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Sökning: WFRF:(Syk Ingvar)

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  • Erlandsson, Johan, et al. (författare)
  • Optimal fractionation of preoperative radiotherapy and timing to surgery for rectal cancer (Stockholm III) : A multicentre, randomised, non-blinded, phase 3, non-inferiority trial
  • 2017
  • Ingår i: The Lancet Oncology. - Elsevier. - 1470-2045. ; 18:3, s. 336-346
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Radiotherapy reduces the risk of local recurrence in rectal cancer. However, the optimal radiotherapy fractionation and interval between radiotherapy and surgery is still under debate. We aimed to study recurrence in patients randomised between three different radiotherapy regimens with respect to fractionation and time to surgery. Methods: In this multicentre, randomised, non-blinded, phase 3, non-inferiority trial (Stockholm III), all patients with a biopsy-proven adenocarcinoma of the rectum, without signs of non-resectability or distant metastases, without severe cardiovascular comorbidity, and planned for an abdominal resection from 18 Swedish hospitals were eligible. Participants were randomly assigned with permuted blocks, stratified by participating centre, to receive either 5 × 5 Gy radiation dose with surgery within 1 week (short-course radiotherapy) or after 4-8 weeks (short-course radiotherapy with delay) or 25 × 2 Gy radiation dose with surgery after 4-8 weeks (long-course radiotherapy with delay). After a protocol amendment, randomisation could include all three treatments or just the two short-course radiotherapy treatments, per hospital preference. The primary endpoint was time to local recurrence calculated from the date of randomisation to the date of local recurrence. Comparisons between treatment groups were deemed non-inferior if the upper limit of a double-sided 90% CI for the hazard ratio (HR) did not exceed 1·7. Patients were analysed according to intention to treat for all endpoints. This study is registered with ClinicalTrials.gov, number NCT00904813. Findings: Between Oct 5, 1998, and Jan 31, 2013, 840 patients were recruited and randomised; 385 patients in the three-arm randomisation, of whom 129 patients were randomly assigned to short-course radiotherapy, 128 to short-course radiotherapy with delay, and 128 to long-course radiotherapy with delay, and 455 patients in the two-arm randomisation, of whom 228 were randomly assigned to short-course radiotherapy and 227 to short-course radiotherapy with delay. In patients with any local recurrence, median time from date of randomisation to local recurrence in the pooled short-course radiotherapy comparison was 33·4 months (range 18·2-62·2) in the short-course radiotherapy group and 19·3 months (8·5-39·5) in the short-course radiotherapy with delay group. Median time to local recurrence in the long-course radiotherapy with delay group was 33·3 months (range 17·8-114·3). Cumulative incidence of local recurrence in the whole trial was eight of 357 patients who received short-course radiotherapy, ten of 355 who received short-course radiotherapy with delay, and seven of 128 who received long-course radiotherapy (HR vs short-course radiotherapy: short-course radiotherapy with delay 1·44 [95% CI 0·41-5·11]; long-course radiotherapy with delay 2·24 [0·71-7·10]; p=0·48; both deemed non-inferior). Acute radiation-induced toxicity was recorded in one patient (<1%) of 357 after short-course radiotherapy, 23 (7%) of 355 after short-course radiotherapy with delay, and six (5%) of 128 patients after long-course radiotherapy with delay. Frequency of postoperative complications was similar between all arms when the three-arm randomisation was analysed (65 [50%] of 129 patients in the short-course radiotherapy group; 48 [38%] of 128 patients in the short-course radiotherapy with delay group; 50 [39%] of 128 patients in the long-course radiotherapy with delay group; odds ratio [OR] vs short-course radiotherapy: short-course radiotherapy with delay 0·59 [95% CI 0·36-0·97], long-course radiotherapy with delay 0·63 [0·38-1·04], p=0·075). However, in a pooled analysis of the two short-course radiotherapy regimens, the risk of postoperative complications was significantly lower after short-course radiotherapy with delay than after short-course radiotherapy (144 [53%] of 355 vs 188 [41%] of 357; OR 0·61 [95% CI 0·45-0·83] p=0·001). Interpretation: Delaying surgery after short-course radiotherapy gives similar oncological results compared with short-course radiotherapy with immediate surgery. Long-course radiotherapy with delay is similar to both short-course radiotherapy regimens, but prolongs the treatment time substantially. Although radiation-induced toxicity was seen after short-course radiotherapy with delay, postoperative complications were significantly reduced compared with short-course radiotherapy. Based on these findings, we suggest that short-course radiotherapy with delay to surgery is a useful alternative to conventional short-course radiotherapy with immediate surgery. Funding: Swedish Research Council, Swedish Cancer Society, Stockholm Cancer Society, and the Regional Agreement on Medical Training and Clinical Research in Stockholm.
