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B Terris

Publications and source records attributed to B Terris.

At least 55 records · Page 3Linked to original sources
PubMed1999

Focal nodular hyperplasia of the liver: a comprehensive pathologic study of 305 lesions and recognition of new histologic forms.

Atypical histologic variants of focal nodular hyperplasia have been reported and are sometimes difficult to recognize. To characterize the morphologic spectrum of focal nodular hyperplasia, we studied 305 lesions surgically resected from 168 patients. Clinicomorphologic correlations were established by statistical analyses. The patients included 150 women and 18 men (sex ratio, 8:1; median age, 38 years). One hundred twenty-eight (76.2%) patients had solitary lesions, and 40 (23.8%) had 2 to 30 lesions. All 305 lesions measured 1 mm to 19 cm in diameter. Only 49% of these lesions had one to three macroscopic scars. Histologically, 245 (80.3%) lesions were of classical form, and 60 (19.7%) lesions were nonclassical. The latter were classified as focal nodular hyperplasia of telangiectatic form (47 lesions), of mixed hyperplastic and adenomatous form (five lesions), and with atypia of large cell type (eight lesions). Several benign or malignant tumors were found in association with these lesions. This large retrospective series of focal nodular hyperplasia shows the relative incidence of its classical and nonclassical forms. The absence of a central scar could explain the difficult preoperative diagnosis of some of the cases. The morphologic diagnostic criteria in this study require further prospective evaluation.

Adolescent↗
PubMed1999

Epithelioid hemangioendothelioma, multiple focal nodular hyperplasias, and cavernous hemangiomas of the liver.

Malignant vascular neoplasms of the liver are uncommon. We report the case of a young woman who developed an epithelioid hemangioendothelioma of the liver associated with multiple focal nodular hyperplasias and hepatic cavernous hemangiomas. Such an unusual association is probably not fortuitous and could support the theory that focal nodular hyperplasia is a reaction to an abnormal vascular supply rather than a true neoplasm.

Adult↗
PubMed1998

Comparative genomic hybridization analysis of sporadic neuroendocrine tumors of the digestive system.

Little information is available on the molecular mechanisms underlying neuroendocrine tumorigenesis. To obtain an overview of the genomic imbalances characterizing these tumors, we studied 20 benign or malignant sporadic endocrine gastroenteropancreatic tumors by comparative genomic hybridization. Chromosomal imbalances were found in all tumors. Gains of chromosomal material were more frequent than losses. The most frequent gains were of chromosomes and chromosome arms 5 (55%), 14 (55%), 17q (55%), and 7 (50%). Losses were most frequent from 11q (30%) and 16p (30%). Gains of chromosome 5 did not occur in nonmetastatic tumors, whereas losses of 9p were observed exclusively in intestinal tumors. In addition, we found two high-level amplifications, of 17q11-21 and 19q13. A complementary FISH analysis revealed that the gain in 17q11-21 included amplification of the protooncogene HER2/neu. As in multiple endocrine neoplasia type-1-associated tumors, deletions of chromosome band 11q13 appear to be involved in the development of sporadic digestive tract neuroendocrine tumors, but our results suggest that other chromosomal regions are also involved.

Adolescent↗
PubMed1998

Effects of diclofenac on experimental streptococcal necrotizing fasciitis (NF) in rabbit.

Aggravation of necrotizing fasciitis (NF) by the administration of non-steroidal antiinflammatory drugs (NSAIDs) has recently been suggested. A rabbit model of streptococcal NF was used to study the effects of parenteral administration of an NSAID on NF evolution and outcome. Of 16 rabbits inoculated with a Streptococcus pyogenes suspension together with staphylococcal alpha toxin, 8 were treated with two doses of 4 mg/kg diclofenac on day 1 after inoculation. Clinical, bacteriological and histological studies were performed until day 10. Under our experimental conditions, NSAID treatment significantly limited NF extension. A specific inverse relationship between the extent of inflammation and bacterial density in NF lesions was observed on day 1 after inoculation in the treated group suggesting that the greater severity of NF in humans treated with an NSAID could be due to the therapeutic delay induced by the misleading clinical effects of the NSAID, and not to inhibition of antibacterial defence.

