There is limited information present to explain temporal improvements in colon cancer survival. This nationwide study investigates the temporal changes in survival over a 35-year period (1970-2004) in Iceland and uses incidence, mortality, surgery rate, stage distribution, lymph node yield, tumor location and histological type to find explanations for these changes. Patients diagnosed with colon cancer in Iceland 1970-2004 were identified (n = 1962). All histopathology was reassessed. Proportions, age-standardized incidence and mortality, relative, cancer-specific and overall survival and conditional survival were calculated. When comparing first and last diagnostic periods (1970-1978 and 1997-2004), 5-year relative survival improved by 12% for men and 9% for women. At the same time surgery rate increased by 12% and the proportion of stage I increased by 9%. Stage-stratified, improved 5-year relative survival was mainly observed in stages II and III and coincided with higher lymph node yields, proportional reduction of stage II cancers and proportional increase of stage III cancers, indicating stage migration between these stages. Improvement in 1-year survival was mainly observed in stages III and IV. Five-year survival improvement for patients living beyond 1 year was minimum to none. There were no changes in histology that coincided with neither increased incidence nor possibly influencing improved survival. Concluding, as a novel finding, 1-year mortality, which previously has been identified as an important variable in explaining international survival differences, is in this study identified as also being important in explaining temporal improvements in colon cancer survival in Iceland.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/ijc.30766

Why is colon cancer survival improving by time? : A nationwide survival analysis spanning 35 years

Background & Aim: The important role of IL-17 in inflammatory response to Helicobacter pylori (H. pylori) colonization has been indicated. We investigated the associations between gastro-duodenal diseases and polymorphisms of IL17A (rs2275913 G>A) and IL17F (rs763780 T>C). Methods: The study was performed in 548 subjects (363 controls and 185 peptic ulcer cases). The multiplex PCR-SSCP method was used to detect gene polymorphisms. Results: Overall, number of rs2275913 A allele was significantly associated with an increased risk for peptic ulcer (OR, 1.50; 95%CI, 1.11-2.01; p=0.0082). The frequency of rs2275913 GA+AA genotype was also significantly higher in ulcer cases than controls (OR, 1.72; 95%CI, 1.09-2.72; p=0.020). The rs2275913 GA+AA genotype conferred an increased risk for the severity of gastric mucosal atrophy in subjects younger than 60 years (OR, 2.83; 95%CI, 1.14-7.04; p=0.025). Both atrophy and metaplasia were increased with age in rs2275913 GA+AA genotype. In NSAIDs/aspirin users, number of rs2275913 A allele was associated with an increased risk for a peptic ulcer (OR, 3.98; 95%CI, 1.48-10.7; p=0.0061). There was no association of rs763780 with the development of peptic ulcer. Conclusions: Our results provide the evidence that rs2275913 is associated with an increased risk for peptic ulcer and the severity of the gastric mucosal atrophy in comparatively younger subjects. In addition, this allele is also associated with the increased risk for peptic ulcer in NSAIDs/aspirin users. ORIGInAL PAPERs

Association of genetic polymorphisms in IL17A and IL17F with gastro-duodenal diseases.

OBJECTIVE: The aim of this study was to determine whether the presence of Helicobacter pylori (H. pylori) infection and multidrug resistance protein 1 (MDR1) C3435T polymorphism had an influence on P-glycoprotein (P-gp) expression in the upper gastrointestinal tract.



METHODS:  A total of 76 patients who underwent upper gastroendoscopy at Sir Charles Gairdner Hospital in Western Australia from October 2010 to July 2011 were enrolled in the study. Antral and duodenal biopsies were collected for P-gp examination. Blood samples were taken and analyzed for MDR1 C3435T polymorphism. H. pylori infection status was confirmed by culture and polymerase chain reaction.



RESULTS:  A significant difference was found in P-gp expression between H. pylori-positive and H. pylori-negative patients (P = 0.028). For the MDR1 C3435T polymorphism, the TT genotype had a significantly lower P-gp expression compared with the CC genotype in antral specimens (P = 0.041). The homozygous TT genotype with H. pylori infection was also significantly different in P-gp expression compared with H. pylori-negative patients (P = 0.029).