  • Hansdotter Andersson, Pernilla, et al. (författare)
  • The COLOFOL trial: study design and comparison of the study population with the source cancer population.
  • 2016
  • Ingår i: Clinical Epidemiology. - Dove Press. - 1179-1349. ; 8, s. 15-21
  • Tidskriftsartikel (refereegranskat)abstract
    • The COLOFOL trial, a prospective randomized multicenter trial comparing two follow-up regimes after curative surgical treatment for colorectal cancer, focuses on detection of asymptomatic recurrences. This paper aims to describe the design and recruitment procedure in the COLOFOL trial, comparing demographic characteristics between randomized patients and eligible patients not included in the study.
  • Acosta, Stefan, et al. (författare)
  • Epidemiology and Prognostic Factors in Acute Superior Mesenteric Artery Occlusion.
  • 2010
  • Ingår i: Journal of Gastrointestinal Surgery. - Springer. - 1873-4626. ; 14, s. 628-635
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Reports on trends in incidence and mortality of acute superior mesenteric artery (SMA) occlusion and evaluation of prognostic factors in recent years are lacking. METHODS: Patients with acute SMA occlusion were identified through the in-patient and autopsy registry between 1970 and 1982 (n = 270), 1987 to 1996 (n = 135), and 2000 and 2006 (n = 100) in Malmö, Sweden. RESULTS: The overall incidence rate decreased from 8.6 to 5.4/100,000 person years and the autopsy rate from 87% to 25% over time. A higher serum creatinine level was associated with a lower probability of undergoing multi-detector row computed tomography with intravenous contrast (MDCTiv) (p = 0.006). Not performing a MDCTiv (odds ratio 4.0; 95% confidence interval [1.0-16.0]) remained as independent prognostic factor for in-hospital mortality. General and vascular surgeons collaborated in 25 out of 61 patients that underwent an intervention, of which 21 (84%) (p < 0.001) survived. CONCLUSIONS: A close collaboration between radiologists and general and vascular surgeons seems to be most important to lower the mortality in patients with acute SMA occlusion.
  • Agren, Magnus S., et al. (författare)
  • Action of matrix metalloproteinases at restricted sites in colon anastomosis repair: an immunohistochemical and biochemical study
  • 2006
  • Ingår i: Surgery. - Elsevier. - 1532-7361. ; 140:1, s. 72-82
  • Tidskriftsartikel (refereegranskat)abstract
    • Background. Dehiscence of colon anastomosis is a common, serious and potentially life-threatening complication after colorectal operation. In experimental models, impaired biomechanic strength of colon anastomoses is preventable by general inhibitors of matrix metalloproteinases (MMPs) and associated with collagen loss, which indicates a possible link between MMP-mediated collagen degradation and dehiscence. The precise localization of collagen degradation within the anastomotic area and the specific MMPs responsible are unknown. Methods. We have analyzed distinct zones within anastomoses using a novel microdissection technique for collagen levels, collagenolytic activity exerted directly by endogenous proteinases, and MMP-8 and MMP-9 immunoreactivity and their collagenolytic activity. Results. The most pronounced collagen loss was observed in the suture-holding zone, showing a 29% drop compared with adjacent micro-areas of 3-day-old anastomoses. Only this specific tissue compartment underwent a dramatic and significant increase in collagenolysis, amounting to a loss of 10% of existing collagen molecules in 24 hours, and was abolished by metalloproteinase inhibitors. The tissue surrounding suture channels was heavily infiltrated with CD68-positive histiocytes that expressed MMP-8 and to a lesser extent MMP-9. The collagenolytic effect of the interstitial collagenase MMP-8 was synergistically potentiated by the gelatinase MMP-9 when added to colon biopsies incubated in vitro. Conclusions. The unique finding of this study was that the specific tissue holding the sutures of a colon anastomosis lost the most collagen presumably through induction and activation of multiple MMPs that may explain the beneficial effects of treatment with non-selective MMP antagonists.