Animals↗
PubMed1998

Association of serum antibodies against p53 protein with poor survival in patients with Zollinger-Ellison syndrome.

BACKGROUND & AIMS: Long-term survival of patients with Zollinger-Ellison syndrome (ZES) is largely determined by the presence or absence of liver metastases. However, because of the lack of precision of these criteria, development of further indicators is still required. Recent evidence showing that autoantibodies directed against the p53 protein could predict poor survival for some types of cancers prompted us to investigate the presence of such antibodies in sera from patients with ZES and their potential value as survival indicator. METHODS: Anti-p53 antibodies were detected in the sera of 44 consecutive patients with ZES using both an enzyme-linked immunosorbent assay (ELISA) and Western blotting. The mean follow-up of these patients was 92 months. RESULTS: Anti-p53 antibodies were detected in 7 of the patients with ZES (16%) by both ELISA and Western blotting. Univariate and multivariate analyses showed that the presence of anti-p53 antibodies (P = 0.0009 and P = 0.017, respectively) and liver metastases (P = 0.0009 and P = 0.012, respectively) was independently associated with shorter survival. CONCLUSIONS: These results suggest that anti-p53 antibodies are an indicator of survival and could be used in combination with staging to determine which patients with ZES have poor prognoses and therefore require reinforced therapy.

Adult↗
PubMed1998

Expression of vascular endothelial growth factor in digestive neuroendocrine tumours.

AIMS: Angiogenesis is a complex multistep process essential for tumour growth. Vascular endothelial growth factor (VEGF) is a potent endothelial cell mitogen and vascular permeability-inducing agent. Recent studies have shown that VEGF expression is correlated to microvessel density and tumour progression. The aim of this study was to analyse VEGF expression in a series of gastrointestinal neuroendocrine tumours. METHODS AND RESULTS: Surgical specimens from 28 gastrointestinal carcinoids and 20 pancreatic endocrine tumours were examined for VEGF expression by immunohistochemistry. Intense cytoplasmic staining for VEGF was observed in several cells of the islets of Langerhans and in neuroendocrine cells of normal digestive mucosa. All midgut carcinoids showed strong VEGF expression in tumoral cells. Positive VEGF immunostaining was observed in 16 of 20 neuroendocrine pancreatic tumours but it was usually much lower than in midgut carcinoids. Western blotting analysis in eight cases identified a major band at 30-32 kDa. No correlation between VEGF expression and tumour stage was found. CONCLUSIONS: This study demonstrates that neuroendocrine cells are a major source of VEGF, particularly in midgut carcinoids. This finding suggests that the presence of VEGF may be required to maintain the differentiated state of capillary vessels in these hypervascular tumours. Such secretion, in conjunction with the other growth factors synthesized by these neuroendocrine tumours, may have an important role in tumour growth.

Adult↗
PubMed1998

Prognostic factors in patients with endocrine tumours of the duodenopancreatic area.

BACKGROUND: The development of endocrine tumours of the duodenopancreatic area (ETDP) is thought to be slow, but their natural history is not well known. The aim of this study was to determine the factors that influence survival of patients with ETDP. PATIENTS/METHODS: Eighty two patients with ETDP (44 non-functioning tumours, 23 gastrinomas, seven calcitonin-secreting tumours, four glucagonomas, three insulinomas, one somatostatinoma) followed from October 1991 to June 1997 were included in the study. The following factors were investigated: primary tumour size, hormonal clinical syndrome, liver metastases, lymph node metastases, extranodular/extrahepatic metastases, progression of liver metastases, local invasion, complete resection of the primary tumour, and degree of tumoral differentiation. The prognostic significance of these factors was investigated by uni- and multi-variate analysis. RESULTS: Twenty eight patients (34%) died within a median of 17 months (range 1-110) from diagnosis. Liver metastases (p = 0.001), lymph node metastases (p = 0.001), progression of liver metastases (p < 0.00001), lack of complete resection of the primary tumour (p = 0.001), extranodular/extrahepatic metastases (p = 0.001), local invasion (p = 0.001), primary tumour size > or = 3 cm (p = 0.001), non-functioning tumours (p = 0.02), and poor tumoral differentiation (p = 0.006) were associated with an unfavourable outcome by univariate analysis. Multivariate analysis identified only liver metastases (risk ratio (RR) = 8.3; p < 0.0001), poor tumoral cell differentiation (RR = 8.1; p = 0.0001), and lack of complete resection of the primary tumour (RR = 4.8; p = 0.0007) as independent risk factors. Five year survival rates were 40 and 100% in patients with and without liver metastases, 85 and 42% in patients with and without complete resection of primary tumour, and 17 and 71% in patients with poor and good tumour cell differentiation respectively. CONCLUSION: Liver metastases are a major prognostic factor in patients with ETDP. Progression of liver metastases is also an important factor which must be taken into account when deciding on the therapeutic approach. The only other independent prognostic factors are tumoral cell differentiation and complete resection of the primary tumour.

