Biomedical subjects

Fausto Sessa

Publications and source records attributed to Fausto Sessa.

7 recordsLinked to original sources

PubMed2006

Ten year survival after excision of squamous cell cancer in Zenker's diverticulum: report of a case.

BACKGROUND: Zenker's diverticulum (ZD) has been increasingly recognized as a site of primary epithelial malignancy. Pitt in 1896 described the first case. METHODS: Between 1990 and 2005, 30 patients affected of esophageal diverticulum were referred to our Department. RESULTS: The pathological results revealed one case of squamous cell carcinoma. On follow-up 10 years after diverticulectomy alone, the patient was alive and well without evidence of recurrence. CONCLUSION: Our case reported provides additional data on clinical decision when the tumor is well localized without full-thickness penetration or extension to the line of resection. In this patient, long-term survival and apparent disease control have been effected by diverticulectomy alone. A case of such long survival is very rare.

Journal Article↗

PubMed2006

Relationship between atrial histopathology and atrial fibrillation after coronary bypass surgery.

BACKGROUND: Postoperative atrial fibrillation is common after coronary surgery. The cellular condition of atrial myocytes might play a part in the postoperative development of atrial fibrillation. Our study aimed to investigate whether patients in whom postoperative atrial fibrillation develops show pre-existent alterations in histopathology of the right atrium and how such changes are expressed in relation to the use of cardiopulmonary bypass. METHODS: Seventy patients undergoing elective coronary revascularization were prospectively randomized to on-pump conventional surgery (conventional coronary artery bypass grafting, n = 35) or off-pump surgery on the beating heart (off-pump coronary artery bypass grafting, n = 35). Samples from the right atrial appendage were immediately collected after opening the pericardium. In the on-pump group samples were also taken after weaning from cardiopulmonary bypass. Focusing on degenerative alterations, histology was studied by means of light microscopy and for confirmation of particular findings by means of electronic microscopy. RESULTS: Twenty-two (31%) patients had postoperative atrial fibrillation, with the rate not being different between the off-pump coronary artery bypass grafting and conventional coronary artery bypass grafting groups (P = .797). Left atrial enlargement and inotropic requirement were related to atrial fibrillation. Interstitial fibrosis, vacuolization, and nuclear derangement of myocytes were the histologic abnormalities associated with the development of postoperative atrial fibrillation. However, in multivariate analysis fibrosis was confounded by myocyte vacuolization (P = .002) and nuclear derangement (P = .016), representing independent atrial fibrillation predictors. As expected, the conventional coronary artery bypass grafting and off-pump coronary artery bypass grafting groups showed similar histology, but more importantly, no atrial changes were detected in relation to cardiopulmonary bypass exposure in the conventional coronary artery bypass grafting group. Atrial histology showed degenerative changes that correlated with advanced age and left atrial enlargement. CONCLUSIONS: Our study supports the contention that atrial fibrillation after coronary surgery is associated with pre-existing histopathologic changes of the right atrium. Patients randomly allocated to off-pump coronary artery bypass grafting procedures showed a similar rate of atrial fibrillation and a similar relationship to atrial histology as did those exposed to cardiopulmonary bypass. Cardiopulmonary bypass did not cause additional changes in tested histology variables.

Aged↗

PubMed2003

Localization of vascular endothelial growth factor and its receptors in digestive endocrine tumors: correlation with microvessel density and clinicopathologic features.

Angiogenesis, a process related to tumor growth and malignancy, is stimulated by several growth factors. Among these is vascular endothelial growth factor (VEGF), which acts on endothelial cells by binding with 2 specific receptors, VEGFR1 and VEGFR2. Recent studies have demonstrated that VEGF expression is correlated with microvessel density (MVD) and tumor progression. Digestive endocrine tumors are heterogeneous neoplasms exhibiting variable biological aggressiveness and behavior that often are not predictable on morphologic grounds alone. The aims of this study were to evaluate the expression of VEGF, VEGFR1, and VEGFR2 in digestive endocrine tumors and to examine its correlation with MVD and malignancy. A total of 84 specimens from endocrine neoplasms and normal gut and pancreatic tissue were immunohistochemically studied using specific antibodies directed against VEGF, VEGFR1, VEGFR2, endothelial antigens, and gastroenteropancreatic hormones. Ultrastructural immunocytochemistry was performed to identify the cellular localization of VEGF and the VEGFRs. In normal tissues, VEGF immunoreactivity was detected in G cells and PP cells. Ultrastructurally, VEGF was localized within secretory granules. The VEGFRs were not significantly expressed by normal endocrine cells. VEGF-immunoreactive (IR) cells were detected in 40 of 83 tumors, mainly G cell and enterochromaffin cell neoplasms. VEGFR1-IR cells were found in 44 of 82 tumors, and VEGFR2-IR cells were found in 55 of 82 tumors, with no predilection for any specific tumor type. The expression of VEGF and its receptors did not correlate with MVD or malignancy. These results suggest that in normal tissues, endothelial functions may be regulated by VEGF produced by some endocrine cells and that a VEGF/VEGFR binding mechanism may be involved in tumorigenesis, but not in tumor progression and aggressiveness.

