cystic tumors of the pancreas, p53 protein overexpression and DNA aneuploidy are rare events, restricted to malignant cases, mostly mucinous cystadenocarcinomas. Our results confirm that this group of tumors is heterogeneous and underline the need for earlier markers of an aggressive behavior.

Adult↗
PubMed1996

Increased expression of CD44v6 in endocrine pancreatic tumours but not in midgut carcinoid tumours.

Aims/background-To analyse the different isoforms of CD44 in various types of endocrine pancreatic and gut carcinoid tumours and to investigate the relation between their expression and tumour dissemination. This study was prompted by the recent observation that inappropriate splicing of the CD44 gene was correlated with tumour progression and metastasis formation in a number of human cancers.Methods-Expression of CD44 isoforms was studied in 38 endocrine pancreatic tumours and gut neuroendocrine tumours using antibodies directed against products of exons v3, v4-v5, v6, v7-v8 as well as against the standard CD44 molecule (CD44H). CD44 gene expression was also analysed by reverse transcription PCR (RT-PCR) in nine endocrine and seven carcinoid tumours.Results-All gastrinomas except one (nine of 10) and about half of the other endocrine pancreatic tumours (seven of 15) expressed CD44v6. Most (10/11) midgut carcinoid tumours were CD44v6 negative, with no detectable immunostaining. CD44v3, CD44v4-v5 and CD44v7-v8 were not expressed in any of these tumours. CD44 mRNA analysis illustrated a complex splice pattern and expression of large CD44 isoforms in CD44v6 positive endocrine tumours, whereas the standard form only was detected in midgut carcinoid tumours. No correlation between CD44 variant expression and tumour metastasis was observed.Conclusions-CD44 variants encoding exon v6 are preferentially expressed both in gastrinomas and in most pancreatic endocrine tumours. In contrast to other tumours, the expression of CD44v6 in pancreatic neuroendocrine tumours does not seem to be correlated with tumour dissemination.

Journal Article↗
PubMed1996

Hepatic angiomyolipoma. A report of four cases with immunohistochemical and DNA-flow cytometric studies.

OBJECTIVE: To describe the pathologic features in four cases of hepatic angiomyolipoma, a rare benign mesenchymal tumor of the liver. DESIGN: Retrospective analysis of surgical specimens from four patients, with immunohistochemical and flow cytometric studies. RESULTS: None of the patients carried a diagnosis of tuberous sclerosis. All four tumors were large and well circumscribed, and one patient had multiple lesions. The neoplasms were composed of numerous vessels and exhibited a predominance of epithelioid smooth muscle cells. The low amount of fat in these four cases was not sufficient to produce characteristic images that would allow diagnosis of angiomyolipoma before surgical resection. All tumors exhibited strong staining with HMB45 and anti-smooth muscle actin antibodies, whereas no positivity was observed with estrogen and progesterone receptor antibodies. Flow cytometry revealed a diploid DNA pattern in all cases. CONCLUSIONS: Our four cases demonstrate that it is difficult to differentiate hepatic angiomyolipoma from other liver tumors when the amount of fat is low. HMB45 positivity of smooth muscle cells appears to be very helpful in reaching a pathological diagnosis of hepatic angiomyolipoma. The DNA-diploid pattern observed in all cases could be considered a new argument for the benign nature of hepatic angiomyolipoma.

Actins↗
PubMed1996

Lymphocytic and collagenous colitis: an immunohistochemical study.

OBJECTIVES: An increase of intraepithelial lymphocytes (IEL) is commonly found in lymphocytic colitis (LC) and collagenous colitis (CC), and has also been observed in the colonic mucosa of some patients with celiac disease or celiac-like disease. Thus, a similar mechanism could play a role in these apparently different entities. The aim of this work was to determine the phenotype of IEL and of lamina propria lymphocytes in the setting of LC and CC. METHODS: Biopsies were taken from all segments of the large bowel and from the ileon of eight patients with CC, four patients with LC, and 10 controls. An immunohistochemical study using monoclonal antibodies directed against IEL, T-cells, helper T-cells, suppressor/cytotoxic T-cells, HLA DR antigens, T-cell-bearing T-cell receptor (TcR) alpha beta, and TcR gamma delta was carried out. RESULTS: There was an increased in mean numbers of IELs in both LC and CC, with significantly more CD 8 IELs than CD 4 IELs. Most IELs were bearing TcR alpha beta; TcR gamma delta-bearing cells were not increased in CC or LC. CD 4+ helper T-cells predominated in the lamina propria. Epithelial cells of colonic mucosa abnormally expressed HLA DR antigens. There were no significant differences between findings in LC and CC. CONCLUSION: This study suggests that the immune abnormalities are similar in LC and CC and that a MHC-restricted immune mechanism could be involved in both diseases. Evidence for this includes: 1) the accumulation of CD 4+ T-cells within the lamina propria, 2) epithelial damage closely related to the increase of CD 8 TcR alpha beta IELs, and 3) abnormal class II MHC molecule expression on epithelial cells of colonic mucosa. Furthermore, the results suggest that the putative immune mechanisms underlying LC or CC are probably different from those that are incriminated in celiac disease.

Adult↗
PubMed1995

PML nuclear bodies are general targets for inflammation and cell proliferation.

