| 1. |
- Adlerberth, Ingegerd, 1959, et al.
(författare)
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Adhesins of Escherichia coli associated with extra-intestinal pathogenicity confer binding to colonic epithelial cells.
- 1995
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Ingår i: Microbial pathogenesis. - 0882-4010. ; 18:6, s. 373-85
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Tidskriftsartikel (refereegranskat)abstract
- Escherichia coli adhesins are virulence factors in intestinal and extra-intestinal infections, but their role in normal intestinal colonization has not been defined. We investigated the intestinal adherence of E. coli with Dr hemagglutinin, S fimbriae, CFA/I or CFA/II, using freshly isolated ileal or colonic enterocytes and cells from the human colonic cell line HT-29. E. coli with S-fimbrial adhesins (Sfa I or Sfa II), P or type 1 fimbriae, adhered in a non-polarized manner, and in similar numbers to colonic and ileal enterocytes. S fimbriae of the variety Sfa II (originating from a meningitis isolate), mediated a stronger binding than Sfa I (of uropathogenic origin). Strains expressing Dr hemagglutinin adhered preferentially to the brush borders, slightly better to colonic than ileal enterocytes. Strains expressing CFA/I or II adhered to colonic and ileal enterocytes, although brush border adherence was predominantly observed with ileal cells. Binding to HT-29 cells paralleled binding to colonic enterocytes for all adhesin specificities except CFA/I. The results suggest that Dr hemagglutinin, P-, type 1- and S-fimbrial adhesins mediate binding to both colonic and ileal enterocytes. These specificities may contribute to the establishment of E. coli in the intestinal microflora, which precedes their spread to extra-intestinal sites.
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| 2. |
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| 3. |
- Cahlin, Christian, 1959, et al.
(författare)
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Growth associated proteins in tumor cells and stroma related to disease progression of colon cancer accounting for tumor tissue PGE2 content.
- 2008
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Ingår i: International journal of oncology. - 1019-6439. ; 32:4, s. 909-18
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Tidskriftsartikel (refereegranskat)abstract
- Connections among specific proteins (Bax, Bcl-2, bFGF, COX-1, COX-2, E-cad, p15, p53, PCNA, TGFbeta3, TUNEL, vWF) in control of cell proliferation, apoptosis, cell adhesion, tumor vascularity and PGE2 content were evaluated in colon cancer as related to disease progression and survival. Tumor tissue and adjacent normal colon mucosa were obtained at curative resection in 22 patients. PGE2 concentrations were assessed in tumor tissue and tumor derived blood, splanchnic blood, peripheral venous blood and urine. Host inflammation was determined (CRP, ESR) in relationship to tumor differentiation and stage. Patients survived as expected according to Dukes A-D staging. Growth-related proteins correlated between tumor cells and stroma as well as between protein factors within tumor cells and tumor stroma. COX-2 predicted tumor tissue content of PGE2 (p<0.002), without reflection in tumor derived blood. Systemic inflammation was predicted by p15, TGFbeta3 and Bcl-2 in tumor tissue (p<0.001). p15 and vWF predicted reduced survival in ungrouped patients (p<0.02), while p15, PCNA, TGFbeta3 and vWF predicted reduced survival (p<0.0001) when patient grouping accounted for high tumor content of PGE2. Our results connect systemic inflammation and survival to COX-2 staining and increased PGE2 in colon cancer. Thus, it seems important to understand proximal signals behind upregulation of COX-2 and subsequent PGE2 production in certain tumor cells in colon cancer.
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| 4. |
- Carlsson, E., et al.
(författare)
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Body composition in patients with short bowel syndrome: an assessment by bioelectric impedance spectroscopy (BIS) and dual-energy absorptiometry (DXA)
- 2004
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Ingår i: European journal of clinical nutrition. - : Springer Science and Business Media LLC. - 0954-3007 .- 1476-5640. ; 58:6, s. 853-9
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To describe body composition in patients with short bowel syndrome (SBS) by using bioelectric impedance spectroscopy (BIS), dual-energy X-ray absorptiometry (DXA) measurements and anthropometrical-derived estimates. SUBJECTS: In all, 19 patients were included, mean age 54 y, range 36-77 (F/M=11/8). Mean BMI was 21.5 kg/m(2). Eight patients were on home parenteral nutrition (HPN). METHODS: Total body water (TBW), intracellular water and extracellular water were assessed by BIS. TBW were derived from DXA. Fat-free mass (FFM) was assessed by BIS and DXA. TBW and FFM were predicted according to an empirical formula. Differences were analysed using the Bland-Altman method. RESULTS: The mean difference between TBW (DXA) and TBW (BIS) was -1.1 l in women and -1.8 l in men. For FFM, the mean difference between FFM (DXA) and FFM (BIS) was -1.7 kg in women and -2.5 kg in men. The mean difference between TBW (DXA) and TBW (BIS) for all patients was -1.2 l and limits of agreement were (-7.80-5.40). Hydration of FFM assessed by BIS gave a mean of 0.75 (0.08). CONCLUSION: The limits of agreement (Bland-Altman) between DXA and BIS were wide, indicating that methods are not interchangeable, which limits its clinical utility. Most of our patients with SBS were maintained in a stable clinical condition within normal limits of body weight and BMI. FFM and TBW did not appear to be altered in ileostomates or those on HPN.
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| 5. |
- Dabrosin-Söderholm, Johan, 1958-
(författare)
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Epithelial barrier dysfunction in ileal Crohn's disease
- 1998
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The study aimed at investigating the intestinal barrier in Crohn's disease, with special reference to epithelial responses to luminal stimuli, and to permeation of proteins.Ileal mucosa from patients undergoing intestinal resection was studied in vitro in Ussing chambers. Intestinal permeability was also studied in vivo, by oral load of lactulose and mannitol.The Ussing chamber was evaluated for intestinal barrier studies. Normal ileal mucosa from patients with colon cancer was subjected to long-term experiments, and investigated in regard to various viability parameters. Mucosal permeability, structural integrity and metabolism were maintained for 90 minutes, and specimens with poor viability were detected by a low transepithelial potential difference. In rat ileal mucosa, luminal sodium caprate, a constituent of milk fat, induced dilatation of the tight junctions as visualised by electron microscopy, and a reversible increase in tight junction permeability. The findings indicate that the Ussing chamber is suitable for studies of the intestinal barrier, including tight junction regulation, provided that experiments are monitored by measurements of transepithelial potential difference and are limited in time.In vitro studies of human ileal mucosa showed that luminal sodium caprate caused uncoupling of oxidative phosphorylation, as shown by a fall in epithelial ATP contents, and mitochondrial swelling seen by electron microscopy, paralleled by an increased permeability. Non-inflamed Crohn's disease specimens had an exaggerated permeability increase and an augmented fall in transepithelial electrical resistance. Confocal microscopy revealed rearrangements of perijunctional filamentous actin, causing dilatation of the tight junctions. In Crohn's disease, a more pronounced reorganisation of actin filaments was seen, suggesting the tight junctions to be hyperreactive to luminal stimuli due to a disturbed cytoskeletal regulation.In vivo, an increased intestinal permeability was induced by ingestion of acetylsalicylic acid. One third of both Crohn's disease patients and their first-degree relatives showed an augmented permeability increase, whereas spouses were equal to controls, suggesting a genetically determined vulnerability of the intestinal barrier.In vitro, non-inflamed ileum from Crohn's disease patients had an increased permeation of ovalbumin. Confocal microscopy suggested this to be caused by an augmented transcytosis, a previously unrecognised defect in the epithelial barrier in Crohn's disease, with a subsequent exposure of antigenic proteins to the subepithelial immunocytes.The Crohn's disease patients without residual inflammation after surgery were followed with endoscopy within twelve months, and all revealed recurrent ileal inflammation.The study indicates a perturbed intestinal barrier in Crohn's disease, possibly genetically determined. The impaired barrier function is demonstrated both by an augmented epithelial transcytosis and by hyperreactive tight junctions. The epithelial barrier dysfunction precedes the recurrent intestinal inflammation in ileal Crohn's disease. The findings suggest an interplay between an impaired epithelial barrier and luminal factors in the initiation of intestinal inflammation.