Adenoma, Islet Cell↗
PubMed1998

[Gene p53 mutations and overexpression of p53 protein in tumors of the Vater's ampulla].

OBJECTIVES AND METHODS: New prognostic markers for tumors of the ampulla of Vater which could distinguish aggressive lesions would be highly useful. The aim of this study was to evaluate the abnormal expression of p53 protein in a series of 34 ampullomas with the monoclonal antibody DO7 directed against p53 protein. Mutations of exons 5 to 8 of p53 gene were also detected by PCR followed by denaturating gel electrophoresis and sequencing. RESULTS: One of 5 adenomas (20%) and 16 of 29 adenocarcinomas (55%) were p53 positive by immunohistochemistry. A constant feature was the presence of p53 positive glands in the surrounding dysplastic mucosa of p53 positive infiltrative lesions. There was no correlation between p53 immunostaining and tumor stage. Among the 19 tumors analyzed, 6 mutations were detected. CONCLUSION: p53 gene mutations and p53 protein immunoreactivity are frequently present in ampullomas. Because these alterations are not correlated to tumor extension and occur at an early stage in the carcinogenesis, their detection does not appear to be contributive for diagnosis of ampullary tumors.

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

The acute promyelocytic leukemia PML-RAR alpha protein induces hepatic preneoplastic and neoplastic lesions in transgenic mice.

The PML-RAR alpha hybrid protein generated by the t(15;17) translocation in acute promyelocytic leukemia (APL) is thought to play a central role in the oncogenic process. However, analysis of the oncogenic activity of the fusion protein in tissue culture assays or in mice has been hampered by its apparent toxicity in multiple murine cells. To circumvent this problem, we generated an inducible line of transgenic mice, MT135, in which the expression of PML-RAR alpha is driven by the metallothionein promoter. After 5 days zinc stimulation, 27 out of 54 mice developed hepatic preneoplasia and neoplasia including foci of basophilic hepatocytes, dysplasia and carcinoma with a significantly higher incidence of lesions in females than in males. The rapid onset of liver pathologies was dependent on overexpression of the transgene since it was not detected in noninduced transgenic animals of the same age. The PML-RAR alpha protein was always present in altered tissues at much higher levels than in the surrounding normal liver tissues. In addition, overexpression of PML-RAR alpha resulted in a strong proliferative response in the hepatocytes. We conclude that overexpression of PML-RAR alpha deregulates cell proliferation and can induce tumorigenic changes in vivo.

Animals↗
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

Somatostatin receptor subtype gene expression in human endocrine gastroentero-pancreatic tumours.

Somatostatin and its analogues are now of current use in the management of endocrine gastroentero-pancreatic (GEP) tumours for the purpose of inhibiting hormone hypersecretion, carrying scintigraphy imaging and attempting to slow down tumour growth. Recent molecular studies have revealed the existence of up to five membrane somatostatin receptor subtypes termed SSTR1-5. However, whether or not scintigraphy imaging and tumour characteristics are correlated with specific subtype(s) remains unclear. SSTR1-5 messenger RNA (mRNA) transcripts were investigated in 38 endocrine GEP tumours (32 islet cell tumours, six carcinoid) using reverse transcriptase polymerase chain reaction (RT-PCR), and their distribution was analysed with respect to tumour characteristics and scintigraphy imaging. SSTR2, SSTR5 and SSTR4 were detected in most cases of endocrine GEP tumours (92%, 84%, and 82% respectively), but SSTR1 and SSTR3 were less frequently observed (66% and 50% respectively). No clear-cut correlation was found between tumour characteristics and subtype mRNA distribution. Moreover, no differences in mRNA subtype distribution were found between the 17 tumours detected by scintigraphy and the four tumours not detected by this method. Somatostatin receptor mRNA subtypes are widely expressed in endocrine GEP tumours, but their distribution is not correlated with tumour characteristics or scintigraphy positivity.

