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D Assisi

Publications and source records attributed to D Assisi.

10 recordsLinked to original sources
PubMed2004

C-MYB, serum P-53M, genetic instability, labeling index and endoscopic findings in patients with adenoma or colorectal cancer.

Structural alterations of c-myb proto-oncogenes and serum p53 mutant level, Mitomycin C-induced chromosomal aberrations and sister chromatid exchanges and proliferative activity of mucosa (H3-thymidine -labeling index LI) are often determined to obtain more information about the diagnosis and prognosis of neoplastic and preneoplastic lesions of the colon. The aim of this study was to evaluate the endoscopic findings of a 5 year follow-up in three groups of subjects (normal, adenoma or cancer patients) and to correlate these findings with the biological alterations in the same subjects between 1990 and 1993. We analyzed 200 subjects (118 Male and 82 Female), 78 normal subjects (group A), 60 patients with adenoma (group B) and 62 with carcinoma (group C). Data regarding endoscopic lesions was collected from June 1998 to December 2000 after a 5 year follow-up and correlated with the biological alterations in the same subjects between 1990--1993. We obtained endoscopic findings from 23/137 subjects (16.8%), 6/137 (4.4%) died from other causes and 108/137 (78.8 %) were negative for lesions. The percentage of disease after 5 years is not statistically different among the three groups (groups A, B and C). There was no statistically significant association between values of the labeling index, structural alterations of c-myb, p-53-M serum levels and chromosomal aberrations and endoscopic findings in the 5 year follow-up. We conclude that the biological markers considered are not able to stratify patients in terms of risk of progression to malignant disease.

Adenoma↗
PubMed2002

Palliative treatment of esophageal tumors.

In malignant dysphagia expandable metal stents are commonly used as palliative treatment, but early and late complications and the improvement of dysphagia have not been well described. This report summarizes our experience with expandable metal stents for malignant dysphagia. From 1995 to 2000, we placed 38 metal stents in 36 patients with malignant dysphagia from unresectable esophageal cancer (94.4%). Dysphagia scores, complications and modality of reintervention were evaluated. Dysphagia scores decreased from 3.2 before the stent placement to 2. Immediate complications occured in one patient because of severe pain, it was not possible to perform endoscopic treatments. Other complications included tracheoesophageal fistula (2 patients), tumor overgrowth (5 patients), new stent placements (2 patients), dislocation (2 patients). In conclusions expandable metal stents are safe and effective in the treatment of malignant dysphagia.

Adenocarcinoma↗
PubMed1999

Colorectal cancer complicating ulcerative colitis: an institutional series.

Ulcerative colitis predisposes to colorectal cancer: the risk increases along with disease duration and extension. Also some subsets of patients are at increased risk, namely patients with early onset of colitis, and patients with primary sclerosing cholangitis. Cancer complicating ulcerative colitis affects evenly all the colon, and is not located more frequently in the rectum and in the sigmoid colon, as well as the sporadic counterpart. Multiple cancers and cancers associated with high grade dysplasia are not infrequent in ulcerative colitis; for this reason, and for controlling the colitis, the treatment of choice is total colectomy, with or without colostomy. The prognosis of cancer complicating ulcerative colitis is similar to the sporadic counterpart. The Authors present a colon cancers series as a complication of colitis occurred at Regina Elena Cancer Institute of Rome, Italy, over the period 1975-1998.

Adult↗
PubMed1999

Endoscopic follow-up in oncological diseases of the gastrointestinal tract: the experience of the Regina Elena Cancer Institute.

In oncology, follow-up refers to the medical procedures aimed to control, over time, both patients at risk of developing cancer, or those already submitted to surgical treatments for neoplastic lesions. The usefulness of an endoscopic follow-up in oncological diseases of the gastrointestinal tract is still being debated and, in some cases, a variety of different protocols are often employed for the same disease. At Regina Elena Cancer Institute, after a critical review of our data and literature, we established and followed guidelines of endoscopic follow-up for patients both at risk and submitted to curative surgery for cancer.

Barrett Esophagus↗
PubMed1997

[Hereditary non polyposis colon cancer (NHP CC) prevalence in South Italy (Campania). Report on a preliminary retrospective study].

The aim of this study was to determine a prevalence of Hereditary Non Polyposis Colo-rectal Cancer (HNPCC) in consecutive one hundred twenty-eight patients living in Campania district and affected by first diagnosed colorectal cancer. Data on 128 patients and their relatives was collected and available for analysys. Our preliminary results seem to demonstrate a low prevalence of HNPCC in Campania and will be verified with a prospective multicentric study in the same area.

