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Abstract Gastric cancer is the second most frequently diagnosed malignancy worldwide and therefore represents a significant healthcare burden. Environmental and genetic factors are involved in the development of gastric cancer. To date only one clear genetic predisposition has been identified involving mutations in the E-cadherin gene. The disease phenotype in patients harbouring E-cadherin mutations appears to be specifically related to diffuse gastric cancer. Little is known genetically about the other forms of gastric cancer. Since there is a growing awareness about the necessity of early intervention criteria have been developed that aid the identification of hereditary forms of gastric cancer. The aim of the current study was to identify minimal inclusion criteria so that nuclear pedigree families can be provided with risk assessment and/or genetic testing. The results reveal that inclusion features described herein such as (a) gastric cancer diagnosed before 46 years of age; (b) two gastric cancers among first degree relatives diagnosed over the age of 50 are useful in identifying suspected hereditary gastric cancer patients.

CHEK2 is a tumor suppressor gene whose functions are central to the induction of cell cycle arrest and apoptosis following DNA damage. Mutations in CHEK2 have been associated with cancers at many sites, including breast and prostate cancers, but the relationship between CHEK2 and gastric cancer has not been extensively studied. In Poland, there are four known founder alleles of CHEK2; three alleles are protein truncating (1100delC, IVS2G>A, del5395) and the other is a missense variant (I157T). We examined the frequencies of four Polish founder mutations in the CHEK2 gene in 658 unselected gastric cancer patients, in 154 familial gastric cancer patients and in 8,302 controls. A CHEK2 mutation was seen in 57 of 658 (8.7 %) unselected patients with gastric cancer compared to 480 of 8,302 (5.8 %) controls (OR 1.6, p = 0.004). A CHEK2 mutation was present in 19 of 154 (12.3 %) familial cases (OR = 2.3, p = 0.001). The odds ratio for early onset (<50 years) gastric cancer was higher (2.1, p = 0.01), than for cases diagnosed at age of 50 or above (OR 1.4, p = 0.05). Truncating mutations of CHEK2 were associated with higher risk (OR = 2.1, p = 0.02) than the missense mutation I157T (OR = 1.4, p = 0.04). CHEK2 mutations predispose to gastric cancer, in particular to young-onset cases.

Ectopic pancreas is the most common type of ectopic tissue in gastrointestinal tract. It is typically asymptomatic, presenting as a small submucosal lesion in prepyloric region of stomach. The diagnosis is usually incidental, during gastroscopy. The patient with symptomatic heterotropic pancreas, mimicking gastric malignancy was described.

Unlabelled: Mutation of the p53 gene belongs to the most common genetic alteration in human cancer. Prognostic significance of serum anti-p53 antibodies in patients with gastric cancer is still a matter of controversy. The aim of the study was to estimate the presence of anti-p53 antibodies in serum of gastric cancer patients and relationship between anti-p53 antibodies and chosen clinical and pathomorphological data age, sex, localization of cancer, histology, stage of disease, metastases to lymph nodes and the time of survival., Material and Method: Serum samples from 71 patients with gastric cancer were analyzed by specific enzyme-linked immunosorbent assay (ELISA) to determine the presence of serum anti-p53 antibodies. The results were statistically compared with clinical and pathological features and postoperative survival., Results: Anti-p53 antibodies were detected in 16 (23%) gastric cancer patients. The presence of p53 antibodies was connected with intestinal tumor type (p < 0.05) and older age (p = 0.0035). There were no association between anti-p53 antibodies, stage and the time of survival., Conclusion: These results suggest that in gastric cancer patients serum anti-p53 antibodies detected by ELISA are not predictor of prognosis.