Adenoma, Islet Cell↗
PubMed1997

[Intraductal papillary mucinous tumors of the pancreas. Clinical and morphological aspects in 30 patients].

AIM: Intraductal papillary-mucinous tumors of the pancreas are rare and characterized by a malignant potential. The aim of this study was to clarify their clinical presentation and the performance of different imaging procedures to determine malignancy and tumor extent. METHODS: Medical records and radiographs of 30 patients with histologically confirmed intraductal papillary-mucinous tumor of the pancreas were reviewed retrospectively. Imaging procedures were compared with pathological data of resected pancreas to evaluate their performances. RESULTS: The most frequent symptom was acute pancreatitis (37%). The onset of symptoms preceded the diagnosis by 2.5 years. Diabetes mellitus and diarrhea were respectively detected in 33 and 23% of the cases. The combination of CT scan, endoscopic retrograde cholangiopancreatography and endosonography allowed correct diagnosis of intraductal papillary-mucinous tumor of the pancreas in 100% of the cases. Tumor extent could be accurately determined considering the location of cystic dilatation of the pancreatic ducts, the presence of intraductal material or parietal irregularity. Actuarial 2-year survival rate was 43% in patients with malignant tumors. Radiological factors predicting malignancy were: vascular invasion, common bile duct dilatation, stricture of the main pancreatic duct and the presence of solid component in the tumor. CONCLUSION: The combination of CT scan, ERCP and endosonography provide accurate diagnosis of intraductal papillary-mucinous tumor of the pancreas as well as assessment of tumor extent and malignancy.

Adenocarcinoma, Mucinous↗
PubMed1997

[Pancreatoblastoma in adults].

Pancreatoblastoma is a rare pancreatic tumor, which usually occurs during childhood. We describe here the ninth adult case in a 21-year-old woman, who died 7 months after diagnosis despite complete surgical resection and adjuvant chemotherapy. Pancreatoblastoma in adults has a poor prognosis, at variance with what may be observed in childhood.

Adult↗
PubMed1996

Interphase cytogenetic studies of human hepatocellular carcinomas by fluorescent in situ hybridization.

Although numerous allelic chromosome losses have been reported in hepatocellular carcinomas (HCC), chromosome analysis by cytogenetic methods has rarely been performed in these tumors, unlike other solid malignant tumors. The purpose of the current study was to analyze primary liver tumors by conventional cytogenetic methods and by a new molecular cytogenetic technique, called fluorescent in situ hybridization (FISH), a technique that has been recently proposed to count the number of chromosome copies in interphase nuclei with chromosome centromeric probes. Primary cultures of tumoral cells were prepared to obtain metaphases. Specific chromosomes probes 7, 17, and 20 were used to perform in situ hybridization on isolated intact tumoral cells. Seven cases of primary liver tumors (six cases of HCC and one case of benign focal hepatic nodular hyperplasia) were investigated. A few metaphases were obtained in five of the seven tumors, and in most cases numerical abnormalities were difficult to interpret. In contrast with in situ hybridization, all cases of HCC showed losses and/or gains of chromosomes. Loss of one to three chromosomes occurred in five tumors. A gain of two chromosomes was observed in two of these five tumors. In only one case, a gain of only three chromosomes occurred. In addition, a loss of chromosome 17 was recorded for the benign tumor. These results demonstrate that FISH with specific probes can provide information on chromosome number in the tumoral cells of primary liver tumors even in the absence of analyzable metaphases. This technique opens new possibilities for the investigation of chromosome abnormalities in HCC.

Adult↗