| 1. |
- Bakke, Ingunn, et al.
(författare)
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Mucosal and faecal neutrophil gelatinase-associated lipocalin as potential biomarkers for collagenous colitis
- 2021
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Ingår i: Journal of gastroenterology. - : Springer Nature. - 0944-1174 .- 1435-5922. ; 56:10, s. 914-927
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Tidskriftsartikel (refereegranskat)abstract
- Background Collagenous colitis (CC) is an inflammatory bowel disease where chronic diarrhoea is the main symptom. Diagnostic markers distinguishing between CC and other causes of chronic diarrhoea remain elusive. This study explores neutrophil gelatinase-associated lipocalin (NGAL) and its mRNA lipocalin2 (LCN2) as histological and faecal disease markers in CC. Methods NGAL/LCN2 were studied in colonic biopsies from CC patients before and during budesonide treatment using RNA sequencing (n = 9/group), in situ hybridization (ISH) (n = 13-22/group) and immunohistochemistry (IHC) (n = 14-25/group). Faecal samples from CC (n = 3-28/group), irritable bowel syndrome diarrhoea (IBS-D) (n = 14) and healthy controls (HC) (n = 15) were assayed for NGAL and calprotectin. Results NGAL/LCN2 protein and mRNA expression were upregulated in active CC vs HC, and vs paired samples of treated CC in clinical remission. IHC and ISH localized increased NGAL/LCN2 mainly to epithelium of active CC, compared to almost absence in HC and treated CC. In contrast, calprotectin was solely expressed in immune cells. Despite great individual differences, faecal NGAL was significantly increased in active CC compared to HC, IBS-D and treated CC and had high test sensitivity. Faecal calprotectin levels were variably increased in active CC, but the values remained below usual clinical cut-offs. Conclusion NGAL/LCN2 is upregulated in the epithelium of active CC and reduced during budesonide-induced clinical remission to the level of HC and IBD-S. This was reflected in NGAL faecal concentrations. We propose NGAL as an IHC marker for disease activity in CC and a potential faecal biomarker discriminating CC from HC and IBS-D.
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| 2. |
- Bledsoe, Adam C., et al.
(författare)
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Mortality and cancer in eosinophilic gastrointestinal disorders distal to the esophagus : nationwide cohort study 1990-2017
- 2022
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Ingår i: Journal of gastroenterology. - : Springer. - 0944-1174 .- 1435-5922. ; 57, s. 735-747
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Tidskriftsartikel (refereegranskat)abstract
- Background: Eosinophilic gastrointestinal disorders (EGIDs) include inflammatory conditions with enteric infiltration of eosinophils and resulting symptoms. This study aims to examine a population-based sample of patients for prevalence, mortality, and cancer risk in EGIDs distal to the esophagus.Methods: Nationwide, population-based cohort study. EGID was identified through relevant biopsy codes from Sweden's all 28 pathology departments through the ESPRESSO cohort. Individuals with EGID were then matched to general population reference individuals with similar age and sex. Study participants were linked to Swedish healthcare registers. Through Cox regression, we calculated adjusted hazard ratios (aHRs) adjusting for sex, age, county, calendar period, and education.Results: In total, 2429 patients (56% female) were found to have EGID distal to the esophagus, representing a prevalence of about 1/4800 in the Swedish population. Mean age was 44 years with 11% children at the time of diagnosis. Mortality was increased 17% in patients with EGIDs compared to reference individuals (aHR = 1.17; 95%CI = 1.04-1.33). Excess mortality was seen in gastric and small bowel eosinophilic disease, but not colonic disease (aHR = 1.81; 95%CI = 1.32-2.48, aHR = 1.50; 95%CI = 1.18-1.89, and aHR = 0.99; 95%CI = 0.85-1.16, respectively). Cause specific mortality was driven by cancer-related death (aHR = 1.33; 95%CI = 1.05-1.69). However, this study failed to show an increase in incident cancers (aHR = 1.14; 95%CI = 0.96-1.35). Comparison of EGID individuals with their siblings yielded similar aHRs.Conclusions: This study found an increased risk of death in patients with EGIDs distal to the esophagus, with cancer death driving the increase. Proximal gut disease seems to confer the greatest risk. There was no increase in incident cancers.