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| 6. |
- Delbro, Dick, 1950, et al.
(författare)
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Demonstration of P2Y4 purinergic receptors in the HT-29 human colon cancer cell line
- 2005
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Ingår i: Autonomic & autacoid pharmacology. - 1474-8665. ; 25:4, s. 163-6
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Tidskriftsartikel (refereegranskat)abstract
- 1 The aim of the current study was to investigate the existence of P 2 Y(4) purinergic receptors in the HT-29 human colon cancer cell line. 2 We utilized Western blots and immunocytochemistry for the analysis. 3 Western blotting demonstrated two bands that could not be found after the antibody had been preabsorbed with the control peptide, suggesting that both bands are related to the P 2 Y(4) purinergic receptor. 4 Immunocytochemistry showed immunoreactivity for the P 2 Y(4) purinergic receptor localized in the cytoplasm of the HT-29 cells. 5 This is the first demonstration of the protein expression of P 2 Y(4) purinergic receptors in a human colon cancer cell line.
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| 7. |
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| 8. |
- Delbro, Dick, et al.
(författare)
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Nuclear expression of mu-opioid receptors in a human mesothelial cell line
- 2009
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Ingår i: Autonomic & Autacoid Pharmacology. - : Wiley. - 1474-8665 .- 1474-8673. ; 29:4, s. 165-170
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Tidskriftsartikel (refereegranskat)abstract
- 1 Possibly acting via mu-opioid receptors (MORs), morphine inhibits the formation ofexperimentally induced postoperative abdominal adhesions in rats. Mesothelial cells mayparticipate in adhesion formation by secreting mediators that interfere negatively withfibrinolysis. Morphine may prevent adhesions by inhibiting the release of pro-adhesionmediators from mesothelial cells. This study aimed to investigate whether human mesothelialcells express MOR-1; if so, such could constitute a site of action for morphine in adhesionprevention.2 Cells from Met-5A, a human mesothelial cell line were seeded and prepared forimmunocytochemistry and Western blotting.3 Immunocytochemistry showed MOR-1 expression in mesothelial cells, predominantly in thenuclei. Western blotting showed two bands (c. 35 and 50 kDa) which correspond to thoseobtained with a control lysate from cells known to express MORs. In addition, we foundMOR-1 expression with nuclear and cytoplasmatic localization in biopsies from humanabdominal adhesions.4 The current findings may suggest that morphine could interact directly with mesothelial cellsvia MOR-1 receptors, and thereby modulate adhesion formation, possibly by interfering withthe release of pro-adhesion factors from these cells
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| 9. |
- Gustafsson Asting, Annika, et al.
(författare)
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EP1-4 subtype, COX and PPAR gamma receptor expression in colorectal cancer in prediction of disease-specific mortality
- 2007
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Ingår i: International journal of cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 121:2, s. 232-40
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Tidskriftsartikel (refereegranskat)abstract
- The importance of prostaglandins in tumor growth and progression is well recognized, including antineoplastic activities by cyclooxygenase (COX) inhibitors. Variation in treatment response to COX inhibition has questioned differences in expression of cell surface and nuclear membrane receptors among tumors with different disease progression. The purpose of this study was to evaluate whether EP(1-4) subtype, PPAR gamma receptor and COX-1/COX-2 expression in colorectal cancer are related to tumor-specific mortality. Reverse transcription-polymerase chain reaction and immunohistochemistry were used to demonstrate expression and protein appearance in tumor tissue compared with normal colon tissue. EP(1) and EP(2) subtype receptor protein was highly present in tumor cells, EP(3) occurred occasionally and EP(4) was not visible. PPAR gamma, EP(2) and EP(4) mRNA were significantly higher in normal colon tissue compared with tumor tissue, without any distinct relationship to Dukes A-D tumor stage. Multivariate analyses indicated that increased tumor tissue EP(2) and COX-2 expression predicted poor survival (p<0.001). COX-1 expression was significantly higher than COX-2 expression in normal colon tissue. Average COX-2 mRNA was not increased in tumor tissue compared with normal colon. However, most tumor cells stained positive for COX-2 protein, which was low or undetectable in normal mucosa cells. COX-1 protein was preferentially visible in stroma. EP(1-4) subtype receptor mRNAs were generally positively correlated to both COX-1 and COX-2 in tumor tissue, but not in normal colon. Our results imply that both prostaglandin production (COX-2) and signaling via EP(1-4) subtype receptors, particularly EP(2), predict disease-specific mortality in colorectal cancer.
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| 10. |
- Gustafsson Asting, Annika, et al.
(författare)
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Prostanoid receptor expression in colorectal cancer related to tumor stage, differentiation and progression.
- 2007
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Ingår i: Acta oncologica (Stockholm, Sweden). - : Informa UK Limited. - 0284-186X .- 1651-226X. ; 46:8, s. 1107-12
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Tidskriftsartikel (refereegranskat)abstract
- INTRODUCTION: Alterations in eicosanoid metabolism is well established in a variety of malignant tumors, particularly colorectal carcinoma. Recent studies in our laboratory have emphasized a role for EP subtype receptors in progression of colorectal cancer and disease specific mortality. Therefore, the aim of the present study was to extend our knowledge to include additional receptor expression (DP1, DP2, FP, IP, TP) for prostanoids (PGD2, TXA2, PGF2alpha, PGI2) in relationship to tumor stage, differentiation and progression of colorectal cancer. MATERIAL AND METHODS: Total RNA from 62 tumors and adjacent normal colon tissue (n = 48) was extracted. Quantification of receptor expression was performed by realtime PCR and related to the expression of an appropriate housekeeping gene (GAPDH). Tumors were assessed according to Dukes A-D (stage I-IV). RESULTS: DP1, DP2, FP and IP receptor subtypes displayed significantly reduced overall expression in tumor tissue compared to normal colon tissue, while the TP receptor subtype showed significantly higher expression in tumor tissue. Overall expression of the prostanoid receptors in tumor tissue was not related to clinical indexes as tumor stage and tumor cell differentiation evaluated by multivariate analyses. Cultured colorectal cancer cell lines with low (HT-29) and high (HCA-7) intrinsic PGE2 production at confluent state did not express DP1 and IP receptor subtypes, but displayed low expression of DP2, FP and TP receptor subtypes. CONCLUSION: The results in the present study indicate imbalanced expression of prostanoid receptors in colorectal cancer compared to normal colon tissue without clear cut relationship to disease progression. Therefore, future studies should be performed on defined cells within the tumor tissue compartment determining whether any prostanoid receptor(s) is useful as a molecular target in treatment or prevention of colorectal cancer.
