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- Linder, Gustav, et al.
(författare)
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Validation of data quality in the Swedish National Register for Oesophageal and Gastric Cancer
- 2016
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Ingår i: British Journal of Surgery. - : Oxford University Press (OUP). - 0007-1323 .- 1365-2168. ; 103:10, s. 1326-1335
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Tidskriftsartikel (refereegranskat)abstract
- Background: The Swedish National Register for Oesophageal and Gastric Cancer (NREV) was launched in 2006. Data are reported at diagnosis (diagnostic survey), at the time of surgery (surgical survey) and at first outpatient follow-up (follow-up survey). The aim of this study was to evaluate data originating from NREV in terms of comparability, completeness, accuracy and timeliness. Methods: Coding routines were compared with international standards and completeness was evaluated by means of a 5-year (2009–2013) comparison with mandatory national registers. Validity was tested by comparison with reabstracted data from source medical records in 400 patients chosen randomly with stratification for hospital size and catchment area population. Timeliness of registration was described. Results: Coding routines followed national and international guidelines. Compared with the Swedish Cancer Registry from 2009 to 2013, 6069 (95·5 per cent) of 6354 patients were registered in NREV at the time of data extraction. Of 60 variables investigated, 10 966 of 12 035 original entries were correct in the reabstraction, resulting in an exact agreement of 91·1 per cent in the register. There were 782 (6·5 per cent) incorrect and 287 (2·4 per cent) missing entries. Median time to registration was 3·9, 3·4 and 4·1 months for diagnostic, surgical and follow-up surveys respectively. Conclusion: NREV has reached a position with good coverage of those with the relevant diagnoses, and contains comparable and valid data. Quality data on each variable are available. Timeliness is an area with potential for improvement.
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- Hess, Timo, et al.
(författare)
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Dissecting the genetic heterogeneity of gastric cancer
- 2023
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Ingår i: EBioMedicine. - : Elsevier. - 2352-3964. ; 92
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Tidskriftsartikel (refereegranskat)abstract
- Background: Gastric cancer (GC) is clinically heterogenous according to location (cardia/non-cardia) and histopathology (diffuse/intestinal). We aimed to characterize the genetic risk architecture of GC according to its subtypes. Another aim was to examine whether cardia GC and oesophageal adenocarcinoma (OAC) and its precursor lesion Barrett's oesophagus (BO), which are all located at the gastro-oesophageal junction (GOJ), share polygenic risk architecture.Methods: We did a meta-analysis of ten European genome-wide association studies (GWAS) of GC and its subtypes. All patients had a histopathologically confirmed diagnosis of gastric adenocarcinoma. For the identification of risk genes among GWAS loci we did a transcriptome-wide association study (TWAS) and expression quantitative trait locus (eQTL) study from gastric corpus and antrum mucosa. To test whether cardia GC and OAC/BO share genetic aetiology we also used a European GWAS sample with OAC/BO.Findings: Our GWAS consisting of 5816 patients and 10,999 controls highlights the genetic heterogeneity of GC according to its subtypes. We newly identified two and replicated five GC risk loci, all of them with subtype-specific association. The gastric transcriptome data consisting of 361 corpus and 342 antrum mucosa samples revealed that an upregulated expression of MUC1, ANKRD50, PTGER4, and PSCA are plausible GC-pathomechanisms at four GWAS loci. At another risk locus, we found that the blood-group 0 exerts protective effects for non-cardia and diffuse GC, while blood-group A increases risk for both GC subtypes. Furthermore, our GWAS on cardia GC and OAC/BO (10,279 patients, 16,527 controls) showed that both cancer entities share genetic aetiology at the polygenic level and identified two new risk loci on the single-marker level.Interpretation: Our findings show that the pathophysiology of GC is genetically heterogenous according to location and histopathology. Moreover, our findings point to common molecular mechanisms underlying cardia GC and OAC/BO.
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