Comment on “Gastric cancer and family history”

No abstract available.

Why do we still have Helicobacter Pylori in our Stomachs?

The existence of any infectious agent in a highly acidic human stomach is contentious, but the chance finding of Helicobacter pylori is by no means an accident. Once H. pylori colonises the gastric mucosa, it can persist for a lifetime, and it is intriguing why our immune system is able to tolerate its existence. Some conditions favour the persistence of H. pylori in the stomach, but other conditions oppose the colonisation of this bacterium. Populations with high and extremely low prevalence of H. pylori provide useful insights on the clinical outcomes that are associated with this type of infection. Adverse clinical outcomes including peptic ulcer disease and gastric cancer depend on a delicate balance between a harmless inflammation and a more severe kind of inflammation. Is the only good H. pylori really a dead H. pylori? The jury is still out.

First case of Helicobacter pylori infection resistant to seven antibiotics in Iran

Treatment of Helicobacter pylori infection with common antibiotics is typically recommended for several digestive conditions, including peptic ulcers. However, reports of resistant H. pylori isolates are increasing, and unfortunately, these do not respond to currently available therapeutic regimens. We report the case of a 31-year-old woman with two peptic ulcers in the duodenal antrum. An H. pylori strain was isolated, and tested for antibiotic resistance using agar dilution and disk diffusion. The isolated strain was found to be resistant to all seven antibiotics that were tested. Therefore, constant monitoring for antibiotic resistance should be performed prior to initiating antibiotic therapy.

[ study of matrix metalloproteinase 9 and CD31 expression through immunohistochemistry in invasive breast cancer]

This study was performed to investigate possible relationships between the manifestation of stromal cells [fibroblasts and/or myofibroblasts] by focusing on expression of their matrix metalloproteinase 9 [MMP9] and possible angiogenesis based on CD31 and CD34 antigen expression during the various steps of hyperplastic changes to precancerous state and invasive breast cancer. Our study included 50 females with invasive ductal carcinoma. Samples were obtained by mastectomy or biopsy and were immunohistochemically stained for the MMP9, CD31, and CD34 antibody. microvessel count [MVC] was also carried out on samples. Statistical analysis of the data was performed using ANOVA and Student's t-test [P < 0.05]. Findings were compared with our "Breast Cancer Data Bank" for reevaluation of their clinical staging. Positive significant correlations were observed between expression of MMP9 and invasive ductal carcinoma in situ [DCIS] and fibrocystic disease +/- ductal intraepithelial neoplasia [FCD +/- DIN] areas [P=0.001]. MMP9 expression in invasive areas was more strongly positive than precancerous areas. Statistically significant correlations were observed between MMP9 expression and CD31 in grade II in invasive areas. MVC was evaluated by CD31 antibody. It was found to be inversely related to increased MVC from invasive areas, DCIS, DIN, and normal areas [P < 0.001]. No significant difference was observed in MVC based on age, tumor size or steroid receptors in stroma of an invasive cancer, DCIS, and FCD +/- DIN. MMP9 expression in invasive areas was more strongly positive than precancerous areas, and negative in normal areas. Angiogenesis can be observed before any significant changes in preinvasive breast lesions. The elevated content of microvessel count of the tumor may be an indicator for worse prognostic factor. The progression from epithelial hyperplasia toward DCIS, and then, invasive carcinoma seems too complex to be assumed a linear progression

Distribution of myofibroblast cells and microvessels around invasive ductal carcinoma of the breast and comparing with the adjacent range of their normal-to-DCIS zones

This study seeks to determine the relationships between manifestation of myofibroblast in the stroma tissue of hyperplastic pre-invasive breast lesions to invasive cancer by investigating clinicopathological data of patients, their effect on steroid receptor expression and HER2, and angiogenesis according to CD34 antigen expression. Handred cases of invasive ductal carcinoma were immunohistochemically investigated for the presence of smooth muscle actin [SMA], ER/PR, HER2, anti-CD34 antibody and microvessel count [MVC]. Patients were scored in four different zones of invasive areas: invasive cancer, DCIS, fibrocystic disease +/- ductal intraepithelial neoplasia [FCD +/- DIN], and normal tissue. There was a significant difference in stromal myofibroblast between all areas except for the stroma of DCIS and FCD +/- DIN [P < 0.001]. We observed positive significant correlations between stromal myofibroblast, HER2 expression, and the numbers of involved lymph nodes in invasive cancer, DCIS, and FCD +/- DIN [P < 0.001]. More myofibroblast were present in grade III cases, with the least frequent observed among grade I cases in the stroma of those with invasive disease, DCIS, and FCD +/- DIN [P < 0.001]. MVC was inversely related to stromal myofibroblast in invasive cancer [P < 0.001] and DCIS [P < 0.001], whereas there was a positive correlation in the stroma of FCD +/- DIN [P = 0.002] and normal areas [P = 0.054]. There was a significant difference in MVC observed in all areas except for DCIS and FCD +/- DIN [P < 0.001]. We noted significant inverse correlations between MVC, HER2 expression, and the numbers of involved lymph nodes in invasive cancer and DCIS [P < 0.001]. Most MVC were present in grade I, with the least frequent observed in grade III cases in the stroma of invasive cancer, DCIS and FCD +/- DIN [P < 0.001]. Angiogenesis can be observed before any significant myofibroblastic changes in the pre-invasive breast lesions. The elevated content of myofibroblast in stroma of tumor; probably may be a worse prognostic factor and the steps from atypical epithelial hyperplasia to DCIS and then to the invasive carcinoma do not appear to be always part of a linear progression