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| 11. |
- Gustafsson Asting, Annika, et al.
(författare)
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Receptor and enzyme expression for prostanoid metabolism in colorectal cancer related to tumor tissue PGE2.
- 2010
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Ingår i: International journal of oncology. - 1791-2423. ; 36:2, s. 469-478
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Tidskriftsartikel (refereegranskat)abstract
- Prostaglandins support progression of colorectal cancer by several mechanisms. This conclusion is based on epidemiological and drug intervention long-term studies or retrieved from animal and cell culture experiments. The aim of the present study was to map receptor and enzyme expression for prostanoid metabolism in the presence of high or low PGE2 content within colon cancer tissue at primary tumor operation and after short-term preoperative provision of non-steroidal anti-inflammatory drug (NSAID). Twenty-three unselected patients with colon cancer were randomly selected to receive indomethacin (NSAID) or sham treatment for 3 days before surgery. Normal colon and tumor tissue were collected at operation for RNA extraction. Tissue PGE2 levels were measured by radioimmunoassay. Gene expression was quantified by microarray and real-time PCR. COX-1 expression increased proportionally to COX-2 expression in colon cancer tissue from untreated patients. Indomethacin reduced PGE2 content in normal and tumor tissue with subsequently decreased IP, HPGD and PPARgamma receptor expression in both tumor and normal colon tissue, while subtype EP1-4 receptors were not significantly influenced by indomethacin treatment. MPGES-1 expression was not related to overall PGE2 content in tumor and colon tissue, but decreased significantly in normal tissue during indomethacin exposure. Reduction of tumor tissue PGE2 was related to significant alteration in expression of several hundred genes indicating decreased cell cycling and increased apoptosis during indomethacin treatment, probably related to upregulation of acute phase reactants in tumor tissue. Increased prostanoid activity in colon cancer tissue is related to cross-talk between tumor and stroma cells.
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| 12. |
- Jung, Bärbel, 1961-
(författare)
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On effectiveness in colorectal surgery : mechanical bowel preparation or not in elective colonic surgery and treatment options for elderly patients with rectal cancer
- 2008
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The management of patients undergoing colorectal surgery has changed in recent decades. Efforts have been made to show that perioperative physiological stress to the patient can be minimised with standardised care programmes and thus improve short term outcome after colorectal surgery. Mechanical bowel preparation (MBP), for instance, has been questioned as part of standard management. There are studies highlighting the effect of cancer treatment and its side effects in the elderly, showing that geriatric patients benefit from oncological therapy in much the same way as younger patients. The impact of this information on surgical and oncological practice in Sweden today is not known. To assess the effectiveness of colorectal surgery we need both randomised controlled trials and population-based cohort studies. We have performed a trial on colonic surgery with and without preoperative mechanical bowel preparation, as well as a nation-wide register study comparing treatment and outcome of rectal cancer in two age groups. In a randomised controlled trial 1505 patients from 21 hospitals were randomised to MBP or no-MBP prior to open elective colonic resection. There were no differences in overall complication rates between the groups: cardiovascular 5.1% with MBP vs. 4.6% without MBP; general infection 7.9% vs. 6.8%; and surgical site complications 15.1% vs. 16.1%. The proportion of patients reaching at least one primary endpoint was 24.5% vs. 23.7% respectively. The patients experience of and postoperative recovery after MBP or no-MBP was evaluated in 105 of the patients in the bowel preparation trial at three of the participating hospitals. Sixty-five patients received MBP and 40 patients did not. In the MBP group 52% needed assistance with bowel preparation. Day 4 postoperatively patients in the no-MBP group perceived more discomfort than patients in the MBP group, p<0.05. Bowel emptying occurred significantly earlier in the no-MBP group than in the MBP group, p<0.05.In an experimental study the effect of MBP on intramucosal bacterial count was evaluated. Macroscopically normal colon mucosa was collected from 37 patients (20 MBP and 17 No-MBP) undergoing elective colorectal surgery at three hospitals. MBP did not influence the median colony count of E. coli, Bacteroides, or total median colony count, information that was previously unknown. These three studies imply that MBP can be omitted before elective colonic resection. In a population-based register study, treatment for rectal cancer in patients ≥ 75 years and those < 75 years was evaluated using data from the Swedish Rectal Cancer Register 1995-2004 (N=15104). This study revealed that preoperative radiotherapy was used less in patients > 75 years. There was also a higher threshold for surgery in this group, and they more often received a permanent stoma compared to younger patients. Outcome in terms of 5-year local recurrence rate and 5-year cancer-specific survival differed very little between the older and younger patient groups who underwent abdominal tumour resection with curative intent. We suggest future studies focusing on ways of reducing surgical and perioperative stress and on quality of life when assessing suitable treatment modalities for rectal cancer.
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| 13. |
- Kodeda, Karl, et al.
(författare)
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Genomic CGH-assessed structural DNA alterations in rectal carcinoma as related to local recurrence following primary operation for cure.
- 2012
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Ingår i: International journal of oncology. - : Spandidos Publications. - 1791-2423 .- 1019-6439. ; 41:4, s. 1397-1404
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Tidskriftsartikel (refereegranskat)abstract
- Several factors determine overall outcome and possible local recurrence after curative surgery for rectal carcinoma. Surgical performance is usually believed to be the most pertinent factor, followed by adjuvant oncological treatment and tumor histopathology. However, chromosomal instability is common in colorectal cancer and tumor clones are assumed to differ in aggressiveness and potential of causing local recurrence. The aim of this study was, therefore, to evaluate if genetic alterations in primary rectal carcinoma are predictive of local recurrences. A large clinical database with linked bio-bank allowed for careful matching of two patient groups (R0) resected for rectal carcinoma. One group had developed early, isolated local recurrences and the other group seemed cured after 93months follow-up. DNA from the primary tumors was analysed with array-CGH (comparative genomic hybridization) including 55,000 genomic probes. DNA from all primary tumors in both groups displayed previously reported and well-recognised DNA aberrations in colorectal carcinoma. Significant copy number gains were confirmed in the 4q31.1-31.22 region in DNA from tumors with subsequent local recurrence. Twenty-two affected genes in this region code for products with high relevance in tumor biology (p53 regulation, cell cycle activity, transcription). DNA from rectal carcinoma displayed well-known aberrations as described for colon carcinoma with no obvious prediction of local rectal recurrence. Gains in the 4q31.1-31.22 DNA region are highly potential for local recurrence despite R0 resection to be confirmed in larger patient materials.