Unlabelled: The Zenker's diverticulum is the pathology of pharyngo-esophageal region with its neck proximal to the cricopharyngeal muscle. The Zenker's diverticulum is the rare finding in upper endoscopy, but choice of treatment may bring some problems. Nowadays, the flexible endoscopy has been in focus of interest for treatment of Zenker's diverticulum., Methods: Our first experience in management of Zenker's diverticulum include 40 patients, age 67-82 years old. All patients had symptoms such as dysphagia, aspiration pneumonia or sputum at night. The procedure consist of endoscopic incision of septum between esophageal lumen and diverticulum using argon beamer until its high was less than 0.5 cm., Results: all patients became free of symptoms. Each patient complained of sore throat after treatment. No serious complications were observed. Only one case of retropharyngeal space emphysema and two cases of perforation were observed, both of them were treated with antybiotics and nasogastric tube feeding., Conclusion: It seems that this method is save and efficacious for treatment of Zenker's diverticulum.

Objectives: The association between interleukin-1 polymorphisms, H. pylori and increased gastric cancer risk remains controversial., Aims: To compare the prevalence of these polymorphisms in individuals with two mutually exclusive diseases connected with infection, gastric cancer, and duodenal ulcer., Methods: 121 gastric cancer and 119 duodenal ulcer patients. Genomic DNA was typed for polymorphisms at position -511, -31 in the interleukin-1beta gene (IL-1 beta) using primer extension and mass-spectrometry. Analysis of the variable number of tandem repeats in intron 2, in its receptor antagonist gene (IL-1RN) was performed by PCR and agarose gel electrophoresis., Results: All subjects were successfully genotyped for the three gene loci. IL-1 beta-511 was found to be in reverse linkage disequilibrium with IL-1 beta-31. The differences between gastric cancer and duodenal ulcer patients concerned only heterozygous variant of IL-1beta and were related to family history of gastric cancer, tumor stage, histology, site. Thus, CT carriers were found to have a higher risk of sporadic [OR 2.21 (95% CI, 1.22-3.99)], early [OR 2.81 (95% CI, 1.14-6.93)], diffuse [OR 2.48, (95% CI 1.21-5.09)] or non-cardia gastric cancer [OR 1.88 (95% CI 1.06-3.33)]. Furthermore, CT genotype was significantly more prevalent in gastric cancer patients with negative than in those with a positive family history (p = 0.039)., Conclusions: The association between the interleukin-1 polymorphisms and gastric cancer risk depends on the family history of gastric carcinoma in the study population. This phenomenon may be in part responsible for differences in results of interleukin-1 studies performed on populations with low and high gastric cancer prevalence.

Unlabelled: Colorectal cancer is a quite common neoplasm. Screening colonoscopies and polypectomies can decrease the incidence of that neoplasm by 75%. Discovering the most frequent reasons and most convincing sources of information about the examinations is important for success of screening programme., Objectives: The aim of this study was to find the connection between some demographic factors, the source of information about the examination and the consent for colonoscopy., Material and Methods: Two groups of subjects, aged 40-65, were included: 1000 subjects, who gave their consent for colonoscopy and 200 subjects, who refused the examination. The sources of information were two kinds of questionnaires: fulfilled before colonoscopy and in case of lack of consent for the examination, which included demographic data, the reason of undergoing or refusal of colonoscopy and the source of information about the examination., Results: The higher educated were the subjects, the more often they agreed for the examination; among subjects after university 87%, and among subjects with elementary education 71% gave their consent for colonoscopy. The most convincing sources of information were the medial sources; 100% of subjects, who found out about the examination from television and radio, gave their consent for colonoscopy. The most frequent reason of undergoing the examination was prophylaxis (54.6%), and the most frequent reasons of refusal was fear of pain (33.5%)., Conclusions: Educational level and the source of information about the examination are the factors that have an important influence on undergoing screening colonoscopy. Identifying the influence of some demographic factors on the consent for colonoscopy and the efficacy of each source of information seems to be very important for the success of screening colonoscopy programme and therefore for discovering adenomatous polyps and colorectal cancer.

