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Biomedical subjects

M Robaszkiewicz

Publications and source records attributed to M Robaszkiewicz.

At least 19 recordsLinked to original sources
PubMed2000

Antibody response of patients with Helicobacter pylori-related gastric adenocarcinoma: significance of anti-cagA antibodies.

The aim of this study was to search for a specific antibody pattern in sera from patients suffering from Helicobacter pylori-related gastric adenocarcinoma (GAC). The serological response of 22 patients suffering from GAC, 31 patients with gastroduodenal ulcer, and 39 asymptomatic subjects was analyzed using immunoblotting performed with three H. pylori strains: strain ATCC 43579; strain B110, isolated from a patient with ulcers; and strain B225, isolated from a patient with GAC. In addition, the latex agglutination test Pyloriset Dry was used to analyze ambiguous sera. H. pylori seropositivity was 75% in the GAC group, 61.3% in the ulcer group, and 56.4% in the asymptomatic group. Anti-CagA antibodies were found more often in the GAC group (48.8%) and in the ulcer group (47.3%) than in the asymptomatic group (21.2%). These percentages depended on the strain used as an antigen: in the GAC group, the anti-CagA frequencies were 93.3, 40, and 13.3% with strains B225, B110, and ATCC 43579, respectively. Thus the presence of anti-CagA antibodies was increased in patients suffering from H. pylori-related GAC, in particular when the CagA antigen was from a GAC strain. These data suggest the existence of a CagA protein specifically expressed by H. pylori strains isolated from GAC patients.

Adenocarcinoma↗
PubMed1999

Prognostic value of the lower esophageal sphincter gradient and acid exposure in the follow-up of antireflux operations.

Eighty-eight consecutive patients with antireflux fundoplication had manometry and pH recording pre- and post-operatively at 6 months and 1, 3 and 5 years for a mean follow-up of 30.6 months. Failure occurred in nine patients (11.4%). For the whole group of patients, surgery produced a significant increase in the lower esophageal sphincter (LES) pressure gradient from 9.5 +/- 6.3 to 14.6 +/- 6.7 mmHg and a significant decrease in acid exposure from 20.6% +/- 17.6% to 5.5% +/- 8.8% at 6 months. There was a similar change in pressure (p < 0.0005) and pH (p < 0.002) in the successful but not in the failure group. Over time, the values remained stable in both groups. Post-operative LES pressure was significantly correlated with the outcome at 6 months (p < 0.02), and the pH was inversely correlated at 5 years (p < 0.039). This study confirms the early predictive value of the post-operative LES pressure. Esophageal acid exposure remains a reliable marker of the outcome. However, recurrences remain unexplained by LES pressure measurement and long-term follow-up using manometry and pH recording does not bring additional valuable data.

Adolescent↗
PubMed1998

[Diagnosis of mediastinal neuro-endocrine tumor using endosonography guided transesophageal puncture biopsy].

Histologic diagnosis of tumors of the mediastinum is mandatory for therapeutic management. The location and the variety of tumors are responsible for diagnostic difficulties. Endosonography guided fine-needle biopsy is an efficient and safe procedure for the diagnosis of peridigestive masses. We report the case of a patient with a neuroendocrine tumor of the mediastinum revealed by a mass syndrome. The diagnosis was performed by endosonography guided needle biopsy.

Biopsy, Needle↗
PubMed1997

[Incidence of inflammatory bowel diseases in Bretagne (1994-1995). ABERMAD. Association Bertonne d'Etude et de Recherche des Maladies de l'Appareil Digesif].

OBJECTIVES: The aim of the study was to determine the incidence and the main clinical data of inflammatory bowel disease in Brittany. METHODS: According to EPIMAD registry's methodology, private and public gastroenterologists (n = 139) of Brittany (2836418 inhabitants) referred all patients consulting for the first time, in 1994 and 1995 with clinical symptoms compatible with inflammatory bowel disease. An interviewer practitioner completed at the gastroenterologist's consulting room a standard questionnaire for each patient. Each case was reviewed separately by four experts to assign a diagnosis of definite, probable, possible Crohn's disease, ulcerative colitis, unclassifiable chronic colitis, or acute colitis (onset of symptoms < 6 weeks). RESULTS: 657 cases were recorded: 205 Crohn's disease (31%), 165 ulcerative colitis (25%) including 75 ulcerative proctitis (46%), 42 unclassifiable chronic colitis (7%), 245 acute colitis (37%). The crude mean annual incidence (per 10(5) inhabitants) based on definite and probable cases only was 2.8 for Crohn's disease and 2.9 for ulcerative colitis. The female/male ratio was 0.9 for Crohn's disease and 0.5 for ulcerative colitis. The median age at time of diagnosis was 27 for Crohn's disease and 36 for ulcerative colitis. The median time between onset of symptoms and diagnosis was equal to 3 months for Crohn's disease and ulcerative colitis. CONCLUSION: In Brittany the observed incidence of ulcerative colitis is similar to that of Crohn's disease and close to that observed in northern France. The incidence of Crohn's disease is lower. However, the real incidence of inflammatory bowel disease is currently underestimated due to the large number of acute colitis requiring a follow up and the cases of Crohn's disease classified as possible not taken into account.