  • Akesson, Oscar, et al. (författare)
  • Morbidity related to defunctioning loop ileostomy in low anterior resection
  • 2012
  • Ingår i: International Journal of Colorectal Disease. - Springer. - 1432-1262. ; 27:12, s. 1619-1623
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim A defunctioning loop ileostomy in low anterior resection reduces the incidence and morbidity of an anastomotic leakage, but complications related to the stoma may occur. We explored stoma-associated complications during the stoma period and after stoma reversal. Methods A retrospective analysis of rectal cancer patients operated with low anterior resection and a defunctioning loop ileostomy at Helsingborg Hospital and Malmo University Hospital from January 2007 to June 2009 was undertaken. Results Ninety-two patients were included, of whom 82 (89 %) underwent stoma reversal. The median stoma period was 6.2 +/- 3.2 months. Sixty-six percent of the patients suffered from minor or major stoma-associated morbidity. The complication rate was significantly related to the stoma time (p < 0.01). Twenty-nine percent (27/92) had at least one episode of dehydration, leading to readmittance in half of the cases. Elderly patients were more prone to develop dehydration. Dehydration most commonly occurred early in the postoperative period (mean, 5.8 weeks). The mean hospital stay for stoma reversal was 6.5 +/- 4.0 days. Forty percent (33/82) had some complication associated with the reversal. Conclusion This study indicates high morbidity associated with defunctioning loop ileostomy. Our data suggest that the stoma time should be limited to reduce complications. Monitoring and early stoma reversal should be considered in elderly patients. Furthermore, stoma reversal is not uneventful, and more studies are needed to address how to minimize complications.
  • Al-Haidari, Amr A., et al. (författare)
  • MiR-155-5p positively regulates CCL17-induced colon cancer cell migration by targeting RhoA
  • 2017
  • Ingår i: Oncotarget. - Impact Journals, LLC. - 1949-2553. ; 8:9, s. 14887-14896
  • Tidskriftsartikel (refereegranskat)abstract
    • Colorectal cancer is the second most common cause of cancer-related death, which is due to migration of tumor cells to distant sites of metastasis. Accumulating data indicate that mciroRNAs play an important role in several aspects of colon cancer cell biology. Herein, we examined the role of miR-155-5p in colon cancer cell migration induced by the CCL17-CCR4 axis in HT-29 colon cancer cells. We found that miR-155-5p knockdown in serum starved colon cancer cells decreased CCL17-induced cell chemotaxis. Moreover, knocking down miR-155-5p markedly decreased CCL17-provoked activation of RhoA in colon cancer cells. Bioinformatics analysis predicted two putative binding sites in the AU-rich element at the 3'-UTR of RhoA mRNA. MiR-155-5p binding to RhoA mRNA was verified using a target site blocker and functionally validated by RNA immunoprecipitation assays, showing that miR-155-5p-dependent regulation of RhoA mRNA is mediated by AU-rich elements present in the 3'-UTR region. Taken together, these results show that miR-155-5p positively regulates RhoA mRNA levels and translation as well as cell migration in serum starved colon cancer cells and indicate that targeting miR-155-5p might be a useful strategy to antagonize colon cancer metastasis.