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| 3. |
- Brusselaers, Nele, et al.
(författare)
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Proton pump inhibitors and the risk of pancreatic cancer
- 2021
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Ingår i: Journal of gastroenterology. - : Springer Science and Business Media LLC. - 0944-1174 .- 1435-5922. ; 56:3, s. 295-296
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 4. |
- Gremel, Gabriela, et al.
(författare)
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The human gastrointestinal tract-specific transcriptome and proteome as defined by RNA sequencing and antibody-based profiling
- 2015
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Ingår i: Journal of gastroenterology. - : Springer. - 0944-1174 .- 1435-5922. ; 50:1, s. 46-57
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The gastrointestinal tract (GIT) is subdivided into different anatomical organs with many shared functions and characteristics, but also distinct differences. We have combined a genome-wide transcriptomics analysis with immunohistochemistry-based protein profiling to describe the gene and protein expression patterns that define the human GIT. METHODS: RNA sequencing data derived from stomach, duodenum, jejunum/ileum and colon specimens were compared to gene expression levels in 23 other normal human tissues analysed with the same method. Protein profiling based on immunohistochemistry and tissue microarrays was used to sub-localize the corresponding proteins with GIT-specific expression into sub-cellular compartments and cell types. RESULTS: Approximately 75% of all human protein-coding genes were expressed in at least one of the GIT tissues. Only 51 genes showed enriched expression in either one of the GIT tissues and an additional 83 genes were enriched in two or more GIT tissues. The list of GIT-enriched genes with validated protein expression patterns included various well-known but also previously uncharacterised or poorly studied genes. For instance, the colon-enriched expression of NXPE family member 1 (NXPE1) was established, while NLR family, pyrin domain-containing 6 (NLRP6) expression was primarily found in the human small intestine. CONCLUSIONS: We have applied a genome-wide analysis based on transcriptomics and antibody-based protein profiling to identify genes that are expressed in a specific manner within the human GIT. These genes and proteins constitute important starting points for an improved understanding of the normal function and the different states of disease associated with the GIT.
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| 5. |
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| 6. |
- Inoue T, T, et al.
(författare)
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Autofluorescence imaging videoendoscopy in the diagnosis of chronic atrophic fundal gastritis
- 2010
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Ingår i: Journal of Gastroenterology. - : Springer Science and Business Media LLC. - 0944-1174 .- 1435-5922. ; 45:1, s. 45-51
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: Diagnosis of chronic atrophic fundal gastritis (CAFG) is important to understand the pathogenesis of gastric diseases and assess the risk of gastric cancer. Autofluorescence imaging videoendoscopy (AFI) may enable the detection of mucosal features not apparent by conventional white-light endoscopy. The purpose of this study was to estimate the diagnostic ability of AFI in CAFG. Methods: A total of 77 patients were enrolled. Images of the gastric body in AFI and white-light mode were taken to assess the extent of gastritis, and biopsies were taken from green (n = 119) and purple (n = 146) mucosa in AFI images. The diagnostic accuracy of green mucosa for CAFG was investigated according to the Sydney system. Results: In per-patient analysis, the accuracy of green mucosa in patients with activity, inflammation, atrophy and intestinal metaplasia was 64, 93, 88 and 81%, respectively. In per-biopsy analysis, the accuracy for activity, inflammation, atrophy and intestinal metaplasia was 55, 62, 76 and 76%, respectively. Green areas in the gastric body exhibited more inflammation (p\0.001), atrophy (p\0.001) and intestinal metaplasia (p\0.001), whereas purple areas rarely contained atrophy or intestinal metaplasia. The kappa statistics for inter- and intra-observer agreement of AFI on assessing the extent of CAFG were 0.66 and 0.47, while those for white-light endoscopy were 0.56 and 0.39. Conclusions: AFI could diagnose the extent of CAFG as a green area in the gastric body, with higher reproducibility compared with white-light endoscopy. Therefore, AFI may be a useful adjunct to endoscopy to identify patients at high risk of developing gastric cancer.
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| 7. |
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| 8. |
- Johansson, Johan, et al.
