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F Potet

Publications and source records attributed to F Potet.

At least 19 recordsLinked to original sources

TP53 gene mutations and p53 protein immunoreactivity in malignant and premalignant Barrett's esophagus.

BACKGROUND/AIMS: Limited data are available regarding TP53 gene alterations in Barrett's esophagus. This study was undertaken to characterize TP53 mutations and p53 protein immunoreactivity in cancers and preinvasive lesions of Barrett's esophageal mucosa. METHODS: Seventeen Barrett's adenocarcinomas were examined by polymerase chain reaction amplification, denaturant gradient gel electrophoresis, and sequencing for the presence of TP53 mutations in exons 5-8. In 9 cases, Barrett's epithelium adjacent to the cancer was investigated. p53 protein immunoreactivity was studied with PAb 1801. RESULTS: Sixteen mutations were found in 15 adenocarcinomas, including 10 missense, 3 nonsense, 1 frameshift, and 2 mutations located within consensus splice donor and acceptor sequences. All nucleotide substitutions were transitions. Eight of the 12 transitions involving a GC base pair occurred within the context of a CpG dinucleotide. p53 immunostaining was present in all 10 cases with missense mutations and in 1 case without a detectable mutation. The surrounding Barrett's mucosa showed TP53 mutations identical to that observed in the carcinoma in only 3 of 5 specimens showing high-grade dysplasia. CONCLUSIONS: TP53 gene mutations and p53 protein immunostaining are present in a majority of Barrett's adenocarcinomas. Our results suggest that these mutations are involved at an early stage during malignant transformation of Barrett's esophagus.

Adenocarcinoma

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

[Sensory fibers sensitive to capsaicin can modulate secretion of the duodenal mucus. A morphometric study in rats].

Many in vitro and in vivo models have been used to study the modulation of intestinal mucosecretion. In such studies, quantification of mucus secretion is usually difficult, due to several technical problems. Whether sensory mechanisms participate in the modulation of intestinal mucosecretion remains unknown. The development and assessment of a morphometric method with computer assisted image analysis that allows to detect and quantitate mucin secretion by duodenal goblet cells are reported. Using this method, the secretory effect of pilocarpine on villus and crypt goblet cells was confirmed. We also determined whether sensory neurons can regulate intestinal mucosecretion by using capsaicin, a vegetal neurotoxin specific of a subpopulation of afferent primary sensory neurons. Intravenous capsaicin administration (10 micrograms/kg) increased mucus secretion by the goblet cells of the duodenal crypts. This suggests that sensory neurons may modulate duodenal mucin secretion. The "local effector function" of these neurons might be involved, in part through the release of substance P because exogenous substance P was able to increase mucin excretion by goblets cells of duodenal villi. Substance P, however, did not exactly mimic the capsaicin effects, suggesting that other factors were involved.

Animals

Drug-induced prolonged cholestasis in adults: a histological semiquantitative study demonstrating progressive ductopenia.

Drug-induced acute hepatitis may be followed by prolonged cholestasis despite the withdrawal of the drug. Eight patients suffering from prolonged cholestasis caused by several drugs were investigated with sequential liver biopsies. At the early stage, lesions of acute cholangitis were observed in most patients; at the chronic phase, ductopenia, defined by the absence of interlobular bile ducts in at least 50% of small portal tracts, was demonstrated in all patients. Ductopenia might be the consequence of acute cholangitis; the degree of ductopenia and the chronicity of the disease might be directly related to the severity of the early acute damage of bile ducts. Consequently, in patients with severe cholestasis related to drugs, research of early morphological signs of acute cholangitis and then of ductopenia seems to be important.

Adult

Adenomas arising in Barrett's esophagus with adenocarcinoma. Report of three cases.