Adolescent↗

PubMed2003

Microsatellite instability and p53 expression in gallbladder carcinomas.

We studied the MSI (microsatellite instability) status and p53 expression in a series of 71 gallbladder cancers (GCs) of different histologic type. All neoplasms were examined combining a microsatellite analysis at mononucleotide locus BAT-26 and an immunohistochemical study for hMSH2, hMLH1, and p53 proteins and markers of gastric and intestinal differentiation. All the 71 GCs were MSS (microsatellite stable). The p53 protein was found in 100% of undifferentiated GCs, 67% of conventional gallbladder adenocarcinomas, 50% of mucinous adenocarcinomas, and 20% GCs with squamous differentiation. All 71 MSS tumors showed presence of immunohistochemical expression of both hMLH1 and hMSH2 gene products. We concluded that microsatellite instability does not play a role in the developing of GC while p53 seems to be the most important alteration found in a large proportion of these cancers, with the only exception of mucinous and squamous gallbladder carcinomas.

Adaptor Proteins, Signal Transducing↗

PubMed2002

Involvement of 1p36 region in two cases of adenocarcinoma of the ampulla of Vater.

Cancer of the ampulla of Vater is an uncommon disease that leads to death in 60% of affected patients. There is general agreement that local spread of the tumour (T stage) is the only significant and independent prognostic factor for this cancer. Although the genetic mechanisms underlying the development of ampullary tumors are still mostly unknown because of their rarity, the genetic anomalies involved in tumor development might serve as additional prognostic markers. Cytogenetic studies may be helpful in identifying specific chromosome regions involved in these cancers. We studied two cases of poorly differentiated ampullary adenocarcinomas using conventional and molecular cytogenetics on direct preparations. The cytogenetic analysis revealed complex chromosome complements in both cases with different cell lines, rearrangements, chromosome markers, and aneuploidies. Interestingly, the involvement of the 1p36 region was a feature of both cases. The molecular studies showed an absence of high microsatellite instability (MSI) and the morphologic and immunohistochemical pattern did not suggest MSI. This study may help to characterized ampullary adenocarcinomas showing complex karyotypes, poor differentiation and poor prognosis. In these tumors, the 1p36 region may play a relevant role in the progression towards a high grade of anaplasia.

Adenocarcinoma↗

PubMed2000

Localization of Hepatocyte Growth Factor and Its Receptor met in Endocrine Cells and Related Tumors of the Gut and Pancreas: An Immunohistochemical Study.

Hepatocyte growth factor (HGF), a stimulator of angiogenesis and cell migration, regulates the growth of a wide variety of cells by binding to its high-affinity receptor met and is involved in the growth and aggressiveness of several tumors. In this study we investigated the expression of HGF and met in normal endocrine cells and related neoplasms of the gut and pancreas to verify their possible role in tumor pathogenesis, growth, and aggressiveness. Normal tissues and 60 different endocrine tumors were immunostained using specific antibodies directed against HGF, met, and various hormones. HGF immunoreactivity (IR) was found in antroduodenal G cells, rectal enterochromaffin (EC) cells, and pancreatic A and B cells, whereas met IR was detected in antral EC and C cells, and in pancreatic B cells; 46 of 60 tumors examined were positive for HGF, and they were mainly represented by ECL-, EC-, and L-cell neoplasms. met IR was identified in 50/60 tumors of various phenotypes. HGF and met coexpression was found in 42/60 cases, most of which were represented by EC-cell tumors. HGF/met coexpression was significantly more frequent in ileocolonic EC-cell tumors, which in the majority of cases were malignant, than in appendiceal EC-cell tumors, which were all benign. Our results demonstrated, for the first time, that HGF and met are specifically distributed in normal gut and pancreatic endocrine cells and, in addition, suggest that HGF and met may be implicated as autocrine/paracrine factors regulating the growth of gastroenteropancreatic endocrine tumors, mainly of ileocolonic EC-cell carcinoids.

Journal Article↗

PubMed1997

Metastatic Psammomatous Somatostatinoma of the Pancreas Causing Severe Ketoacidotic Diabetes Cured by Surgery.

A case of somatostatin-producing pancreatic tumor associated with severe insulin-dependent diabetes mellitus and ketoacidotic coma is reported. The tumor, a 10-cm expansile mass arising from the pancreatic tail of a 70-yr-old woman, was first detected by ultrasonography, performed because of abdominal pain, and subsequently confirmed by computed tomography and fine-needle tumor aspiration. Pathologic investigation showed a predominantly solid-trabecular structure with scattered microacini and psammomatous bodies. A large proportion of tumor cells expressed somatostatin and/or calcitonin. Following resection of the primary tumor and three peripancreatic lymph nodes with metastases, the patient recovered rapidly from her diabetic syndrome and remained in substantially good health during a subsequent 8-yr follow-up period, without evidence of tumor recurrence.

Journal Article↗