Prevalence of EPIYA motifs in Helicobacter pylori strains isolated from patients with dyspeptic disorders in northern Iran

Cytotoxin-associated gene A [CagA]-positive strains of Helicobacter pylori are associated with gastroduodenal diseases. Evidences have suggested that the type of H. pylori CagA EPIYA motifs may be associated with recurrent dyspepsia [i.e. gastritis, peptic ulcer, or gastric cancer]. We investigated the prevalence of different EPIYA motifs [A, B, C, or D] in H. pylori strains isolated from patients with recurrent dyspepsia who underwent upper gastrointestinal [GI] endoscopy. We investigated the prevalence of different EPIYA motifs [A, B, C, or D] in H. pylori strains isolated from patients with recurrent dyspepsia who underwent upper gastrointestinal [GI] endoscopy. H. pylori strains were isolated from biopsy specimens of 220 patients with recurrent dyspepsia. The presence of glmM gene, as a housekeeping gene, CagA gene, and pattern of CagA EPIYA motifs were determined using polymerase chain reaction [PCR] method. The association between the type of motifs and disease state was determined by the Chi-square test, Fisher's exact test, and logistic regression. CagA-positive H. pylori strains were identified in 125 [57%] of patients, including 36 [28.6%] gastritis, 31 [24.6%] duodenal ulcer, and 58 [46.4%] gastric cancer. The frequency of pattern of CagA EPIYA motifs were detected as 39 [31.2%] AB motifs, 54 [43.2%] ABC motifs, 32 [25.6%] ABCC motifs,and no D motifs. The risk of gastric cancer occurrence was estimated to be 2.57 times higher in patients infected by strains with ABCC motif when compared with gastritis and duodenal ulcer patients [p=0.03]. Moreover, patients with C-containing motifs were 2.27 times more likely to be afflicted with gastric cancer than with duodenal ulcer. AB motif was more associated with gastritis and duodenal ulcer than ABC and ABCC motifs. The results suggested that CagA-EPIYA ABCC might be associated with gastric cancer, while EPIYA-AB might be associated with duodenal ulcer

[Evaluation on antibiotic resistance of helicobacter pylori isolated from patients admitted to tooba medical center, Sari]

Helicobacter pylori, which infect approximately one half of the world's population, are an important risk factor in chronic gastritis, peptic ulcer disease, and gastric cancer. H. pylori eradication is now widely recommended as the most effective treatment of peptic ulcer disease. One of the most important reasons for treatment failure is H. pylori resistance to the antimicrobials usage in therapy. The aim of this study was to determine susceptibility patterns of H. pylori isolates in 6 routine anti-microbial agents in Northern Iran. 125 patients from Tooba Medical Center in Sari with endoscopic evidence of dyspepsia complaints were used for obtaining gastric biopsies specimens. Biopsies were sent to the laboratory in thioglycolate broth [transport medium]. Bacteria were primarily cultured on Columbia agar supplemented with 7% horse blood, 7% fetal calf serum. Urease, Catalase and Oxidase activities were used for H. pylori identification. Bacterial suspensions equivalent to 3 Mc. Farlands were spread on plates, along with antibiotic disks and placed in the diameter zone. Inhibition was measured after 3 days of incubation in micro-aerophilic condition. H. pylori were isolated from 116[92.8%] subjects, a total of 125 biopsy specimens. Resistance to metronidazole, amoxicillin, clarithromycin, tetracycline, furazolidone and ciprofloxacin were 71%, 35%, 25%, 9%, 24% and 25%, respectively. Multiple resistance [amoxicillin-clarithromycin-metronidazole] were found in [6]5% of the isolates. Comparison of our data with previous results showed that prevalence of H. pylori resistance to clarithromycin, furazolidone and metronidazole has increased in Iran considerably. Resistance to amoxicillin in our study was too high in comparison with foreign studies. The present study demonstrates the need for continuous monitoring of the antimicrobial susceptibility in H. pylori in order to determine the optimal drug regimens