Acute promyelocytic leukemia is associated with a t(15;17) translocation that generates a fusion product between PML and the retinoic acid receptor alpha. Recently, PML was shown to concentrate within subnuclear domains, referred to as nuclear bodies, that are disorganized in acute promyelocytic leukemia cells. This observation provided the first evidence that alteration of a nuclear structure may play a role in human pathogenesis. In an attempt to clarify the role of PML and, more generally, of the associated nuclear bodies, we used immunohistochemistry to explore the expression of PML in normal, inflammatory, and neoplastic human tissues. With the exception of endothelial cells and macrophages that contain a high amount of PML protein, a weak speckled labeling pattern was observed in the nucleus of all cell types analyzed. By contrast to normal tissues, the level of PML expression was considerably enhanced in inflammatory tissues, predominantly around the mononuclear cell infiltrate, as well as during either normal or pathological proliferative states, in particular in tumoral pathology. Surprisingly, in most hepatocellular carcinoma, a cytoplasmic delocalization of PML was observed. Finally, the number of PML nuclear bodies increased up to twice their normal value as quiescent cultured cells were stimulated to grow upon serum addition. Altogether these results strongly suggest that the PML-associated nuclear bodies are implicated both in the inflammatory process and in cell growth control.

Adenocarcinoma↗
PubMed1995

Absence of c-Ki-ras gene mutation in malignant and premalignant Barrett's oesophagus.

Aims-To establish the prevalence of c-Ki-ras gene mutations in codons 12 and 13 in 28 surgically resected Barrett's adenocarcinomas and 18 associated preneoplastic lesions in Barrett's oesophagus.Methods-Mutations were detected using the polymerase chain reaction followed by restriction fragment length polymorphism analysis. Human colon carcinoma cell lines with well characterised mutations in codons 12 and 13 were used as positive controls and to test the sensitivity of the method.Results-c-Ki-ras gene mutations were not detected in any of the 28 specimens of Barrett's adenocarcinoma or in the 18 specimens of Barrett's oesophagus (nine non-dysplastic cases, three cases with low and six with high grade dysplasia).Conclusions-These results suggest that the c-Ki-ras gene is not involved in the development of cancer in Barrett's oesophagus.

Journal Article↗
PubMed1994

Otogenic meningoencephalitis induced by Streptococcus pneumoniae in gerbils.

OBJECTIVE: Study and development of a gerbil model of pneumococcal meningoencephalitis secondary to acute middle ear (ME) otitis. Preliminary data raised the hypothesis of a direct bacterial dissemination from the ME focus to the central nervous system. This infection pattern was examined. DESIGN: Animals were inoculated bilaterally by transbulla challenge with a serotype 3 strain of Streptococcus pneumoniae at various inoculum sizes. The incidence and course of meningeal complications were studied in relation to the course of ME otitis. RESULTS: After inoculation of 40 bacteria per ear, lethal meningeal complications occurred in 14 (29%) of 48 cases. A 76% rate (25 of 33 animals) of early meningeal involvement was observed after inoculation of 10(4) bacteria per ear. Actual involvement of brain was confirmed histologically for both infection schemes. Bacterial counts 20 to 22 hours after infection with the higher inoculum showed various phases of the extension of the ME infection to brain tissue, cerebrospinal fluid, and bloodstream. Bacterial counts in ME and brain tissue were strongly correlated (P < .001). Nine of the 25 animals with infection of the central nervous system had positive brain tissue cultures without bacteremia. CONCLUSION: Gradations in inflammatory aspects of the meninges and cerebral parenchyma, together with bacteriologic findings, indicate a primary invasion of meningeal spaces that can result in lethal encephalitis and septicemia. This model might be useful for preclinical therapeutic assays on pneumococcal meningeal complications, including infections due to strains with abnormal susceptibility to antibiotics.

Animals↗
PubMed1994

Overexpression of the p53 tumor suppressor gene product in esophageal and gastric carcinomas.

PURPOSE: p53 protein has been reported as frequently overexpressed in esophageal and gastric carcinomas. However, the correlation between p53 protein expression and clinico-pathological features of the tumors is debated in this heterogeneous group of cancers. The aim of this study was to establish the prevalence of p53 protein overexpression in a series of resected esophageal squamous carcinomas (n = 78), adenocarcinomas developed on Barrett's esophagus (n = 20), adenocarcinomas of the cardia (n = 36), and adenocarcinomas of the antrum (n = 30), and to correlate this expression with the clinico-pathological and flow-cytometric characteristics of the tumors. METHODS: Immunohistochemical staining was performed on frozen sections with a monoclonal antibody directed against wild type and mutated p53 protein (Pab 1801). An adjacent frozen specimen was used for flow cytometric determination of the DNA-ploidy and S phase fraction. RESULTS: p53 protein nuclear expression was detected in 76% of esophageal squamous carcinomas, in 75% of adenocarcinomas developed in Barretts esophagus, in 56% of adenocarcinomas of the cardia, and in 27% of adenocarcinomas of the antrum. Only the number of positive adenocarcinomas of the antrum was significantly lower when compared to the other three types of tumors (p = 0.001). No significant correlation was observed between p53 protein expression and most of the clinico-pathological and flow-cytometric parameters (sex, age, tobacco smoking, chronic alcohol consumption, size of the tumor, grade of differentiation, depth of infiltration, presence of lymph node metastases, UICC stage, DNA-ploidy, S phase fraction). p53 protein expression was more frequent in Lauren's intestinal adenocarcinomas (67%) when compared to the diffuse type tumors (24%) (p = 0.002). CONCLUSIONS: Our results confirm that overexpression of p53 protein is a common feature of esophageal and gastric carcinomas. The high prevalence of p53 protein overexpression found in cardiac adenocarcinoma when compared to antral adenocarcinoma reinforces the hypothesis of distinct carcinogenetic mechanisms in these two cancers. In particular the lack of correlation between p53 expression and tumor stage suggests that p53 protein overexpression is an early event in these tumors.

Adenocarcinoma↗