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| 14. |
- Kodeda, Karl, et al.
(författare)
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Local recurrence of rectal cancer: a population based cohort study of diagnosis, treatment and outcome.
- 2012
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Ingår i: Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland. - : Wiley. - 1463-1318. ; 14:5, s. 230-7
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Tidskriftsartikel (refereegranskat)abstract
- Aim: Local recurrence is an important endpoint of rectal cancer treatment, but details of this form of treatment failure are less well described. The aim of this study was to acquire deeper knowledge of local recurrence regarding symptoms, diagnostic work-up, clinical management, health-care utilization and outcome. Method: Of 671 patients with rectal cancer, 57 were diagnosed with local recurrence within 5 years after surgery. Their records were analysed. Results: At diagnosis of local recurrence 49(86%) of 57 patients were symptomatic and 40 (70%) were diagnosed between scheduled follow-up visits. The predominant symptom was pain. Forty five of the 57 (79%) had a palpable tumour. Most were deemed incurable at presentation and less than 10 (18%) were operated on with curative intent. Five years after the initial rectal cancer surgery, two patients were alive, with one free of disease. Despite the need for multiple interventions, including surgery, only 4 out of 40 patients were classified as being well palliated in the terminal stage. Conclusion: Follow-up after rectal cancer surgery by annual clinical examination is not sufficient to detect local recurrence when it is asymptomatic. Local recurrence of rectal cancer is often associated with intractable symptoms. These patients require frequent interventions and can rarely be cured if diagnosed at an advanced stage. Strategies for early detection of local recurrence and the management thereof require improvement.
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| 15. |
- Kodeda, Karl, et al.
(författare)
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Rectal washout and local recurrence of cancer after anterior resection.
- 2010
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Ingår i: The British journal of surgery. - : Oxford University Press (OUP). - 1365-2168 .- 0007-1323. ; 97:10, s. 1589-97
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND:: Adenocarcinomas of the rectum shed viable cells, which have the ability to implant. Intraoperative rectal washout decreases the amount and viability of these cells, but there is no conclusive evidence of the effect of rectal washout on local recurrence after rectal cancer surgery. METHODS:: Data were analysed from a population-based registry of patients who had anterior resection from 1995 to 2002 and were followed for 5 years. Rectal washout was performed at the discretion of the surgeon. National inclusion of patients with rectal cancer and follow-up was near complete (approximately 97 and 98 per cent respectively). RESULTS:: A total of 4677 patients were analysed (3749 who had washout, 851 no washout and 77 with information missing); 52.0 per cent of patients in the washout group and 41.4 per cent in the no-washout group had preoperative radiotherapy (P < 0.001). Local recurrence rates were 6.0 and 10.2 per cent respectively (P < 0.001). Univariable and multivariable logistic regression analyses produced odds ratios that favoured washout: 0.56 (95 per cent confidence interval (c.i.) 0.43 to 0.72) and 0.61 (0.46 to 0.80) respectively (both P < 0.001). In multivariable analysis restricted to patients who had curative surgery, the odds ratio was 0.59 (95 per cent c.i. 0.44 to 0.78; P < 0.001). CONCLUSION:: There was a more favourable outcome in patients after rectal washout than without. Copyright (c) 2010 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd.
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| 16. |
- Kodeda, Karl, et al.
(författare)
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Regional Differences in Local Recurrence Rates after Rectal Cancer Surgery.
- 2009
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Ingår i: Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland. - : Wiley. - 1463-1318.
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Tidskriftsartikel (refereegranskat)abstract
- Abstract Aim To analyse a substantial regional difference in local failure rate after rectal cancer surgery focusing on management. Methods National, population-based, prospective registry data were used, including comprehensive five year follow-up of 3,783 patients operated on in the period 1998-2000. Local recurrence rates were compared using crude rate, Kaplan-Meier estimates and competing risk methodology. Resected patients (651 regional and 3,132 national) were analysed and subgroup comparisons of management were performed. Results The crude local recurrence rate was 13.7 percent in the regional cohort and 7.1 percent in the national cohort. The absolute difference of 6.6 percent may partly be explained by systematic errors of underreporting (
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| 17. |
- Lagerstedt, Kristina, 1976, et al.
(författare)
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Genes with relevance for early to late progression of colon carcinoma based on combined genomic and transcriptomic information from the same patients.
- 2010
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Ingår i: Cancer informatics. - 1176-9351. ; 9, s. 79-91
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Genetic and epigenetic alterations in colorectal cancer are numerous. However, it is difficult to judge whether such changes are primary or secondary to the appearance and progression of tumors. Therefore, the aim of the present study was to identify altered DNA regions with significant covariation to transcription alterations along colon cancer progression. METHODS: Tumor and normal colon tissue were obtained at primary operations from 24 patients selected by chance. DNA, RNA and microRNAs were extracted from the same biopsy material in all individuals and analyzed by oligo-nucleotide array-based comparative genomic hybridization (CGH), mRNA- and microRNA oligo-arrays. Statistical analyses were performed to assess statistical interactions (correlations, co-variations) between DNA copy number changes and significant alterations in gene and microRNA expression using appropriate parametric and non-parametric statistics. RESULTS: Main DNA alterations were located on chromosome 7, 8, 13 and 20. Tumor DNA copy number gain increased with tumor progression, significantly related to increased gene expression. Copy number loss was not observed in Dukes A tumors. There was no significant relationship between expressed genes and tumor progression across Dukes A-D tumors; and no relationship between tumor stage and the number of microRNAs with significantly altered expression. Interaction analyses identified overall 41 genes, which discriminated early Dukes A plus B tumors from late Dukes C plus D tumor; 28 of these genes remained with correlations between genomic and transcriptomic alterations in Dukes C plus D tumors and 17 in Dukes D. One microRNA (microR-663) showed interactions with DNA alterations in all Dukes A-D tumors. CONCLUSIONS: Our modeling confirms that colon cancer progression is related to genomic instability and altered gene expression. However, early invasive tumor growth seemed rather related to transcriptomic alterations, where changes in microRNA may be an early phenomenon, and less to DNA copy number changes.
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| 18. |
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| 19. |
- Lagerstedt, Kristina, 1976, et al.
(författare)
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The role of combined allelic imbalance and mutations of p53 in tumor progression and survival following surgery for colorectal carcinoma
- 2005
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Ingår i: International journal of oncology. - 1019-6439. ; 27:6, s. 1707-15
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Tidskriftsartikel (refereegranskat)abstract
- The role of p53 mutations in disease progression and survival of colorectal cancer is unclear, since numerous studies have reported different conclusions. However, few reports, if any, have evaluated disease progression and survival in relationship to 'functional' and 'non-functional' p53 status defined by genetic and molecular indications. Malignant colorectal tumors, from 72 unselected patients who underwent primary and potentially curative elective tumor resections, were either classified as p53 functional (p53+/+, p53+/-) or non-functional (p53-/-) based on DNA sequence analysis of all p53 exons, including determination of allelic imbalance of p53 (LOH), according to four DNA markers; 2 within the coding gene and two markers in the immediate flanking regions of p53. Tumor frequency of microsatellite instability was also analyzed according to Dukes' A-D stages. Dukes' staging predicted survival as expected, while the conceptual p53 status, functional p53 vs non-functional p53, did not clear-cut predict disease specific survival. p53 mutations alone or allelic imbalance inside the reading frame of the gene were unpredictive of survival, while allelic imbalance downstream of p53 predicted reduced survival (p < 0.05). The present study demonstrates that base mutations in combination with allelic imbalance within the reading frame of p53 do not predict survival or progression of colorectal cancer, while allelic imbalance upstream coding parts of the gene predicted disease-specific survival in univariate analysis. Thus, structural alterations within the gene seem less important than alterations in regions with potential control elements.