The aim of the study was a screening assessment of the nutritional status of patients admitted to hospitals and discharged from hospitals. The study was carried out in 4 university hospitals, 4 woivodeship hospitals and 4 district hospitals. In randomly selected 3310 patients (every 10th patient admitted to hospital) anthropometric parameters were assessed: body height, body mass, body mass index (BMI), waist-hip ratio (WHR), arm circumference, blood morphological and biochemical parameters were determined (erythrocyte, white blood cell and lymphocyte count in blood, albumin and haemoglobin concentration in serum). The mean values of the assessed parameters in the whole studied population of patients admitted to various types of hospitals were not different from the normative values for adults, however, a gradual decrease of the values of certain parameters in the over 70 years age group was observed. Although, the mean values of the studied parameters of the nutritional status were within the accepted normal range, 10.43% of the studied patients had BMI below 20 kg/m2, and 20.7% of the patients the serum albumin level was below 3.5 g/dl on admission, which could suggest protein-energy malnutrition. In a yet higher proportion of patients (21%) lymphocyte count was below 1500/mm3. During hospital stay tendency became even more pronounced. On discharge from hospital the proportion of patients with BMI below 20 kg/m2 rose to 11.21%, and with serum albumin level below 3.5 g/dl rose to 28.6%. Only the proportion of patients with low lymphocyte count remained unchanged during hospital stay and was 21.1% on discharge. In the studied population 42.29% of the patients reported receiving of additional food beyond hospital diet.

Aim: The expression of p53 protein was compared in primary gastric carcinomas and coexisting regional and distant metastases. The purpose of the study was to evaluate whether p53 staining in regional lymph-node metastases might improve the value of p53 as a prognostic marker and determine the behaviour of its protein during gastric cancer progression., Material and Methods: 60 gastric cancer patients were included into the study. In all patients the expression of p53 was assessed in primary tumours and in regional lymph-node metastases. Additionally in 12 patients the p53 expression was determinated in distant metastases. The number of all secondary tumours studied was 153. Formalin fixed, paraffin embedded material and three-stage immunohistochemical methods were used., Results: p53 accumulation was detected in 24 (40%) of primary gastric carcinomas. In each patient p53 expression in primary regional and distant metastatic tumours was identical., Conclusions: Our results show that assessment of p53 in lymphnode metastases does not improve prognostic value of p53 in gastric carcinoma and support the view that p53 alterations occur before and maintain during metastatic spread.

The purpose of the study was a more thorough assessment of the nutrition state of patients admitted to hospitals in Poland. The study was carried out in four hospitals at teaching centre level, in four hospitals at province level, and in four county hospitals. The patients for the study were selected randomly from 3310 adult patients (every 10th patient admitted to these hospitals). For the study 210 patients (122 women and 88 men) were qualified. Their mean age was 54 +/- 16 years (range 15-82 years). The patients were subjected to various biochemical tests including determination of antioxidant vitamins (vitamins A, E and C), vitamin B12, folic acid, ferritin, and homocysteine and blood lipids. Vitamin deficiency accepted as vitamin malnutrition was found in the case of vitamin C in 51.8% of the patients, folic acid in 32%, vitamin E in 10%, vitamin B12 in 6.8%, vitamin A in 1.4%. Vitamin deficiency was equally frequent in patients with malnutrition, overweight or with obesity. Lipid profile disturbances were found in 51% and high homocysteine level in 63% of the studied patients.

Colorectal cancer is one of the most common neoplasms that often occurs in several members of family. In this communication we present the case of synchronous colorectal cancers with similar localization and similar clinical course in monozygotic twins.

Colorectal cancers (CRCs) are one of the most common forms of cancer in Poland and one of the leading causes of death. The tumors have been attributed to genetic, dietary, and other environmental factors, but recently growth factors such as gastrin have also been implicated in the carcinogenesis. The relationship between plasma amidated and nonamidated gastrin in CRCs is controversial. This study was designed (1) to determine the plasma levels of progastrin and amidated gastrin in 50 CRC patients before and 3-6 months after removal of the tumor, (2) to determine the tumor concentrations of these gastrin peptides and the level of expression for gastrin mRNA and gastrin/CCK(B) receptor mRNA, (3) to examine the expression of cyclooxygenase COX-1 and COX-2 mRNA in CRC tissue, and (4) to compare the prevalence of Hp and its cytotoxic protein, CagA, and cytokines (TNFalpha, IL-1beta, and IL-8) in CRCs, before and after removal of tumor. It was found that the CRC, its resection margin, and the plasma contained severalfold higher levels of progastrin than of amidated gastrins and that the removal of the CRC tumor resulted in a marked reduction in plasma progastrin level without a significant alteration in plasma levels of amidated gastrins. Both gastrin and CCK(B)-R mRNA were detected in the cancer tissue and resection margin by RT-PCR, and similarly, COX-1 and COX-2 mRNA were expressed in these tissues of most CRCs. The seroprevalence of Hp, especially that expressing CagA, and levels of IL-1beta, but not other cytokines, were significantly higher in CRC patients than in 100 age-, gender-, and profession-matched controls and did not change significantly about 3-6 months after tumor resection. We conclude that (1) the CRC and its margin contain large amounts of progastrin and show gene expression of gastrin, CCK(B)-R, and COX-2; (2) removal of the CRC markedly reduces the plasma concentrations of progastrin; (3) the Hp infection rate is higher in CRC, and this may contribute to colorectal cancerogenesis via enhancement of progastrin and gastrin release; and (4) plasma progastrin concentrations might serve as a biomarker of CRC.