(författare)
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Pancreatic acinar metaplasia in the distal oesophagus and the gastric cardia: prevalence, predictors and relation to GORD
- 2010
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Ingår i: JOURNAL OF GASTROENTEROLOGY. - : Springer Science and Business Media LLC. - 0944-1174 .- 1435-5922. ; 45:3, s. 291-299
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Tidskriftsartikel (refereegranskat)abstract
- The nature of pancreatic acinar metaplasia (PAM) in the gastro-oesophageal junction (GOJ) remains obscure. We aimed to estimate its prevalence and investigate into its risk factors in a population-based series of first-time endoscopy patients. We investigated consecutive patients, endoscoped for the first time, representing defined catchment area populations. Biopsies were taken immediately below the GOJ and from the distal oesophagus. Endoscopy room-based cross-sectional clinical data were supplemented with exposure data from 160 population controls. Associations, expressed as odds ratios (OR), were modelled with multivariable logistic regression. A subsample of 26 patients underwent oesophageal pH monitoring. Among 644 patients (mean age 53 years, 43% men), PAM was found in 121 patients (19%), exclusively above the GOJ in 40 (6%), below GOJ in 67 (10%), and both above and below GOJ in 14 (2%). PAM exclusively above the GOJ and PAM exclusively below the GOJ were both borderline associated with age (2% increase in prevalence per year). PAM exclusively above the GOJ was significantly associated with female gender (OR 2.8, 95% CI 1.3-6.3) and presence of Helicobacter pylori immediately below the GOJ (OR 2.6, 95% CI 1.3-5.4). Out of 21 patients with Barretts oesophagus (BO), 8 (38%) had PAM above the GOJ. The mean value for percentage time with oesophageal pH andlt; 4.0 was 7.3% (95% CI 4.3-10.2%) among patients who had PAM above the GOJ (reference value 3.4%). Pancreatic acinar metaplasia might be an age-dependent lesion, associated with H. pylori, female gender and gastro-oesophageal reflux if located above the GOJ.
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| 9. |
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| 10. |
- Ludvigsson, Jonas F., et al.
(författare)
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Risk of lymphoproliferative malignancy in celiac patients with a family history of lymphoproliferative malignancy
- 2013
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Ingår i: Journal of gastroenterology. - : Springer Science and Business Media LLC. - 0944-1174 .- 1435-5922. ; 48:12, s. 1324-1331
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Tidskriftsartikel (refereegranskat)abstract
- Individuals with celiac disease (CD) are at increased risk of lymphoproliferative malignancy (LPM). We examined if a family history of LPM or any cancer influenced the risk of LPM in individuals with CD. We identified 28,996 individuals with biopsy-verified CD (equal to villous atrophy, Marsh histopathology stage 3), of whom 616 had family history of LPM. Cox regression then estimated hazard ratios (HRs) for LPM in these 616 compared with two control groups. We also examined the risk of LPM in CD individuals with a family history of any cancer (n = 8,439). During follow-up, 2/616 CD individuals with a family history of LPM, and 235/28,380 CD individuals without a family history of LPM developed LPM themselves. CD individuals with a family history of LPM were not at increased risk of LPM compared to general population controls (HR = 1.18; 95 % CI = 0.27-5.10), or compared to CD individuals without a family history of LPM (adjusted HR = 0.31; 95 % CI = 0.08-1.23). We found no increased risk of LPM in CD individuals with a family history of any cancer. This study found no evidence that a family history of LPM or any cancer increases the risk of future LPM in individuals with CD. Despite the large number of study participants, this study is nevertheless limited by few positive events due to a low absolute risk of LPM even in individuals with CD.
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| 11. |
- Maret-Ouda, John, et al.