English Abstract↗
PubMed1994

[Ulcerative rectocolitis diagnosed in the elderly. Case studies].

Fourteen patients with idiopathic ulcerative colitis (UC) diagnosis made over 60 years of age have been extrapolated from 255 (5.49%) consecutive. Some clinical parameters (sex; symptoms of onset; delay in diagnosis; extension of disease; density of relapses; therapy with cortisone) have been compared between the 14 patients with ultra sixtieth year of age diagnosis (A group) and the 241 patients with a diagnosis made previously (B group). There were no significant differences concerning the symptoms at onset and the delay in diagnosis. In group A a larger prevalence of the male (M/F 3.66 against 1.46) and distal localization (64% against 53%) have been reported. The density of relapse and therapy with cortisone (p < 0.025) prevailed in B group. In conclusion, limited to our experience, the UC in A group is less severe than in B group.

Adult↗
PubMedDate not supplied

[The Lynch syndrome].

Lynch syndrome is a peculiar disease, accounting for 5% of the total burden of colon cancer. Characteristics of this disease are autosomal dominant transmission, early onset, and frequent right colon localization. Diagnostic criteria, aimed to collaborative studies, are based on these features (so called Amsterdam criteria). Lynch syndrome has specific biomolecular features (microsatellite instability); mismatch repair genes have been identified as responsible of this syndrome. Lynch syndrome causes high risk for extracolonic malignancies, particularly for endometrial cancer, supposed to be related to mutation of hMSH2 gene. Another feature of Lynch syndrome tumours is better survival with respect to sporadic counterpart. Genetic test allows identifying the state of mutation carriers and selects the patients to submit to screening. Endoscopic screening has been demonstrated to reduce incidence of colorectal malignancies in this syndrome.

Colorectal Neoplasms, Hereditary Nonpolyposis↗
PubMedDate not supplied

Current trends in screening and secondary prevention of colorectal cancer.

Colorectal cancer is one of the most frequent neoplasms in Western countries with an estimated 400,000 deaths per year worldwide. Several randomized studies have demonstrated that screening programs with FOBT (Fecal Occult Blood Test) reduce mortality from 18 to 33%, whereas case-control and cohort studies with endoscopy have shown a mortality reduction ranging from 60 to 76%. The target population for secondary prevention is men and women aged more than 50 years and younger subjects in case first-degree relatives are affected or the family pedigree raises the suspicion of a genetic syndrome. This report summarizes the results of different screening strategies for average risk patients (FOBT, anamnestic risk questionnaire, sigmoidoscopy, colonoscopy and virtual colonoscopy) and the surveillance protocols applicable to high-risk patients, particularly for hereditary syndromes such as HNPCC and FAP.

Colonography, Computed Tomographic↗
PubMedDate not supplied

Activation of c-MYC and c-MYB proto-oncogenes is associated with decreased apoptosis in tumor colon progression.

BACKGROUND: An increasing amount of evidence suggests that progression from normal mucosa to colorectal cancer is accompanied by morphological and genetic alterations. Genetic abnormalities affect malignant transformation via a gradual imbalance of normal tissue homeostasis involving programmed cell death (PCD) or apoptosis. Therefore, it has been hypothesized that alterations in apoptosis may contribute to carcinogenesis. The aim of the present work was to investigate the relationship between frequency of spontaneous apoptosis during transition adenoma-to-carcinoma of the colorectal tract and the incidence of activation of c-myc and c-myb proto-oncogenes, involved both in colon tumorigenesis and apoptosis. MATERIALS AND METHODS: Ninety-five tissue specimens (60 polyps and 35 adenocarcinomas) were removed with autologous normal adjacent mucosa from colon cancer patients. Genomic DNA was extracted and analyzed for both apoptosis frequency (DNA fragmentation assay) and proto-oncogene activation (Southern blot analysis). On the same samples, Bcl-2 protein expression was evaluated by immunohistochemistry. RESULTS: Our results showed that: i) a significant relationship exists between apoptosis and genesis of colorectal cancer since, compared to adenomatous polyps and adjacent normal mucosa, cell death is markedly inhibited in tumors (p = 0.01); ii) during colon tumor progression, apoptosis and amplifications of c-myc/c-myb genes are inversely related; iii) Bcl-2 expression is retained in colon tumors even though at a significantly lower level with respect to adenomatous polyps. CONCLUSION: These results indicate that failure of the normal apoptotic process together with de-regulation of c-myc and c-myb proto-oncogenes might promote the development of colorectal tumors.

Adenocarcinoma↗