Malt-lymphoma, gastrin and COX-2 interaction. Low grade, mucosal associated lymphoid tissue (MALT)-lymphoma is an unique among gastric malignancies where causal involvement of Helicobacter pylori (H. pylori) infection has been proposed based on complete regression of the tumor following the eradication therapy. In this report ten primary, low-grade MALT-lymphomas have been examined before and 6 months after one week of successful eradication therapy (clarithromycin + amoxicillin + omeprazole). Gastric biopsy samples from tumor and intact antrum and corpus mucosa were obtained during endoscopy before and after eradication for assessment of expression of gastrin and gastrin receptor (CCKB-R) as well as cyclooxygenase (COX)-1 and COX-2 using RT-PCR. The gastric lumen and serum gastrin and mucosal and tumor tissue PGE2 biosynthesis were determined by RIA before and after H. pylori eradication. Eradication of H. pylori resulted in complete endoscopic and histological remission of MALT-lymphoma in 9 out of 10 patients as assessed 6 months after this eradication. Before eradication, the mRNA expression for gastrin and CCKB-R as well as mRNA expression for COX-1 and COX-2 were observed in tumor tissue and infected mucosa, while corpus mucosa expressed only CCKB-R and antrum mucosa only gastrin. Six months upon the eradication when MALT-lymphoma completely regressed both endoscopically and histologically in 9 of 10 tested subjects, the expression of gastrin and COX-2 disappeared from the former area of MALT-lymphoma tumor. Gastrin mRNA remained detectable only in antrum mucosa, CCKB-R mRNA in corpus mucosa and COX-1 mRNA both in antrum and corpus mucosa. Gastric luminal and serum gastrin levels and gastric mucosa and tumor PGE2, which were greatly elevated before eradication, became normalized after this procedure. This study demonstrates that low-grade MALT-lymphoma is linked to H. pylori infection which may promote the expression and excessive release of gastrin and COX-2 expression that could be involved in the pathogenesis of MALT-lymphoma.