(författare)
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Proton pump inhibitor use and risk of pneumonia : a self-controlled case series study
- 2023
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Ingår i: Journal of gastroenterology. - : Springer. - 0944-1174 .- 1435-5922. ; 58, s. 734-740
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Tidskriftsartikel (refereegranskat)abstract
- Background: Recent research indicates that use of proton pump inhibitors (PPIs) is associated with pneumonia, but existing evidence is inconclusive because of methodological issues. This study aimed to answer whether PPI-use increases risk of pneumonia while taking the methodological concerns of previous research into account.Methods: This population-based and nationwide Swedish study conducted in 2005-2019 used a self-controlled case series design. Data came from national registries for medications, diagnoses, and mortality. Conditional fixed-effect Poisson regression provided incidence rate ratios (IRR) with 95% confidence intervals (CI) for pneumonia comparing PPI-exposed periods with unexposed periods in the same individuals, thus controlling for confounding. Analyses were stratified by PPI-treatment duration, sex, age, and smoking-related diseases. Use of histamine type-2 receptor antagonists (used for the same indications as PPIs) and risk of pneumonia was analysed for assessing the validity and specificity of the results for PPI-therapy and pneumonia.Results: Among 519,152 patients with at least one pneumonia episode during the study period, 307,709 periods of PPI-treatment occurred. PPI-use was followed by an overall 73% increased risk of pneumonia (IRR 1.73, 95% CI 1.71-1.75). The IRRs were increased across strata of PPI-treatment duration, sex, age, and smoking-related disease status. No such strong association was found between histamine type-2 receptor antagonist use and risk of pneumonia (IRR 1.08, 95% CI 1.02-1.14).Conclusions: PPI-use seems to be associated with an increased risk of pneumonia. This finding highlights a need for caution in using PPIs in individuals with a history of pneumonia.
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| 12. |
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| 13. |
- Schol, J., et al.
(författare)
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Postinfectious onset in functional dyspepsia is a risk factor for weight loss
- 2022
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Ingår i: Journal of Gastroenterology. - : Springer Science and Business Media LLC. - 0944-1174 .- 1435-5922. ; 57:3, s. 156-163
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Tidskriftsartikel (refereegranskat)abstract
- Background: Functional dyspepsia (FD) is differentiated into two subgroups: the postprandial distress syndrome (PDS) and epigastric pain syndrome (EPS). Acute gastroenteritis and Helicobacter pylori (HP) infection have been identified as risk factors for FD. It is unclear how these risk factors relate to Rome IV subgroups and their clinical impact. We aimed to study the association of postinfectious FD (PI-FD) and HP status with clinical profiles and weight loss. Methods: Consecutive FD patients were assessed for symptom frequency and severity. Patients were identified as PDS, EPS or the overlap group according to severity scores. Additionally, PI history and HP status were determined. Results: In a cohort of 459 FD-patients, 36% were characterized as having PDS, 9% as having EPS and 55% showed overlap. PI onset and positive HP status were reported by, respectively, 20% and 14% of patients, not significantly differing between subgroups (respectively, p = 0.31 and p = 0.40). Weight loss was reported by 63% in PDS, 36% in EPS and 56% in overlap patients (p = 0.011). Only early satiety severity correlated with more severe weight loss in the PDS (r 0.31, p < 0.0001) and overlap group (r 0.38, p < 0.0001). PI-FD patients were more likely to experience weight loss (OR 2.27, p = 0.0013). HP status was not significantly associated with weight loss (p = 0.90). Conclusion: In this cohort, PI onset of FD symptoms emerged as a risk factor for weight loss, but was not associated with the symptom patterns of PDS, EPS or overlap subgroups. Patients with HP infection were not more likely to experience important weight loss. © 2022, Japanese Society of Gastroenterology.
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| 14. |
- Tanash, Hanan A., et al.
(författare)
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Liver disease in adults with severe alpha-1-antitrypsin deficiency
- 2019
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Ingår i: Journal of Gastroenterology. - : Springer Science and Business Media LLC. - 0944-1174 .- 1435-5922. ; 54:6, s. 541-548
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Tidskriftsartikel (refereegranskat)abstract
- Background: The proportion of adults with liver disease due to severe alpha-1-antitrypsin deficiency (AATD), with PiZZ phenotype, is not clear. The markers of the AATD liver disease, how it progresses, and measures for its prevention have not been established. The aim of this study was to analyze the risk of liver disease in individuals with severe AAT deficiency (PiZZ). Methods: Longitudinal clinical and laboratory data were obtained from the Swedish National registers, by cross-linkage between the Swedish national AATD register, the Swedish National Patient Register, the National Cancer Register and the National Causes of Death Register. Results: A total of 1595 PiZZ individuals were included in the analyses. The mean follow-up time was 12 years (range 0.3–24). The mean number of follow-ups was 5 (range 2–15). Two or more liver function tests (LFTs) were available in 1123 individuals, and 26% of them (n = 290) had repeated elevated LFTs during the follow-up. The prevalence of any liver disease was 10% (n = 155). Liver cirrhosis was found in 7% of the individuals (n = 116) and hepatocellular carcinoma in 2% (n = 29). The mean age at the onset of liver disease was 61 (SD 15) years. In multivariate analyses, the male gender, age over 50 years, repeated elevated LFTs, hepatitis virus infection, and a diagnosis of diabetes were associated with increased risk of developing liver disease in adulthood (p < 0.01). Conclusion: The prevalence of liver disease in adult PiZZ individuals is 10%. Age over 50 years, the male gender, repeated elevated liver enzymes, hepatitis, and the presence of diabetes mellitus are risk factors for developing liver disease.