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| 20. |
- Lagerstedt, Kristina, 1976, et al.
(författare)
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Tumor Genome Wide DNA Alterations Assessed by Array CGH in Patients with Poor and Excellent Survival Following Operation for Colorectal Cancer.
- 2007
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Ingår i: Cancer informatics. - 1176-9351. ; 3, s. 341-55
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Tidskriftsartikel (refereegranskat)abstract
- Genome wide DNA alterations were evaluated by array CGH in addition to RNA expression profiling in colorectal cancer from patients with excellent and poor survival following primary operations.DNA was used for CGH in BAC and cDNA arrays. Global RNA expression was determined by 44K arrays. DNA and RNA from tumor and normal colon were used from cancer patients grouped according to death, survival or Dukes A, B, C and D tumor stage. Confirmed DNA alterations in all Dukes A - D were judged relevant for carcinogenesis, while changes in Dukes C and D only were regarded relevant for tumor progression.Copy number gain was more common than loss in tumor tissue (p < 0.01). Major tumor DNA alterations occurred in chromosome 8, 13, 18 and 20, where short survival included gain in 8q and loss in 8p. Copy number gains related to tumor progression were most common on chromosome 7, 8, 19, 20, while corresponding major losses appeared in chromosome 8. Losses at chromosome 18 occurred in all Dukes stages. Normal colon tissue from cancer patients displayed gains in chromosome 19 and 20. Mathematical Vector analysis implied a number of BAC-clones in tumor DNA with genes of potential importance for death or survival.The genomic variation in colorectal cancer cells is tremendous and emphasizes that BAC array CGH is presently more powerful than available statistical models to discriminate DNA sequence information related to outcome. Present results suggest that a majority of DNA alterations observed in colorectal cancer are secondary to tumor progression. Therefore, it would require an immense work to distinguish primary from secondary DNA alterations behind colorectal cancer.
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| 21. |
- Langenskiöld, Marcus, 1972, et al.
(författare)
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Differential Prognostic Impact of uPA and PAI-1 in Colon and Rectal Cancer.
- 2009
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Ingår i: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine. - : Springer Science and Business Media LLC. - 1423-0380. ; 30:4, s. 210-220
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Tidskriftsartikel (refereegranskat)abstract
- Background and Objectives: Degradation of extracellular matrix is important for tumour growth and invasion, which in part is regulated by the plasminogen activation system. The aim of the study was to evaluate the protein expression of urokinase plasminogen activator (uPA) and plasminogen-activating inhibitor-1 (PAI-1) in plasma, tumour-free mucosa and tumour tissue regarding their prognostic value in colon and rectal cancer. Methods: Patients (n = 221) undergoing surgery for colorectal cancer were prospectively included. Samples were assayed by ELISA technique. Results: PAI-1 in tumour tissue (p = 0.006), plasma (<0.0001) and uPA in tumour-free mucosa (p = 0.006) were associated with survival in rectal cancer in univariate analysis. An uPA expression level below 1.1 ng/mg (log rank test, p < 0.0001) in tumour-free mucosa was associated with poor survival in rectal cancer. This was true also for patients without disseminated disease (M(0), p = 0.02). PAI-1 in plasma correlated with metastatic disease (p < 0.0001). uPA and PAI-1 were not associated with survival in either tumour tissue, mucosa or plasma in patients with colon cancer. Conclusions: uPA and PAI-1 have a differential prognostic impact in colon and rectal cancer. Preoperative mucosal uPA and plasma PAI-1 protein expression could possibly be used as prognostic factors in rectal cancer.
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| 22. |
- Lönnroth, Christina, 1946, et al.
(författare)
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Downregulation of Prominin 1/CD133 expression in colorectal cancer by NSAIDs following short-term preoperative treatment
- 2012
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Ingår i: International Journal of Oncology. - : Spandidos Publications. - 1019-6439 .- 1791-2423. ; 41:1, s. 15-23
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Tidskriftsartikel (refereegranskat)abstract
- Expression of Prominin 1/CD133 is associated with poor prognosis and chemoresistance in several types of solid tumors. The aim of the present study was, therefore, to evaluate Prominin 1/CD133 expression in colorectal carcinoma after short-term preoperative treatment by non-steroidal anti-inflammatory drugs (NSAIDs). Patients aimed at curative operation for colon cancer were randomized to receive NSAIDs (indomethacin 50 mg x2 or celecoxib 100 mg x2) three days preoperatively. Antisecretory prophylaxis (esomeprasol 40 mg x1) was provided to all patients and served as sham intake. CD133 expression in tumor tissue was also assessed in tumors from Dukes B patients selected for either long or short postoperative survival. No patients received perioperative chemoradiotherapy. Tumor tissue was collected at surgery for quantification of mRNAs (Prom I and Wnt4) by qPCR. Immunohistochemistry stained for CD133, Ep-CAM, CD34 and CD45. PGE(2) content in tumor tissue was determined. Transcript of CD133 in tumor tissue was lower in patients treated with NSAIDs (0.28 +/- 0.07 vs. 0.51 +/- 0.08; p<0.03) as well as some other stem cell-related transcripts. In treated patients 36% of all tumors stained positive for CD133 compared to 71% in sham-treated control patients (p<0.05). Short survivors with Dukes' B tumors displayed 78% CD133 expression as compared to 33% of tumors in long-term survivors (p<0.002). Tumor tissue PGE(2) content was negatively related to patient survival. Our results show that short-term preoperative NSAID treatment downregulates colon cancer tissue expression of Prominin 1/CD133, a stem cell marker indicative of survival prognosis as confirmed.
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| 23. |
- Lönnroth, Christina, 1946, et al.
(författare)
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Preoperative low dose NSAID treatment influences the genes for stemness, growth, invasion and metastasis in colorectal cancer.