  • Al-Haidari, Amr A., et al. (författare)
  • Neutrophil extracellular traps promote peritoneal metastasis of colon cancer cells
  • 2019
  • Ingår i: Oncotarget. - Impact Journals, LLC. - 1949-2553. ; 10:12, s. 1238-1249
  • Tidskriftsartikel (refereegranskat)abstract
    • Cytoreductive surgery is the only curative option for patients with peritoneal carcinomatosis, however, intraperitoneal recurrence rate is high making new ways to prevent cancer recurrence an urgent need. Recent evidence suggests that neutrophils are involved in cancer progression. The purpose of our study was to examine the role of neutrophils in the spread of colon cancer cells in the peritoneal cavity. The number of metastatic noduli in the peritoneal cavity was quantified in mice injected with murine colon cancer cells (CT-26) intraperitoneally after surgical laparotomy and treated with a neutrophil depleting antibody or DNase I. In addition, peritoneal metastases were harvested from patients with peritoneal carcinomatosis. Scanning and transmission electron microscopy showed extensive neutrophil extracellular trap (NET) formation in peritoneal colon cancer metastases in mice and patients. Neutrophil depletion markedly reduced the number of metastases in laparotomised animals. Administration of DNase I decreased the number of metastatic nodules by 88% in laparotomised animals as well as NET-induced chemokinedependent colon cancer cell migration and adhesion in vitro. Finally, CT-26 cancer cells were found to express the avβ3 integrin and inhibition of av integrin abolished NET-induced adhesion of colon cancer cells to vitronectin. Taken together, our data show that NETs play an important role in colon cancer cell metastasis in the peritoneal cavity and regulate colon cancer cell migration and adhesion to extracellular matrix proteins. These novel findings suggest that targeting NETs might be an effective strategy to antagonize intrabdominal recurrences of colon cancer after cytoreductive surgery in patients with peritoneal carcinomatosis.
  • Al-Haidari, Amr, et al. (författare)
  • CCR4 mediates CCL17 (TARC)-induced migration of human colon cancer cells via RhoA/Rho-kinase signaling.
  • 2013
  • Ingår i: International Journal of Colorectal Disease. - Springer. - 1432-1262. ; 28:11, s. 1479-1487
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Accumulating data suggest a role of chemokines in tumor cell metastasis. CCR4 has been implicated in hematologic malignancies and recently also in solid tumors. Herein, we hypothesized that CCR4 might be expressed and support migration of colon cancer cells. METHODS: We used quantitative RT-PCR and flow cytometry to determine mRNA and surface expression of CCR4 on colon cancer cell lines (HT-29) and (AZ-97). Total RhoA and active RhoA protein levels in CCL17-stimulated colon cancer cells were quantified using ELISA and G-LISA assays. Migration assays were performed to evaluate colon cancer cells chemotaxis. In vitro tumor growth was assessed using proliferation assay. RESULTS: Our results show clear-cut mRNA levels and surface expression of CCR4 on a colon cancer cell line (HT-29) and on tumor cells (AZ-97). CCR4 ligand CCL17 (TARC) was a potent stimulator of colon cancer cell migration. This CCL17-induced colon cancer cell migration was inhibited by pre-incubation of the colon cancer cells with an antibody directed against CCR4 or an antagonist against CCR4. CCL17-induced signaling in colon cancer cells revealed that CCL17 increased mRNA formation of RhoA-C in colon cancer cells. Our results also found that CCL17 increased total RhoA and active RhoA protein levels in colon cancer cells. The Rho-kinase inhibitor Y-27632 abolished CCL17-induced colon cancer cell chemotaxis. In addition, inhibition of isoprenylation by GGTI-2133 markedly reduced colon cancer cell migration triggered by CCL17. CONCLUSIONS: Our novel data indicate for the first time that the CCL17-CCR4 axis might be involved in the spread of colon cancer cells.
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