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| 15. |
- Ugai, Tomotaka, et al.
(författare)
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Prognostic role of detailed colorectal location and tumor molecular features : analyses of 13,101 colorectal cancer patients including 2994 early-onset cases
- 2023
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Ingår i: Journal of gastroenterology. - : Springer. - 0944-1174 .- 1435-5922. ; 58, s. 229-245
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Tidskriftsartikel (refereegranskat)abstract
- Background: The pathogenic effect of colorectal tumor molecular features may be influenced by several factors, including those related to microbiota, inflammation, metabolism, and epigenetics, which may change along colorectal segments. We hypothesized that the prognostic association of colon cancer location might differ by tumor molecular characteristics.Methods: Utilizing a consortium dataset of 13,101 colorectal cancer cases, including 2994 early-onset cases, we conducted survival analyses of detailed tumor location stratified by statuses of microsatellite instability (MSI), CpG island methylator phenotype (CIMP), and KRAS and BRAF oncogenic mutation.Results: There was a statistically significant trend for better colon cancer-specific survival in relation to tumor location from the cecum to sigmoid colon (Ptrend = 0.002), excluding the rectum. The prognostic association of colon location differed by MSI status (Pinteraction = 0.001). Non-MSI-high tumors exhibited the cecum-to-sigmoid trend for better colon cancer-specific survival [Ptrend < 0.001; multivariable hazard ratio (HR) for the sigmoid colon (vs. cecum), 0.80; 95% confidence interval (CI) 0.70–0.92], whereas MSI-high tumors demonstrated a suggestive cecum-to-sigmoid trend for worse survival (Ptrend = 0.020; the corresponding HR, 2.13; 95% CI 1.15–3.92). The prognostic association of colon tumor location also differed by CIMP status (Pinteraction = 0.003) but not significantly by age, stage, or other features. Furthermore, MSI-high status was a favorable prognostic indicator in all stages.Conclusions: Both detailed colonic location and tumor molecular features need to be accounted for colon cancer prognostication to advance precision medicine. Our study indicates the important role of large-scale studies to robustly examine detailed colonic subsites in molecular oncology research.
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| 16. |
- Vanhoutvin, S. A. L. W., et al.
(författare)
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Alternative procedure to shorten rectal barostat procedure for the assessment of rectal compliance and visceral perception : a feasibility study
- 2012
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Ingår i: Journal of gastroenterology. - : Springer-Verlag Tokyo Inc.. - 0944-1174 .- 1435-5922. ; 47:8, s. 896-903
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Barostat methodology is widely used for assessing visceral perception. Different barostat protocols are described with respect to the measurement of rectal compliance and visceral perception. The choice of protocols affects the duration, which is normally 60-90 min, and accuracy of the procedure. This study aimed to shorten the procedure by using the semi-random distension protocol for both compliance and visceral perception measurement and a correction based on rectal capacity (RC) instead of minimal distension pressure (MDP).METHODS: Twelve irritable bowel syndrome (IBS) patients (7 females) and 11 healthy controls (8 females) underwent a barostat procedure. Compliance was determined during both a staircase distension and a semi-random protocol. Visceral perception data were compared as a function of pressure or relative volume, corrected for MDP or RC, respectively.RESULTS: Compliance measurement using the semi-random protocol instead of the staircase distension protocol resulted in an overestimation in healthy volunteers, but not in IBS patients. The overall conclusion that IBS patients had a lower compliance compared to controls was not different between protocols. Data presentation of the visceral perception scores as a function of corrected volume instead of pressures corrected for MDP did not alter the conclusion that sensation scores in IBS patients were higher as compared to healthy controls.CONCLUSIONS: This study showed that barostat procedures may be shortened by approximately 20 min, without losing the ability to discriminate between healthy controls and IBS patients. A correction for RC instead of MDP may improve the accuracy of the procedure.