- 2014
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Ingår i: International journal of oncology. - : Spandidos Publications. - 1791-2423 .- 1019-6439. ; 45:6, s. 2208-2220
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Tidskriftsartikel (refereegranskat)abstract
- Preclinical data, and an increasing list of clinical investigations, show anti‑inflammatory agents to favourably influence the biology of colorectal tumor. We have earlier reported on re‑expression of activated immune cells after three days preoperative treatment of patients with colorectal carcinoma, randomized to receive oral NSAID(indomethacin or celebrex). Antisecretory prophylaxis(esomeprasol) was provided to all patients and served as sham treatment. Concomittant to MHC locus activation, Prominin1/CD133, a marker associated with stemness and poor prognosis in several solid tumors, was downregulated. The aim of the present study was to evaluate expression of additional regulators belonging to the stem cell niche, OCT4, SOX2 and BMP7, aswellas some microRNAs, reported to act as tumor suppressors or oncomiRs. Peroperative tumor biopsies were analyzed by microarrays, quantitative real‑time PCR and immunohistochemistry(IHC). The stem cell master regulator SOX2 was increased by NSAIDs(p<0.01), aswellas the tumor suppressor miR‑630(p<0.01), while BMP7, a marker for poor prognosis in CRC, was downregulated by NSAID(indomethacin, p<0.02). The upregulation of SOX2, but not of its heterodimer binding partner OCT4, could imply a negative feed‑back loop, with a switch‑off for stemness preservation of tumor cells. This is supported by the overall evaluation of gene expression profiles with subsequent events, indicating less aggressive tumors following NSAID treatment.
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| 24. |
- Lönnroth, Christina, 1946, et al.
(författare)
-
Preoperative treatment with a non-steroidal anti-inflammatory drug (NSAID) increases tumor tissue infiltration of seemingly activated immune cells in colorectal cancer.
- 2008
-
Ingår i: Cancer immunity : a journal of the Academy of Cancer Immunology. - 1424-9634. ; 8
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Tidskriftsartikel (refereegranskat)abstract
- This study evaluates HLA gene expression and tumor infiltration by B-cells, macrophages, dendritic cells, T-helper and cytotoxic T-lymphocytes in response to short-term preoperative treatment with cyclooxygenase inhibitors. Patients with colorectal carcinoma were randomized to receive oral NSAID (indomethacin or celebrex) for three days preoperatively; controls received esomeprazol. Peroperative tumor biopsies and normal colon tissue were analyzed by microarray, quantitative PCR and immunohistochemistry. Efficacy of short-term systemic NSAID treatment was confirmed by measurement of PGE2 production in blood monocytes from healthy volunteers. NSAID treatment upregulated genes at the MHC locus on chromosome 6p21 in tumor tissue, but not in normal colon tissue, from the same patient. 23 of the 100 most upregulated genes belonged to MHC class II. HLA-DM, -DO (peptide loading), HLA-DP, -DQ, -DR (antigen presentation), granzyme B, H, perforin and FCGR3A (CD16) (cytotoxicity) displayed increased expression, as did CD8, a marker of cytotoxic T-lymphocytes, while HLA-A and -C expression were not increased by NSAID treatment. MHC II protein (HLA-DP, -DQ, -DR) levels and infiltration by CD4+ T-helper cells of tumor stroma increased upon NSAID treatment, while CD8+ cytotoxic T-lymphocytes increased in both tumor stroma and epithelium. Molecules associated with immunosuppressive T regulatory cells (FOXP3, IL-10) were significantly decreased in indomethacin-exposed tumors. Standard oral administration of NSAID three days preoperatively was enough to increase tumor infiltration by seemingly activated immune cells. These findings agree with previous information that high prostanoid activities in colorectal cancer increase the risk for reduced disease-specific survival following tumor resection.
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| 25. |
- Nordgren, Camilla, et al.
(författare)
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Efterfrågas rätt kunskap och kompetens
- 2021
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Ingår i: Socionomen. - : Akademikerförbundet SSR. - 0283-1929. ; :1
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Tidskriftsartikel (populärvet., debatt m.m.)
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| 26. |
- Nordgren, Camilla, et al.
(författare)
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Need for Knowledge- What, Where and How? Social Workers Handle Service and Support för Individuals With Disability
- 2022
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Ingår i: British Journal of Social Work. - Oxford : Oxford University Press. - 0045-3102 .- 1468-263X. ; 52:7, s. 4108-4126
-
Tidskriftsartikel (refereegranskat)abstract
- This article investigates the need and sources of knowledge among LSS administrators in Sweden (i.e. social workers handling service and support for individuals with disability according to the Swedish Disability Act [LSS]). Changing and challenging working conditions and issues concerning professional status warrant the aim. A questionnaire distributed via gatekeepers in a number of municipalities demonstrated that knowledge about ‘disability’, ‘law’, ‘ethics’ and ‘augmentative and alternative communication’ was rated highly. This result is particularly interesting given that many social work education programmes do not have compulsory courses in disability. Colleagues appear to be relied upon as essential sources of support and knowledge, but the knowledge sharing seems unorganised. Findings are discussed in relation to communities of practice (CoP) and shows that, due to the lack of essential knowledge from formal education and the strong dependence on colleagues, a locally developed praxis might be established. Inadequate theoretical and research-based knowledge, together with this local praxis knowledge, may result in the LSS administrators’ work becoming inadequate. A specialist education in disability studies is proposed as a prerequisite for being employed as an LSS administrator, and the inclusion of a theoretical and scientific framework in the regular CoP interaction is also recommended.
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| 27. |
- Nordgren, Camilla, et al.
(författare)
-
Utsatthet och ojämlikhet trots politiska ambitioner
- 2024. - 1
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Ingår i: Funktionsförmåga, funktionshinder och socialt arbete. - Malmö : Gleerups Utbildning AB. - 9789151112152 ; , s. 141-154
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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| 28. |
- Novotny, Ann, 1982-, et al.
(författare)
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A pharmacological analysis of the cholinergic regulation of urokinase-type plasminogen activator, and plasminogen activator inhibitor-1 secretion in the human colon cancer cell line, HT-29
- 2010
-
Ingår i: European Journal of Pharmacology. - : Elsevier BV. - 0014-2999 .- 1879-0712. ; 646:1-3, s. 22-30
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Tidskriftsartikel (refereegranskat)abstract
- Urokinase-type plasminogen activator (uPA) is an important factor for tumour cell invasion and metastasis. We recently showed that acetylcholine is an autocrine/paracrine growth factor for the human colon cancer cell line, HT-29, in part via the α7 subtype of the nicotinic acetylcholine receptors. In the current study, we investigated whether acetylcholine participates in the regulation of the protein expressions of also uPA and its receptor (uPAR) in the HT-29 cell line. Such were investigated by immunocytochemistry and Western blotting, and quantitation of uPA secretion was undertaken by ELISA. Stimulation of the cells for 24 h with nicotine caused increased uPA secretion with peak effect (78% above the control) occurring at a nicotine concentration of 10 nM. This effect was markedly inhibited by α-Bungarotoxin, thus showing the involvement of α7 nicotinic acetylcholine receptors. Basal uPA secretion was found to be partly dependent on ongoing activation of nicotinic receptors, suggesting tonic production of acetylcholine. Conversely, there was no cholinergic influence on the expression of uPAR. The current findings demonstrate novel aspects of receptor-mediated regulation of tumour metastatic potential via uPA secretion. This may suggest future pharmaceutical strategies in treatment of colorectal cancer.
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| 29. |
- Novotny, Ann, 1982, et al.
(författare)
-
A pharmacological analysis of the cholinergic regulation of urokinase-type plasminogen activator secretion in the human colon cancer cell line, HT-29.