Adenocarcinoma of the esophagus is a well known complication of Barrett's esophagus, and results from a dysplasia-carcinoma sequence. This report describes 3 patients with adenomatous polyps arising in Barrett's esophagus. One patient presented with multiple sessile or pedunculated polyps giving a polyposis appearance; the other two patients had single polyps associated with distinct adenocarcinoma arising in Barrett's esophagus. Polyps consisted of adenomatous proliferation with adenocarcinoma in the 3 patients. Review of the literature identified twelve previously reported cases. These cases show that although rare, adenomas may arise in Barrett's esophagus, and are most likely premalignant lesions such as other adenomas of the gastrointestinal tract.

Adenocarcinoma

Concurrent superficial squamous cell carcinoma of the esophagus and early gastric adenocarcinoma. Report of a case.

We report a patient with concurrent superficial carcinomas of the esophagus and stomach. The tumors occurred in a 68-year-old woman. The esophageal tumor was an intramucosal squamous cell carcinoma, and the gastric tumor an intramucosal adenocarcinoma, type III in the Japanese classification of early gastric cancer. This is the first reported case of associated superficial esophageal and gastric cancers originating from a Western country. Such an association may be more frequent than realized, and therefore it is important to examine both the stomach and esophagus if a patient has one of these tumors.

Adenocarcinoma

Acute colitis associated with prolonged administration of neuroleptics.

We describe a 29-year-old patient who developed acute colitis limited to the sigmoid and left colon with features mimicking ischemic injury after a prolonged administration of trifluoroperazine and levomepromazine, two phenothiazines in association with haloperidol, another neuroleptic, and biperidene, an anticholinergic compound. The discontinuation of these drugs was followed by a prompt and complete recovery, and no other cause of acute colitis was found. The subsequent administration of sultopride, a neuroleptic from the benzamide family and then the readministration of haloperidol were well tolerated. No colonic disorder occurred for the following months. This case strongly supports the view that neuroleptic agents, in particular phenothiazines, may induce acute colitis and that haloperidol, a butyrophenone derivative, or sultopride, a benzamide-related neuroleptic, can be administered thereafter without recurrence of the disease.

Adult

[Colonic elastoma. A pathologic study of 7 cases].

The occurrence of elastic tissue abnormalities in the digestive tract is not common. There are sometimes observed in genetically transmitted connective tissue diseases in which numerous systemic complications are associated as in Ehlers-Danlos and in Grönblad-Strandberg syndromes. We report 7 cases of an unusual lesion localized in the colon in which abnormally increased amounts of elastic tissue were observed. This elastosis raises many nosological and diagnostic difficulties. We propose the term "colonic elastoma" to describe this lesion. The review of the literature allows to consider several etiopathogenetic possibilities.

Adult

[Diarrhea with malabsorption and exudative enteropathy caused by intestinal myeloid involvement in a patient with myeloproliferative syndrome].

A 41-year-old woman with a myelodysplastic syndrome complained of diarrhea with malabsorption and protein-losing enteropathy after splenectomy. No cause was found and various therapeutic regimens were not effective. Pathological examination of biopsies from stomach, small intestine, and large bowel showed infiltrations interpreted as inflammatory on routine technics. Blast cell infiltration was found on electron microscopy. Treatment by citarabine induced normalization of leukocytosis, and diarrhea disappeared. Six months after the onset of illness, she developed acute myeloblastic leukemia and died of infectious pneumonia. Blastic infiltration of the lamina propria could be responsible for the determinism of symptoms, because of the lack of another etiology, the intensity of the blastic infiltration and the effect of cytotoxic therapy, even in the absence of new biopsies.

Adult

Esophageal squamous carcinoma in five patients with Barrett's esophagus.

Adenocarcinoma of the esophagus is a well-known complication of Barrett's esophagus. This report describes five patients (three men and two women) with Barrett's esophagus and squamous carcinoma of the esophagus. All patients had hiatal hernia, and three had a history of tobacco and alcohol use. The tumors were located in the Barrett's mucosa in one case, at the squamocolumnar junction in two cases, and in the squamous-lined mucosa above the Barrett's mucosa in two cases. One patient also had focal adenocarcinoma associated with the squamous carcinoma of the esophagus. Review of the literature identified 11 previously reported cases. Occurrence of esophageal squamous carcinoma in Barrett's esophagus patients suggests a possible relationship between these two conditions, and the need for a careful evaluation of the squamous esophageal mucosa and the squamocolumnar junction at the time of endoscopy.