Acute Disease↗
PubMed1997

TP53 and oesophageal cancer.

Mutations of the tumor suppressor gene TP53 have been detected in tumor tissues of a large variety of human malignancies and contribute to the development, progression and probably the prognosis of the disease. The pattern of somatic mutations in the TP53 gene in human tumors most often consists of a point mutation in one allele accompanied by loss or rearrangement of the second allele. Esophageal cancer is one of the most commonly mutated cancer, p53 mutations having an incidence greater than 80% in squamous cell carcinoma. The profile of distribution of these mutations in the TP53 gene is of interest to establish correlation between the exposure to carcinogens responsible for DNA mutations. The other form of esophageal cancer, Barrett's esophageal is a good model to study the role of TP53 in mammalian tumorigenesis.

Barrett Esophagus↗
PubMed1996

Molecular analysis of the TP53 gene in Barrett's adenocarcinoma.

The TP53 gene is the most frequently mutated gene in human cancers. Barrett's esophagus provides an excellent model by which to understand the genetic events that lead from dysplasia to cancer. We screened for mutations in the TP53 gene by a combination of denaturing gradient gel electrophoresis and DNA sequencing in ten cases of adenocarcinoma arising in Barrett's mucosa. We have identified missense mutations in five of the ten samples, three transitions (R282W, G245S, R248W) and two transversions (E286Q and C176F). In one case we have analyzed biopsy specimens taken from the same site, one year before the patient developed an intra mucosal carcinoma. The mutation that was identified in this high grade dysplastic area was identical to that detected in the cancer. This would suggest TP53 mutations occur as an early genetic event in the development of Barrett's adenocarcinoma.

Adenocarcinoma↗
PubMed1995

Multicentre prospective controlled study of Barrett's oesophagus and colorectal adenomas. Groupe d'Etude de l'Oesophage de Barrett.

Previous studies have suggested that patients with Barrett's oesophagus may be at increased risk of colorectal neoplasia, though the association is disputed. In a multicentre prospective study we compared the prevalence of colorectal adenomas in patients with Barrett's oesophagus and controls. Barrett's oesophagus patients (n = 104) had histological confirmation of columnar epithelium extending more than 3 cm above the gastro-oesophageal junction. The 537 controls were patients with symptoms suggesting irritable bowel syndrome. No participant had a personal history of colonic neoplasm. Each patient underwent colonoscopy. Histologically proven adenomas were found in 26 Barrett's patients (25%) and 75 controls (14%). Three colorectal cancers were discovered in each group. The prevalence of adenomas was greater in the Barrett's oesophagus group than in the control group (p < 0.01) but the relation became non-significant after adjustment for age and sex and control for other known risk factors by a logistic regression model (odds ratio 1.4 [0.7-2.7]). The relative risk of adenoma was significantly higher in patients older than 59 than in younger patients (2.2 [1.3-3.5]) and in men than in women (3.4 [2.0-5.7]). Other factors contributing significantly to the risk of adenoma were a family history of colorectal cancer (2.3 [1.1-4.8]), rectal bleeding (2.1 [1.1-3.9]), previous colonic investigation (0.3 [0.1-0.7]), and complete as opposed to partial colonoscopy (6.4 [0.8-48.3]). We conclude that Barrett's oesophagus is not an independent risk factor for colorectal neoplasia and, therefore, is not, in itself an indication for colorectal screening.

Adenoma↗
PubMed1995

p53 protein accumulation in oesophageal squamous cell carcinomas and precancerous lesions.

AIMS: To investigate the immunohistochemical expression of p53 protein in oesophageal squamous cell carcinomas and in dysplastic areas of the oesophageal mucosa surrounding the tumours. METHODS: Biopsy samples were obtained from 20 patients with an oesophageal squamous cell carcinoma. Blocks of the tumours and of the surrounding mucosa were immunostained with the monoclonal antibody DO-7. RESULTS: Fourteen of the 20 carcinomas were positive for p53 (70%). The frequency of p53 overexpression increased with the differentiation of the tumour. Nine out of 13 dysplastic specimens were positive for p53 (69%): eight cases with severe dysplasia and one case with moderate dysplasia. No p53 immunostaining was detected in normal oesophageal epithelium. All p53 positive dysplastic specimens were taken from the mucosa adjacent to tumours that were also immunostained. In moderate dysplastic mucosa the p53 positive cells were located in the proliferative basal zone, whereas in severe dysplasia the immunostained cells increased in number and spread to upper cell layers of the epithelium. CONCLUSION: This study supports the hypothesis that TP53 gene is frequently involved in the development of oesophageal squamous cell carcinoma and that p53 protein accumulation is an early event in human oesophageal carcinogenesis.