CONCLUSIONS:  P-gp expression in the upper gastrointestinal tract is associated with H. pylori infection, and the TT genotype appeared to be associated with lower P-gp expression than the CC genotype in the stomach.

P-glycoprotein expression in Helicobacter pylori-positive patients: The influence of MDR1 C3435T polymorphism

Objective. P-gp, encoded by ABCB1 gene, is an ATP-binding membrane pump, which exports substrates from the cell including drugs and xenobiotics. Changes in the function of P-gp as a result of polymorphism could have an impact in some diseases' risks and treatment outcomes. The aim of the study was to determine the significance of the ABCB1 gene SNPs: 1236 and 2677 for peptic ulcer risk and development of Helicobacter pylori infection in peptic ulcer patients. Material and methods. One hundred and ninety-five biopsy specimens obtained from peptic ulcer patients (investigated group) were genotyped using sequencing for common SNPs of ABCB1: 1236 and 2677. Genotyping data were compared with the results from healthy subjects (control) and with the presence of H. pylori infection, which was estimated by urease test. Results. No statistically significant difference in frequency of genotypes and alleles for the SNPs were found between the investigated group and the control. However, in the peptic ulcer p...

Investigation of ABCB1 1236 and 2677 SNPs in patients with peptic ulcer.

BACKGROUND/AIMS Tumor necrosis factor α (TNF-α) encoded by TNFA is a key mediator in inflammation, a precursor condition for peptic ulceration. Promoter polymorphisms of TNFA that influence its transcriptional activity and TNF-α production are known. TNFA-308G>A (rs1800629) and TNFA-1031T>C (rs1799964), which are responsible for increased TNFA transcription, could influence the risk of peptic ulceration. This study aimed to investigate these polymorphisms and to evaluate their association with peptic ulcer disease and Helicobacter pylori infection in the Polish population. METHODS Gastric mucosa specimens obtained from 177 Polish peptic ulcer patients were used to conduct rapid urease tests and to assess the investigated polymorphisms by polymerase chain reaction-restriction fragment length polymorphism. Genotyping data were compared with the results obtained from healthy individuals of Polish origin. RESULTS There were no significant differences in genotype and allele frequency of the investigated polymorphisms between peptic ulcer patients and healthy individuals. No associations between the frequencies of particular genotypes and alleles for both single-nucleotide polymorphisms (SNPs) and the presence of H. pylori infection in peptic ulcer patients and in subgroups of men and women with peptic ulcer disease were found. CONCLUSIONS The investigated SNPs are not risk factors for either peptic ulcer or H. pylori infection development in the Polish population. The results require verification in a larger cohort.

Investigation of -308G>A and -1031T>C Polymorphisms in the TNFA Promoter Region in Polish Peptic Ulcer Patients

C3435T polymorphism of the ABCB1 gene: impact on genetic susceptibility to peptic ulcers

A 65-kDa tumor-associated protein (P65) is a potential non- specific tumor marker expressed by many types of tumor cells. Our recent studies indicate that P65 gene expression is connected with poor prognosis for the patients with colorectal cancer. In the present study P65 gene expression was determined by means of RT-PCR in the group of 22 gastric cancer and adjacent normal gastric mucosa. Its presence was correlated with some parameters of clinical staging. P65 gene expression was also determined in 102 tissue antral gastric endoscopic biopsy specimens from the patients suspected of H. pylori infection. The presence of H. pylori infection was determined by urease test. We found that in the group of gastric cancers, similarly to colorectal cancer, P65 gene expression was connected with poor clinicopathological parameters as T3, lymph nodes and distant metastases. There was no dependence between P65 gene expression and H. pylori infection. However, more often P65 gene expression was detected in the group of infected men than women. There was also a statistically significant dependence between age and P65 gene expression in the group of people above 60 years old. It could be then postulated that P65 gene expression is connected with poor prognosis for the patients suffering from gastric cancer and that this expression does not depend on H. pylori infection.

Expression of the P65 gene in gastric cancer and in tissues with or without Helicobacter pylori infection.

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C3435T polymorphism of the ABCB1 gene: impact on genetic susceptibility to peptic ulcers

Investigation of ABCB1 1236 and 2677 SNPs in patients with peptic ulcer.

Expression of the P65 gene in gastric cancer and in tissues with or without Helicobacter pylori infection.