Adenocarcinoma

Pleomorphic carcinoma of the small bowel. The limitations of immunohistochemical specificity.

We report 3 cases of poorly differentiated tumors of the small bowel with histological, immunohistochemical, and ultrastructural studies. The patients were male, aged 45, 57, and 63. In all 3 cases, histological features of spindle cell, epithelioid cell and giant cell areas favoured a diagnosis of carcinoma, although a malignant stromal tumor could not be firmly excluded. Immunohistochemistry demonstrated in the 3 cases a strong expression of both "epithelial" (cytokeratin) and "stromal" (vimentin) markers; one tumor expressed the epithelial membrane antigen, and another one desmin. Electron microscopy showed no specific features in one case. The case positive for desmin demonstrated intracytoplasmic lumina, allowing the diagnosis of carcinoma. In spite of a non-specific immunohistochemical pattern, we finally considered these 3 tumors as of epithelial origin, corresponding to the rare and recently described pleomorphic carcinoma of the small bowel. This report emphasizes the difficult diagnosis of some poorly differentiated tumors, particularly in the gastro-intestinal tract. Such problems had until recently been resolved by ultrastructural and mostly by immunohistochemical studies. However, an increasing number of reports, together with our 3 cases, show unexpected reactivity of tumors with theoretically specific immunoreactions, such as those directed against intermediate filaments. Coexpression of intermediate filaments could be due to cross reactivity of molecules bearing common epitopes, or to the presence of different filaments in the same cell type; recent immunoblotting studies favour this latter hypothesis.

Carcinoma

Recurrence of Fabry's disease in a renal allograft eleven years after successful renal transplantation.

A case of Fabry's disease in a renal transplant recipient with a follow-up period of 11 years is reported. The patient suffered from renal, skin, peripheral nerve lesions, and asymptomatic cardiomegaly. Fabry's disease symptoms disappeared after transplantation. Improvement of renal function was rapidly observed, and it remained satisfactory during the whole posttransplantation period. The patient died of a severe, uncontrolled infection and of biliary peritonitis. Autopsy showed a polyvisceral accumulation of sphingolipids deposits. The engrafted kidney was histologically free of disease. Ultrastructurally, it revealed numerous sphingolipid inclusions in the endothelial cells of capillaries. The explanation of this complication could be attributed to: (1) high circulating levels of plasma substrates locally overwhelming the enzymatic capability of the graft endothelial cells; and (2) the endothelial cells originated from the recipient but not from the donor, an occurrence that has been described after transplantation. Rejection and the newly formed deposits in the endothelial cells may lead to the loss of the engrafted organ. As a consequence of the increasing possibility of organ transplantation, this complication should be detected by studying the blood vessels ultrastructurally in order to evaluate the condition of the transplant.

Adolescent

Hypertrophic gastropathy with gastric adenocarcinoma: Menetrier's disease and lymphocytic gastritis?

Lymphocytic gastritis is a form of gastric inflammation characterised by a pronounced increase in lymphocytes in gastric surface and foveolar epithelium. Lymphocytic gastritis is often associated with endoscopic evidence of 'varioliform gastritis'. Lymphocytic gastritis has recently been reported to be associated with other forms of hypertrophic gastropathies. We present a case of hypertrophic gastropathy with gastric adenocarcinoma, with both Menetrier's disease and lymphocyte gastritis. Immunohistochemical studies showed that the intraepithelial lymphocytes were predominantly alpha/beta T cells as in the normal stomach and not gamma/delta T cells as in coeliac sprue. This case together with the six recently published cases suggests that Menetrier's disease and lymphocytic gastritis may be part of the same disease spectrum.

Adenocarcinoma