- 2010
-
Ingår i: European journal of pharmacology. - : Elsevier BV. - 1879-0712 .- 0014-2999. ; 646:1-3, s. 22-30
-
Tidskriftsartikel (refereegranskat)abstract
- Urokinase-type plasminogen activator (uPA) is an important factor for tumour cell invasion and metastasis. We recently showed that acetylcholine is an autocrine/paracrine growth factor for the human colon cancer cell line, HT-29, in part via the alpha7 subtype of the nicotinic acetylcholine receptors. In the current study, we investigated whether acetylcholine participates in the regulation of the protein expressions of also uPA and its receptor (uPAR) in the HT-29 cell line. Such were investigated by immunocytochemistry and Western blotting, and quantitation of uPA secretion was undertaken by ELISA. Stimulation of the cells for 24h with nicotine caused increased uPA secretion with peak effect (78% above the control) occurring at a nicotine concentration of 10nM. This effect was markedly inhibited by alpha-Bungarotoxin, thus showing the involvement of alpha7 nicotinic acetylcholine receptors. Basal uPA secretion was found to be partly dependent on ongoing activation of nicotinic receptors, suggesting tonic production of acetylcholine. Conversely, there was no cholinergic influence on the expression of uPAR. The current findings demonstrate novel aspects of receptor-mediated regulation of tumour metastatic potential via uPA secretion. This may suggest future pharmaceutical strategies in treatment of colorectal cancer.
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| 30. |
- Novotny, Ann, 1982, et al.
(författare)
-
Is acetylcholine a signaling molecule for human colon cancer progression?
- 2011
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Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 0036-5521 .- 1502-7708. ; 46:4, s. 446-455
-
Tidskriftsartikel (refereegranskat)abstract
- Objective. Non-neuronal acetylcholine (ACh) has been suggested to be a mediator for the development of various types of cancer. We analyzed a possible role for this molecule in carcinogenesis and/or progression of human colon cancer, in patient biopsies harvested from the colon during surgery. We addressed whether ACh synthesis (by choline acetyltransferase) and/or degradation (by ACh esterase), as well as the expression of the alpha alpha 7-subtype of the nicotinic ACh receptors, and the peptide ligand at the alpha alpha 7 receptors, secreted mammalian Ly6/urokinase-type plasminogen activator receptor-related protein-1, respectively, are deranged in tumor tissue as compared with macroscopically tumor-free colon tissue. Methods. A total of 38 patients were grouped for analysis based on their respective Dukes stage (either Dukes A ++ B or C ++ D). A mucosal tissue sample was harvested from macroscopically tumor-free colon tissue (i.e. control tissue), as well as from the tumor, and protein lysates were prepared for quantitative Western blotting. Full-thickness specimens were taken for immunohistochemistry. Results. For all the above named markers, there was a significant difference between control and tumor tissue with regard to protein levels, and there was, in addition, a significant difference in protein levels between the Dukes A ++ B and C ++ D groups. Conclusion. The current findings may suggest a role for ACh in colon carcinogenesis/cancer progression; the data obtained could have prognostic and/or therapeutic significance for this disease.
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| 31. |
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| 32. |
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| 33. |
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| 34. |
- Nylund, Gunnar, 1959, et al.
(författare)
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Expression of P2Y2 purinoceptors in MCG 101 murine sarcoma cells, and HT-29 human colon carcinoma cells
- 2004
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Ingår i: Autonomic neuroscience. - : Elsevier BV. - 1566-0702. ; 112:1-2, s. 69-79
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Tidskriftsartikel (refereegranskat)abstract
- We investigated how agonists at purinoceptors may affect tumour cell metabolism. This was investigated in vitro in tumour cell lines by microphysiometry, which method monitors extracellular acidification rate (ECAR), on-line. The cell lines investigated were the murine sarcoma, MCG 101, and the human colon cancer, HT-29. In MCG 101, adenosine-5'-triphosphate (ATP) or uridine-5'-triphosphate (UTP) caused a concentration-dependent increase in ECAR, most likely due to the ligation of P2Y(2) receptors, which response was blocked by suramin. In HT-29, ATP or UTP elicited a concentration-dependent, biphasic change in ECAR (increase/decrease). The pharmacological analysis suggests the involvement of P2Y(2) receptors, although other P2 receptor subtypes cannot be entirely excluded. This biphasic response to UTP or ATP was resistant to suramin. The expression of P2Y(2) receptors was demonstrated in both cell lines by immunocytochemistry and Western blot. The current study, thus, shows the functional and morphological expression of a purinoceptor subtype with partly different effects on metabolism in two different tumour cell lines.
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| 35. |
- Nylund, Gunnar, 1959, et al.
(författare)
-
Functional expression of mu-opioid receptors in the human colon cancer cell line, HT-29, and their localization in human colon.
- 2008
-
Ingår i: Digestive diseases and sciences. - : Springer Science and Business Media LLC. - 0163-2116 .- 1573-2568. ; 53:2, s. 461-6
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Tidskriftsartikel (refereegranskat)abstract
- We have investigated the functional expression of mu-opioid receptors (MORs) in the human colon cancer cell line, HT-29. As revealed by immunocytochemistry, immunoreactivity was present in both the cytoplasm and nuclei of the cells. Challenge with morphine for 24 h (1 nM to 1 microM) barely affected cell proliferation, while the secretion of urokinase type plasminogen activator (a protease involved in invasion/metastasis) was markedly augmented by a concentration of 0.1 microM. Human colon cancer tissue from 14 consecutively operated patients was investigated by immunohistochemistry. MORs were found in the nuclei of colonocytes and immune cells of the lamina propria in tumor-free tissue. In tumor tissue, immunoreactivity was found in the membrane and often in the nuclei of tumor cells. The current findings suggest that morphine administration could affect tumor progression by interfering with, for example, invasive properties. Our demonstration of a nuclear expression of the MORs appears to be a novel finding.
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| 36. |
- Nylund, G., et al.
(författare)
-
P2Y2- and P2Y4 purinergic receptors are over-expressed in human colon cancer
- 2007
-
Ingår i: Autonomic & autacoid pharmacology. - 1474-8665. ; 27:2, s. 79-84
-
Tidskriftsartikel (refereegranskat)abstract
- 1. A characteristic of cancer is altered signal transduction leading to uninhibited growth. Adenosine-5'-triphosphate (ATP), a natural ligand at P2X- and P2Y purinergic receptors may regulate cell growth in non-neoplastic, as well as neoplastic tissues. In the human colon cancer cell line, HT-29, we previously demonstrated the expression of purinergic receptors of the P2Y(2)- and P2Y(4) subclasses. 2. The aim of the current study was to investigate whether these two purinergic receptors are expressed also in human colon cancer, and, if so, how such expression is related to that in tumour-free colonic tissue. 3. The immunohistochemical findings of both P2Y(2)- and P2Y(4) receptors in the tumours from three patients, prompted us to conduct an investigation of a consecutive series of patients utilizing Western blotting for protein detection and densitometry for quantitation. 4. Both P2Y(2)- and P2Y(4) purinergic receptors could be identified in tumour-free tissue, and both were significantly over-expressed in each of the 10 colon cancers.