Background: Tumors arising in the colorectal area have worldwide distribution and concern mostly older population being attributed to genetic, dietary and hormonal factors but most recently also to infection with Helicobacter pylori (HP). Both, HP discovery and molecular biology of colorectal cancer have been recently considered as two of ten greatest advances of gastroenterology at the dawn of 3rd millenium but little information is available regarding the relationship between the HP and colorectal cancer. Since HP infection is usually accompanied by an increase in plasma level of gastrin, which is also recognized as a trophic hormone for the colonic epithelium and a potent mitogen capable to induce cyclooxygenase-2 (COX-2), we decided 1) to compare the seroprevalence of HP, its cytotoxic protein, CagA, and cytokines (TNFalpha, IL-1beta and IL-8) in colorectal cancer patients, before and after removal of cancer, with those in age- and gender-matched controls; 2) to determine the gene expression of gastrin and gastrin receptors (CCK(B)-R) in colorectal cancer tissue, 3) to assess the plasma levels and tumor tissue contents of gastrin, 4) to examine the mRNA expression of cyclooxygenase COX-1 and COX-2 cancer tissue and intact colonic mucosa., Material and Methods: The trial material included 80 patients with colorectal cancers and 160 age- and gender-matched controls. Anti-HP IgG, anti-CagA IgG seroprevalence and cytokine levels were estimated by ELISA tests. Gene expressions of gastrin, CCK(B)-R, COX-1, COX-2 and Bax and Bcl2 was examined using RT-PCR, while gastrin was measured by RIA., Results: The HP IgG seroprevalence, especially that expressing CagA, was significantly higher in colorectal cancer patients than in controls and did not change one week after tumor resection while plasma cytokines were significantly reduced after this operation. Gastrin and CCK(B)-R mRNA were detected in the cancer tissue and the resection margin and similarly COX-2 mRNA was expressed in most of cancers and their resection margin but not in intact colonic mucosa where only COX-1 was detected. The colorectal cancer tissue contained several folds more immunoreactive gastrin than cancer resection margin and many folds more than the intact colonic mucosa., Conclusions: 1) Colorectal carcinoma and its resection margin overexpress gastrin and receptors for gastrin (CCK(B)-R), and COX-2; 2) here, we propose that an increased plasma level of gastrin should be considered as suitable biomarker of colorectal cancer, 3) HP infection may contribute to colonic cancerogenesis by enhancing expression of gastrin and COX-2, they may account for stimulation of the tumor growth, angiogenesis and reduction in apoptosis as evidenced an increased ratio of mRNA expression for anti-apoptotic Bcl2 over proapoptotic Bax proteins and 4) HP positive patients who develop colorectal cancer should be subjected to the HP eradication; this is expected to reduce hypergastrinemia and to attenuate COX-2 expression. Our final conclusion would be: treatment of patients with colorectal cancer with COX-2 selective inhibitors now gained a strong support as a preventive measure.

Background: Epidemiological and animal studies demonstrated a link between gastric cancer (GC) or mucosal associated lymphoid tissue (MALT) lymphoma and chronic infection with Helicobacter pylori (H. pylori). The exact mechanism responsible for the development of GC and MALT-lymphoma in H. pylori-infected patients still remains obscure. This report is designed to overview the molecular biology, especially the gene expression and histochemical manifestation of gastrin and other growth factors such as transforming growth factor alpha (TGF alpha) and hepatocyte growth factor (HGF) in the GC before and after eradication of H. pylori. Furthermore, gene expression of cyclooxygenase-1 (COX-1) and COX-2 and apoptosis-related proteins such as Bax and Bcl-2 are discussed., Material and Methods: The findings originate from two series of patients; Series I involving 337 GC patients and 400 age- and gender-matched controls and series 2 including 20 MALT-lymphoma patients and 40 matched controls., Results: An overall H.pylori-seropositivity reached about 80% in GC and about 90% in MALT-lymphoma, significantly higher than in non-cancer controls (60%). The prevalence of CagA-positive strains was about twice as high (about 70%) in GC and MALT-lymphomas as in sex- and age-matched controls. Expression of gastrin was detected in antrum of all tested patients but also in majority (90%) of GCs and MALT-lymphomas tumor tissue. HGF and TGF alpha were expressed more frequently in GC tissue than in normal fundic mucosa. COX-1 was similarly expressed in GC and MALT as in intact mucosa, while COX-2 mRNA was detected only in tumor tissue, being attenuated by H.pylori eradication in GC and abolished by this therapy in MALT-lymphoma. The plasma levels of alpha-amidated gastrin in GC and MALT were several folds higher than in controls. Gene expression of bcl-2 was detected in all, while bax--only in about 50% of GC samples., Conclusions: Infection with H. pylori, especially that expressing CagA-positivity, is primum movens in developing GC and MALT-lymphoma and the upregulation of growth factors, particularly of gastrin, and COX-2 and dysregulation of the Bax/Bcl-2 system seem to contribute to gastric cancerogenesis.