Adult↗
PubMed1995

[Overexpression of protein p53 and Barrett esophagus. A frequent and early event in the course of carcinogenesis].

OBJECTIVES AND METHODS: In Barrett's oesophagus, the risk of malignancy is evaluated histologically with the presence of dysplasia. The abnormal expression of p53 protein could represent a useful new marker. The aim of this study was evaluate the abnormal expression of p53 protein in a series of 52 oesophagectomy specimens with Barrett's oesophagus, either non-dysplastic (n = 3), dysplastic (n = 8), or malignant (n = 41). The immunohistochemical study was made on deparaffinized sections with the monoclonal anti-p53 antibody DO7. RESULTS: The 3 non-dysplastic cases were p53 negative; 1 case of low-grade dysplasia in 5 was positive, as were the 3 cases of high grade dysplasia and 33 of 41 cancers (80%), including 13 superficial cancers in 14 (93%) and 20 invasive cancers in 27 (74%). A common feature was the presence of rare p53 positive crypts in low grade dysplastic areas and non-dysplastic specialized mucosa that surrounded high grade dysplasia and cancers. CONCLUSIONS: Our results confirm the high frequency of the abnormal expression of p53 protein in cancer developed in Barrett's oesophagus. This expression is a consequence of alterations of the TP53 gene, and has an important role in the carcinogenesis of Barrett's mucosa; it is likely to represent an early event. Prospective studies are needed to evaluate its interest in the surveillance of patients with Barrett's oesophagus.

Barrett Esophagus↗
PubMed1995

[Therapeutic management and survival of gastric adenocarcinoma in the province of Finistère between 1984 and 1989].

OBJECTIVES: The aim of this study was to analyze the evolution of treatment regimens and survival rates of stomach adenocarcinoma recorded in the Finistère cancer registry from 1984 to 1989. METHODS: In a population of 838,627 inhabitants, 1,280 patients with a gastric cancer were registered; 1,164 patients (693 males and 471 females) had an adenocarcinoma. Survival rates were estimated by the actuarial method, and compared using the logrank test and the Cox model. RESULTS: Surgical resection was the main treatment for 661 patients (57%). The frequency of curative resection increased from 25% between 1984 and 1986 to 35% after 1986. Among the other patients, 39 (3%) were treated by chemotherapy and/or radiotherapy, and 53 patients (4%) by endoscopy alone; 253 patients had only symptomatic treatment. The survival rates of all patients were 43% at 1 year and 20% at 5 years. The median survival was 9.2 +/- 0.6 months. In patients with cancer managed surgically, the factors associated with a better prognosis were young age, long duration of symptoms before diagnosis, ulcerated macroscopic aspect, limited tumour extension and curative surgical resection. In other patients, 2 factors were associated a with better prognosis: the absence of metastases and an endoscopic palliative treatment. CONCLUSIONS: Surgical resection is the main treatment of gastric adenocarcinoma. Although the frequency of surgery increased, the prognosis of gastric adenocarcinoma did not improve within this 6-year period.

Adenocarcinoma↗
PubMed1994

[Barrett esophagus. Current situation of the risk and surveillance policy].

Barrett's oesophagus is a condition in which a metaplastic columnar mucosa replaces the normal squamous epithelium of the lower oesophagus. Barrett's oesophagus develops as a complication of gastro-oesophageal reflux and predisposes to the development of oesophageal adenocarcinoma. Most adenocarcinomas arising in Barrett's mucosa are far advanced at the time of diagnosis, and prognosis is consequently poor. Regular endoscopic surveillance of patients with Barrett's oesophagus is recommended to detect the oesophageal malignancy in an early presymptomatic stage. The concept of screening is based on the notion that regular surveillance can reduce the mortality, but there is yet little evidence that this is the case in Barrett's oesophagus. Screening is generally carried out by regular endoscopy with multiple biopsies in an attempt to detect dysplasia. Unfortunately, dysplasia is not an ideal biomarker of malignant potential in Barrett's oesophagus. There is an interest in research into more sensitive and effective predictors of heightened risk for development of malignancy. DNA content flow cytometry and p53 protein expression might be useful in managing the cancer risk in Barrett's patients. However these new techniques need further evaluation before they can be applied to routine clinical investigation.

Adenocarcinoma↗