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| 37. |
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| 38. |
- Pettersson, Ann, 1982-, et al.
(författare)
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Expression of the endogenous, nicotinic acetylcholine receptor ligand, SLURP-1, in human colon cancer.
- 2008
-
Ingår i: Autonomic & Autacoid Pharmacology. - : Wiley. - 1474-8665 .- 1474-8673. ; 28:4, s. 109-116
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Tidskriftsartikel (refereegranskat)abstract
- 1. Secreted mammalian Ly-6/urokinase plasminogen activator receptor-related protein-1 (SLURP-1) is a recently discovered endogenous ligand at the alpha7 subunit of the nicotinic acetylcholine receptors. Previous reports have shown that SLURP-1 is expressed in normal human keratinocytes seemingly with a pro-apoptotic function. Conversely, such expression was markedly attenuated in transformed cells and it was suggested that the molecule could convey protection against malignant transformation. 2. In this study, we demonstrated the mRNA expression (by RT-PCR) and protein expression (by Western blotting and immunocytochemistry) of SLURP-1 in the human colon cancer cell line, HT-29. 3. Furthermore, we demonstrated the expression of SLURP-1 (by immunohistochemistry) in tumour cells of human colon cancer tissue, and, to a greater extent, in immune and smooth muscle cells of adjacent, macroscopically tumour-free colon tissue. 4. The current findings suggest that SLURP-1 participates in the regulation of gut immune functions and motility, as well as possibly playing a role in colon carcinogenesis/cancer progression.
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| 39. |
- Pettersson, Ann, 1982, et al.
(författare)
-
Is acetylcholine an autocrine/paracrine growth factor via the nicotinic alpha7-receptor subtype in the human colon cancer cell line HT-29?
- 2009
-
Ingår i: European journal of pharmacology. - : Elsevier BV. - 1879-0712 .- 0014-2999. ; 609:1-3, s. 27-33
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Tidskriftsartikel (refereegranskat)abstract
- We used immunochemistry to demonstrate expression of acetylcholine's nicotinic alpha7-receptor subtype in human colon cancer cell line HT-29. Moreover, RT-PCR and immunochemistry showed that choline acetyltransferase and acetylcholine esterase, the enzymes responsible for acetylcholine synthesis and degradation, respectively, localise in HT-29 cells. Bromoacetylcholine bromide, an inhibitor of choline acetyltransferase, significantly attenuated basal cell growth. Our findings suggest that acetylcholine might serve as an autocrine/paracrine-or speculatively, even intracrine-signalling molecule in cell line HT-29, thus contributing to carcinogenesis/cancer progression.
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| 40. |
- Pettersson, Ann, 1982-, et al.
(författare)
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Nicotine induced modulation of SLURP-1 expression in human colon cancer cells.
- 2009
-
Ingår i: Autonomic neuroscience : basic & clinical. - : Elsevier BV. - 1872-7484 .- 1566-0702. ; 148:1-2, s. 97-100
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Tidskriftsartikel (refereegranskat)abstract
- The secreted mammalian Ly-6/urokinase plasminogen activator receptor-related protein-1 (SLURP-1) is an endogenous ligand at the alpha 7 subunit of the nicotinic acetylcholine receptor (nAChR). SLURP-1 has anti-tumourigenic properties. In the current study, we demonstrate that the challenge of HT-29 human colon cancer cells with nicotine for 24 h to increase cell growth via the alpha 7nAChRs, caused a marked reduction of the protein expression of SLURP-1. We suggest that there is an interplay between acetylcholine and SLURP-1 in the HT-29 cells, both molecules serving as autocrine growth controlling ligands at the alpha 7nAChR, where acetylcholine regulates the release of SLURP-1.
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| 41. |
- Staaf, Annika, et al.
(författare)
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Oförutsebar rättssäkerhet : En granskning av handläggning enligt LSS
- 2023
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Ingår i: Retfærd. - : Jurist- og Økonomforbundets Forlag. - 0105-1121. ; 46:4, s. 71-86
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Tidskriftsartikel (refereegranskat)abstract
- Artikelns resultat baserar sig på en enkätstudie till handläggare inom funktionshinderområdet i Sverige och redovisar deras arbetssituation, med fokus på konsekvenser for enskildas rättssäkerhet. Det övergripande syftet med artikeln ar att belysa aspekter av rättssäkerhet i ärenden enligt LSS. Rättssäkerhet är ett begrepp som givits flera betydelser, framfär allt en formell och en materiell definition (Peczenik, 1995). Vi argumenterar för att den materiella definitionen hör bättre samman med lagmotivens, liksom funktionsrättskonventionens (CRPD) fokus på mänsklig värdighet och likvärdigt bemötande vad avser LSS tillämpning. Resultaten visar att flera LSS-handläggare inte anser att deras hemkommuner fattar rättssäkra beslut och att utförda bedömningar är lite av gissningar eftersom tydliga riktlinjer saknas. Vidare anges att arbetsledare ger instruktioner om vilka insatser som får beviljas och vilka som ska avslås, utifrån budgethänsyn snarare än bedömningar av behov. Enkätsvaren redovisar också situationer där brukare blivit kränkande bemötta. Sammantaget leder detta till en oförutsebar rättssäkerhet for brukaren.
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| 42. |
- Svensson, Svante, 1947-, et al.
(författare)
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Prof. Carl Nordling 1931-2016
- 2018
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Ingår i: Journal of Electron Spectroscopy and Related Phenomena. - : Elsevier. - 0368-2048 .- 1873-2526. ; 224, s. 107-108
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Tidskriftsartikel (populärvet., debatt m.m.)
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| 43. |
- Wahlqvist, Mats, 1954, et al.
(författare)
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Patient-centred attitudes among medical students: Gender and work experience in health care make a difference
- 2010
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Ingår i: Medical Teacher. - 1466-187X. ; 32:4
-
Tidskriftsartikel (refereegranskat)abstract
- Abstract Background: Previous studies of medical students’ patient-centred attitudes show a decline across undergraduate education and overall higher scores for female students. Aims: To assess undergraduate students’ patient-centred attitudes at various stages of education and to explore possible associations between attitudes and age, gender and work experience in health care. Methods: In autumn 2005, medical students in Gothenburg (n=797) were asked to answer Patient-Practitioner Orientation Scale (PPOS), a validated instrument exploring attitudes towards the doctor-patient relationship. Data including gender, age, current term and students’ work experience in health care were collected. Results: Six hundred students of 797 (75%) answered the questionnaire. No decrease of students’ PPOS score across the curriculum was observed. PPOS scores from female students were higher compared to males (p<0.0001) and female scores were significantly higher in the later terms compared with earlier (p=0.0011). Female students had more experience from working in health care (p=0.0023). Extended work experience was associated with higher PPOS only among females (p=0.0031). Conclusions: No decline of students’ patient-centred attitudes may indicate an ongoing shift. Gender differences in patient-centred attitudes were reproduced. Work experience in health care presents a new gender difference. These gender differences should be considered when training patient-centred attitudes and skills.
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