To characterize the toxicity of phosphorothioate antisense oligodeoxynucleotides ([S]ODNs) in vivo, the mice received intravenously 26-mer bcr-abl antisense oligodeoxynucleotides (1 mg/mice/day) for 9 consecutive days. The organs and tissues were removed on the indicated days (+1, +7, +30) after the treatment. Our investigation revealed middle elevation of aminotransferases activity, lactate dehydrogenase level, total protein level and globulin level, decrease of glucose, albumin and blood urea nitrogen level in the peripheral blood. The mild anaemia and thrombocytopenia were observed too. The most significant treatment-related findings in the antisense treated mice were splenomegaly, reactive hepatitis and atrocytosis of kidney. These findings together with previous results demonstrate little and temporary toxicity effects mainly in organs known from cumulating of [S]ODNs.

Argon plasma coagulation (APC) has been introduced for the local endoscopic treatment of gastrointestinal malignancy recently. It is mainly used as a palliative therapy, especially in case of stenosis. Despite a lot of publications concerning APC the clinical usefulness of this method in a small malignant tumors remains unclear. The patient with early diagnosed carcinoma of gastric, efficiently treated using argon plasma coagulation is described.

Numerous epidemiological studies demonstrated the association between Helicobacter pylori (H. pylori) infection and gastric cancer but the mechanism of the involvement of H. pylori in gastric cancerogenesis remains virtually unknown. This study was designed to determine the seropositivity of H. pylori and cytotoxin associated gene A (CagA), serum gastrin and gastric lumen gastrin levels under basal conditions and following stimulation with histamine in gastric cancer patients and controls. 100 gastric cancer patients aging from 21 to 60 years and 300 gender- and age-adjusted controls hospitalized with non-ulcer dyspepsia (NUD) entered this study. 13C-Urea Breath Test (UBT), serum immunoglobulin (IgG) antibodies to H. pylori and CagA were used to assess the H. pylori infection and serum levels of IL-1beta, IL-8 and TNFalpha were measured by enzyme-linked immunosorbent assay (ELISA) to evaluate the degree of gastric inflammation by H. pylori . Gastrin-17 mRNA and gastrin receptors (CCK(B)) mRNA expression in gastric mucosal samples taken by biopsy from the macroscopically intact fundic and antral mucosa as well as from the gastric tumor was determined using RT-PCR. The overall H. pylori seropositivity in gastric cancer patients at age 21-60 years was about 92%, compared, respectively, to 68%, in controls. A summary odds ratio (OR) for gastric cancer in H. pylori infected patients was about 5.0 . The H. pylori CagA seropositivity in gastric cancer patients was about 58.5% compared to 32.4% in controls, giving the summary OR for gastric cancer in CagA positive patients about 8.0. The prevalence of H. pylori- and H. pylori CagA-seropositivity was significantly higher in cancers than in controls, irrespective of the histology of gastric tumor (intestinal, diffuse or mixed type). Median IL-1beta and IL-8 reached significantly higher values in gastric cancer patients (9.31 and 30.8 pg/ml) than in controls (0.21 and 3.12, respectively). In contrast, median serum gastrin in cancers (as total group) was several folds higher (62.6 pM) than in controls (19.3 pM). Also median luminal gastrin concentration in gastric cancer patients was many folds higher (310 pM) than in controls (20 pM). This study shows for the first time that cancer patients are capable of releasing large amounts of gastrin into the gastric lumen to increase luminal hormone concentration to the level that was recently reported to stimulate the growth of H. pylori. There was no any correlation between plasma gastrin levels and gastric luminal concentration of gastrin suggesting that: 1) luminal gastrin originates from different source than plasma hormone, most probably from the cancer cells, 2) cancer cells are capable of expressing gastrin and releasing it mainly into the gastric juice and 3) the gastric cancer cells are equipped with gastrin-specific (CCK(B)) receptor so they exhibit the self-growth promoting activity in autocrine fashion. This notion is supported by direct detection of gastrin mRNA and gastrin receptor (CCK(B)-receptors) mRNA using RT-PCR in cancer tissue. To our knowledge this is the first study showing an important role of gastrin as self-stimulant of cancer cells in patients infected with H. pylori. Basal and histamine maximally stimulated acid outputs were significantly lower in gastric cancer patients than in controls despite of enhanced gastrin release, particularly in cancer patients and this might reflect the mucosal inflammatory changes (increased serum levels of proinflammtory interleukins - IL-1beta and IL-8), that are known to increase gastrin release. We conclude that: 1) H. pylori infected patients, particularly those showing CagA-seropositivity, are at greatly increased risk of development of gastric cancer, 2) H. pylori-infected cancer patients produce significantly more IL-1beta and IL-8 that might reflect an H. (ABSTRACT TRUNCATED)