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| 17. |
- Yeh, Ka Ming, et al.
(författare)
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Cystic fibrosis transmembrane conductance regulator modulates enteric cholinergic activities and is abnormally expressed in the enteric ganglia of patients with slow transit constipation
- 2019
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Ingår i: Journal of gastroenterology. - : SPRINGER JAPAN KK. - 0944-1174 .- 1435-5922. ; 54:11, s. 994-1006
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Tidskriftsartikel (refereegranskat)abstract
- Background Cystic fibrosis transmembrane conductance regulator (CFTR) was recently found in the enteric nervous system, where its role is unclear. We aimed to identify which enteric neuronal structures express CFTR, whether CFTR modulates enteric neurotransmission and if altered CFTR expression is associated with slow transit constipation (STC). Methods Immunofluorescence double labeling was performed to localize CFTR with various neuronal and glial cell markers in the human colon. The immunoreactivity (IR) of CFTR and choline acetyltransferase (ChAT) on myenteric plexus of control and STC colon was quantitatively analyzed. In control colonic muscle strips, electrical field stimulation (EFS) evoked contractile responses and the release of acetylcholine (ACh) was measured in the presence of the CFTR channel inhibitor, CFTR(inh)-172. Results CFTR-IR was densely localized to myenteric ganglia, where it was co-localized with neuronal markers HuC/D and beta-tubulin, and glial marker S-100 but little with glial fibrillary acidic protein. Vesicular ACh transport was almost exclusively co-localized with CFTR, but neurons expressing nitric oxide synthase were CFTR negative. Significant reductions of CFTR-IR (P amp;lt; 0.01) and ChAT-IR (P amp;lt; 0.05) were observed on myenteric ganglia of STC compared to control. Pre-treatment of colonic muscle strips with CFTR(inh)-172 (10 mu M) significantly inhibited EFS-evoked contractile responses (P amp;lt; 0.01) and ACh release (P amp;lt; 0.05). Conclusions Co-localization of CFTR-IR with cholinergic markers, inhibition of EFS-induced colonic muscle contractility and ACh release by CFTR(inh)-172 suggest that CFTR modulates enteric cholinergic neurotransmission. The downregulation of CFTR and ChAT in myenteric ganglia of STC correlated with the impaired contractile responses to EFS.
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| 18. |
- Zhou, Jin, et al.
(författare)
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The prognostic significance of peroxisome proliferator-activated receptor beta expression in the vascular endothelial cells of colorectal cancer
- 2014
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Ingår i: Journal of gastroenterology. - : Springer Verlag (Germany). - 0944-1174 .- 1435-5922. ; 49:3, s. 436-445
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Tidskriftsartikel (refereegranskat)abstract
- Currently, little is known regarding the role of peroxisome proliferator-activated receptor-beta (PPAR beta) in the vascular endothelial cells (VECs) of colorectal cancers (CRCs). The aim of this study was to investigate the relationship of PPAR beta expression in the VECs of CRCs in terms of the prognosis and clinicopathological features of CRC patients. The expression and localization of PPAR beta in the primary cancers and the matched normal mucosal samples of 141 Swedish CRC patients were analyzed in terms of its correlation with clinicopathological features and the expression of angiogenesis-related genes. This study also included 92 Chinese CRC patients. PPAR beta was predominantly localized in the cytoplasm and was significantly downregulated in the VECs of CRC compared to that of the normal mucosa. The low expression levels of PPAR beta in the VECs of CRC were statistically correlated with enhanced differentiation, early staging and favorable overall survival and were associated with the increased expression of VEGF and D2-40. The patients exhibiting elevated expression of PPAR beta in CRC cells but reduced expression in VECs exhibited more favorable survival compared with the other patients, whereas the patients with reduced expression of PPAR beta in CRC cells but increased expression in VECs exhibited less favorable prognosis. PPAR beta might play a tumor suppressor role in CRC cells in contrast to a tumor promoter role in the VECs of CRCs.
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