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Pulmonary lymphangitic carcinomatosis is a special type of diffuse metastasis of carcinoma in the lymphatic vessels of the lungs. Lymphangitic carcinomatosis is commonly observed in malignancies of the breast, lung, pancreas, colon and cervix as a strong marker for poor prognosis. Presenting with common respiratory symptoms, it may be easily misdiagnosed as other pulmonary interstitial diseases. Pulmonary lymphangitic carcinomatosis is a rare manifestation of metastatic gastric cancer. The presented case describes a patient with pulmonary lymphangitic carcinomatosis in the course of stomach cancer. The primary diagnosis was established based on the exclusion of other interstitial lung diseases, with the use of imaging techniques as well as biochemical, microbiological and cytological findings. The patient’s general condition was very severe, rendering him bedridden and therefore not eligible for any treatment, including chemotherapy. He died suddenly before final verification of the diagnosis. Pulmonary lymphangitic carcinomatosis should be suspected in patients with advanced gastric cancer, presenting with symptoms and signs of respiratory disease. Imaging techniques are mostly helpful to establish the diagnosis.
Protein kinase B (PKB/Akt) is a serine-threonine kinase functioning downstream of phosphatidylinositol 3-kinase (PI-3 kinase) in response to mitogen or growth factor stimulation. In several cell types, it plays an important anti-apoptotic role. TPA is a potent regulator of the growth of many different cell types. Here, we detected that TPA could induce cell apoptosis in the gastric cancer cell line, BGC-823. We also found that TPA inhibited the expression of PKB/Akt in a TPA concentration- and time-dependent manner. Furthermore, TPA inhibited the phosphorylation of PKB at Ser473, but did not affect the phosphorylation of Thr308. It only attenuated the expression of PKB/Akt and the phosphorylation of Ser473 in the cell nucleus, whereas it did not change the PKB/Akt distribution in BGC-823 cells. These results suggest that PKB/Akt inhibition by TPA may be the important factor in the mechanism of effect of TPA on gastric cell lines.
The presence of spiral-shaped micro-organisms in the human stomach was described over 100 years ago by Polish clinical researcher, Professor W. Jaworski at Cracow Jagiellonian University. Their presence was then confirmed in animals by G. Bizzazero, but was not really taken seriously until the late 1970s, when J.R. Warren, a pathologist in Perth, Australia, noted the appearance of spiral bacteria overlaying gastric mucosa, chiefly over inflamed tissue. Warren and B.J. Marshall cultured these organisms in 1982 from 11 patients with gastritis and were able to demonstrate a strong association between the presence of Helicobacter pylori (H. pylori) and the finding of inflammation in gastric biopsies. People, who did not exhibit gastritis, also did not have the organism, a finding which was confirmed in a number of studies. Originally called Campylobacter pyloridis, the name was changed to Campylobacter pylori, and then later to Helicobacter pylori (H. pylori) as specific morphologic, structural, and genetic features indicated that it should be placed in a new genus. Marshall elegantly fulfilled Koch's postulates for the role of H. pylori in antral gastritis with the self administration of H. pylori, and also showed that it could be cured by use of antibiotics and bismuth salts. Most persons who are infected with H. pylori never suffer any symptoms related to the infection; however, H. pylori causes chronic active, chronic persistent, and atrophic gastritis in adults and children. Infection with H. pylori also causes duodenal and gastric ulcers. Infected persons have a 2- to 6-fold increased risk of developing gastric cancer and mucosal-associated-lymphoid-type (MALT) lymphoma compared with their uninfected counterparts. The role of H. pylori in non-ulcer dyspepsia remains unclear. These practical aspects of H. pylori were subjects of two international symposia organized by us in 1995 and 1997 in Cracow, helping to promote research and Polish consensus regarding treatment of H. pylori infection.
The PKB signaling pathway is essential for cell survival and the inhibition of apoptosis, but its functional mechanisms have not been fully explored. Previously, we reported that TPA effectively inhibited PKB activity and caused PKB degradation, which was correlated with the repression of PKB phosphorylation at Ser473. In this study, we focus on how PKB is regulated by TPA in gastric cancer cells. One of the TPA targets, PKCα, was found to mediate the inhibition of PKB phosphorylation and degredation caused by TPA. Furthermore, TPA induced the import of PKCα into the nucleus, where PKCα exerted an inhibitory effect on PKB expression and phosphorylation. As a result, cancer cell proliferation was arrested. Our study characterizes a novel function of PKCα in mediating the negative regulation of PKB by TPA, and suggests a potential application in the clinical treatment of gastric cancer.
The aim of the present study was to assess the possible correlation of p53 with CEA and Ca 19-9 serum levels as well as with selected clinicopathological data. 46 patients, who were gastrectomized due to gastric cancer between 1998 and 2001, were analyzed. The concentration of CEA and Ca 19.9 was estimated in serum. Mean percentage of p53-positive cells in present group was 33,69 %. The comparison of mean percentage of p53-positive cells with IHC reaction intensity revealed statistically significant, directly proportional correlation, with p<0,001. Mean CEA and Ca 19-9 serum concentration were 1,75± 1,71 ng/ml, and 17,34±44,73 U/ml respectively. No significant correlation between p53-expression, CEA and Cal9-9 was noted respecting several clinicopathological data of tumors. However clear trend of higher CEA and Cal9-9 values in groups of potentially worse prognosis (T3-T4; Nl-2; III grade of disease) was observed.
Background. Within the last few decades, the prevalence of obesity has increased rapidly throughout the world. Epidemiological studies indicate a relationship of several types of cancer with obesity. The study aimed was to analyse the relation between body mass index (BMI) and the risk of developing gastric cancer. Material and methods. A multicenter case-control study was conducted between 2010 and 2015 in Poland. The study included 152 patients with gastric cancer and 152 patients with normal results of esophagogastroduodenoscopy performed in the same period and matched for age, education and sex. BMI was calculated by using patients’ height and weight. An analysis of environmental factors associated with the risk of gastric cancer was performed. Results. The group with the diagnosis of gastric cancer was characterised by significantly higher regular consumption of alcohol and was found to include a higher percentage of smokers compared to the control group. In a subgroup analysis, it was found that there was a significantly higher body mass index among both men and women diagnosed with gastric cancer. A relation between gastric cancer and both overweight (BMI 25.0-29.9 kg / m²) and obesity (BMI≥30 kg / m²) was established. In a multivariate analysis, this was an independent risk factor for gastric cancer. Conclusions. We suggest that BMI should be considered as an independent risk factor for developing gastric adenocarcinoma, which should lead to further research leading to the development of recommendations for the prevention of gastric cancer for people with high BMI.
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