The purpose of the study was to assess risk factors for intestinal metaplasia arising from H. pylori-related chronic gastritis in a subset of the population referred to endoscopic examinations due to dyspeptic complaints. We aimed specifically to establish whether H. pylori itself may be responsible for the occurrence of intestinal metaplasia and to which extent the metaplasia may be associated with life style factors such as cigarette smoking, alcohol consumption or dietary habits. The study was carried out in a sample of 1290 outpatients referred for the first time to gastroenterologic outpatient clinics in 6 university centers in Poland. The study methods covered standardized health interviews, endoscopy and histology of gastric antral specimens taken at endoscopy. The interviews performed by trained interviewers sought information on tobacco and alcohol intake, diet, socioeconomic status, and other variables. In non-ulcer dyspepsia subjects there was 54.9% H. pylori related gastritis and 25.1% of non-H. pylori-related gastritis. The corresponding rates in the group of ulcer dyspepsia were 67.5% and 20.5%. The increased risk of chronic gastritis in antrum was associated with Helicobacter pylori infection (OR = 2.28; 95% CI:1.93-2.69), and with gastric peptic ulcer (OR = 1.88; 95% CI:1.20-2.94). In the non-ulcer dyspepsia the prevalence of metaplasia was 11.1% and in ulcer dyspepsia 19.7%. The risk of intestinal metaplasia within antrum depended greatly upon the presence of gastric peptic ulcer (OR = 3.85; 95% CI:2.35-6.32) and increased with age (OR = 1.05; 95% CI:1.04-1.07), smoking cigarettes currently or in the past (OR = 1.42; 95% CI:1.10-1.84), higher frequency of drinking vodka (OR = 1.32, 95% CI:1.01-1.75) and antral chronic gastritis (OR = 1.31; 95% CI:1.00-1.70), however, it was inversely related to daily consumption of fresh fruits or vegetables (OR = 0.59; 95% CI:0.38-0.93). The results of the study suggest that there is no sufficient evidence supporting the hypothesis about an association between H. pylori gastritis and intestinal metaplasia, however, the transition of gastritis to metaplasia depends greatly on life style factors such as cigarette smoking or vodka drinking and is impeded by daily consumption of fresh fruits or vegetables.

The purpose of this study was to correlate the presence of p53 antibodies in sera of patients with colorectal adenocarcinoma with size, site and stage of the tumour, age and sex of a patient and the level of carcinoembryonic antigen (CEA) in the serum. p53 antibodies were detected using enzyme-linked immunoabsorbent assay (ELISA). Serum p53 antibodies were detected in 30 of 145 patients (21%), mostly in Astler-Coller stage B1 (28% of patients). No association was found between p53 antibody status in stage A+B1+B2 vs stages C1+C2+D (22% vs 19%) i.e. between patients without and with metastases to regional lymph nodes and/or distant metastases. Serum p53 antibodies were detected in 9 of 34 patients (26%) with tumour localised in the right part vs 21 of 109 patients (19%) with tumours in the left part of the colon and in 18 of 96 (19%) of patients with tumours localised in rectosigmoideum vs 12 of 47 (26%) with tumours in the remaining colon. There was no significant correlation between serum anti p53 antibody and CEA statuses. Increased level of serum CEA was seen in 46/145 (32%) patients. Patients with C1+C2+D stage cancers had high serum CEA level more frequently than did patients with A+B1+B2 stage tumours (44% vs 19% respectively, p < 0.001). Of 102 cases with normal CEA level, 19 (19%) were positive for anti p53 antibodies. These results together with the literature data [11, 20] indicate that approximately 27% CEA negative patients may have serum p53 antibodies. Therefore simultaneous assessment of serum p53 antibodies and CEA seems to be useful for monitoring high risk patients and for postoperative patient monitoring.