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| 42. |
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| 43. |
- Mälarstig, Anders, et al.
(författare)
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Tumour-derived adhesion factor in colorectal cancer
- 2009
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Ingår i: Molecular Medicine Reports. - : Spandidos Publications. - 1791-2997 .- 1791-3004. ; 2:6, s. 971-976
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Tidskriftsartikel (refereegranskat)abstract
- Tumour-derived adhesion factor (TAF) has been shown to be associated with breast, prostate and colorectal cancer (CRC), acting as tumour suppressor or tumour promoter by mechanisms not as yet understood. Here, we comparatively analyzed the expression profile of TAF in plasma, tumour and paired normal tissue from patients with CRC. In addition, we investigated the relationship between TAF and systemic inflammation, mirrored by the elevation of interleukin-6 (IL-6) and TAF levels in plasma. Levels of TAF and IL-6 were determined by ELISA. Immunohistochemistry was performed to investigate the site of TAF expression. We also used a TaqMan system to investigate a TAF single nucleotide polymorphism (rs2041437) with a potential effect on CRC. TAF protein levels were significantly (Pless than0.001) higher in colorectal tumours than in normal tissue, and were increased in patients with Dukes stages B and C compared to A. Immunohistochemistry revealed heterogeneous TAF expression mainly in the epithelial cells of the cancer and normal tissue. The plasma TAF level was reduced in CRC patients compared with the controls (P=0.002), independent of the inflammatory marker IL-6. Regarding genotype and allelic distributions, significant differences between CRC patients and control subjects or associations between clinical characteristics and TAF levels in tissue and plasma were not observed. In conclusion, altered TAF protein expression in cancer tissue may be a potential biomarker in colorectal carcinogenesis. Further research exploring the regulation of TAF is required to evaluate whether TAF is linked to clinical outcome.
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| 44. |
- Nguyen, Song Van, et al.
(författare)
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Clinicopathological and prognostic value of CD44 gene polymorphism (rs187115) in Swedish patients with colorectal cancer
- 2023
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Ingår i: Nucleosides, Nucleotides & Nucleic Acids. - : Taylor & Francis. - 1525-7770 .- 1532-2335. ; 42:10, s. 807-817
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Tidskriftsartikel (refereegranskat)abstract
- Cluster of differentiation (CD) 44 plays a crucial role in apoptosis, cell-cell interactions, angiogenesis, metastasis and proliferation. The aim of the present study was to examine the influence of CD44 gene polymorphism rs187115 on colorectal cancer (CRC) susceptibility and the association with various clinical features including long-term survival in Swedish patients with CRC. Genotypes were screened, using TaqMan single nucleotide polymorphism (SNP) assays based on polymerase chain reaction, in 612 CRC patients and 575 healthy controls.The carriers of G allele, genotypes (AG + GG), were found to be associated with an increased risk of CRC with an odds ratio (OR) of 1.35 (95% confidence interval (CI) = 1.01-1.81; p = 0.039) and found to be more common in patients with mucinous cancer compared with non-mucinous cancer, OR = 1.69 (95% CI = 1.02-2.80; p = 0.011). By using Kaplan-Meier analysis, the patients with genotype GG showed shorter cancer-specific and recurrence free survival with a hazard ratio (HR) of 1.25 (95% CI = 1.02-1.54; p = 0.036) and 1.52 (95% CI = 1.12-2.06; p = 0.007), respectively, in comparison with the carriers of A allele (AG + AA). The present findings demonstrated that the variant G allele of CD44 gene polymorphism rs187115 was related to risk for CRC and associated to mucinous cancer and predict worse prognosis in Swedish patients with CRC.
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| 45. |
- Nowak-Sliwinska, Patrycja, et al.
(författare)
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Consensus guidelines for the use and interpretation of angiogenesis assays
- 2018
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Ingår i: Angiogenesis. - : Springer. - 0969-6970 .- 1573-7209. ; 21:3, s. 425-532
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Forskningsöversikt (refereegranskat)abstract
- The formation of new blood vessels, or angiogenesis, is a complex process that plays important roles in growth and development, tissue and organ regeneration, as well as numerous pathological conditions. Angiogenesis undergoes multiple discrete steps that can be individually evaluated and quantified by a large number of bioassays. These independent assessments hold advantages but also have limitations. This article describes in vivo, ex vivo, and in vitro bioassays that are available for the evaluation of angiogenesis and highlights critical aspects that are relevant for their execution and proper interpretation. As such, this collaborative work is the first edition of consensus guidelines on angiogenesis bioassays to serve for current and future reference.
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| 48. |
- Rennel, Emma, et al.
(författare)
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Endocan is a VEGF-A and PI3K regulated gene with increased expression in human renal cancer
- 2007
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Ingår i: Experimental Cell Research. - : Elsevier BV. - 0014-4827 .- 1090-2422. ; 313:7, s. 1285-1294
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Tidskriftsartikel (refereegranskat)abstract
- An in vitro model of VEGF-A-induced angiogenesis was used to generate transcription profiles of human microvascular endothelial cells. Microarray analysis showed increased transcription of genes known to regulate angiogenesis, but also genes that previously have not been firmly associated with angiogenesis such as endocan, pinin, plakophilin, phosphodiesterase 4B and gelsolin. Increased endocan mRNA levels in response to VEGF-A in endothelial cells and in human renal cancer have previously been reported. We now show increased endocan protein levels in VEGF-A treated endothelial cells and in human renal clear cell carcinoma. Increased protein expression was observed both in tumor cells and in a subset of tumor vessels, while expression in normal kidney tissue was low. VEGF-A seemed to be a specific inducer of endocan transcription since FGF-2, PDGF-BB, HGF/SF and EGF did not alter expression levels. Inhibition of PI3K with LY294002 caused a 12-fold increase in endocan transcription suggesting a repressive function of PI3K. In contrast inhibition of Src or MEK, which are signaling pathways activated by VEGF-A, did not influence basal or VEGF-A-induced endocan levels. In conclusion our study shows that, among angiogenic growth factors, VEGF-A is a specific inducer of endocan transcription which is translated into increased protein levels in VEGF-A treated endothelial cells. Increased endocan protein expression in human renal cancer suggests a role in tumor growth.
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| 49. |
- Shamoun, Levar, et al.
(författare)
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Association of gene and protein expression and genetic polymorphism of CC chemokine ligand 4 in colorectal cancer
- 2021
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Ingår i: World Journal of Gastroenterology. - : Baishideng Publishing Group. - 1007-9327 .- 2219-2840. ; 27:30, s. 5076-5087
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND Leukocytes, such as T cells and macrophages, play an important role in tumorigenesis. CC chemokine ligand (CCL) 4, which is produced by lymphocytes and macrophages, has been found to be expressed in the mucosa of the gastrointestinal tract and is a potent chemoattractant for various leukocytes. AIM To examine CCL4 expression and its genetic polymorphism rs10491121 in patients with colorectal cancer (CRC) and evaluate their prognostic significance. METHODS Luminex technology was used to determine CCL4 Levels in CRC tissue (n = 98), compared with paired normal tissue, and in plasma from patients with CRC (n = 103), compared with healthy controls (n = 97). Included patients had undergone surgical resection for primary colorectal adenocarcinomas between 1996 and 2019 at the Department of Surgery, Ryhov County Hospital, Jönköping, Sweden. Reverse transcription quantitative PCR was used to investigate the CCL4 gene expression in CRC tissue (n = 101). Paired normal tissue and TaqMan single nucleotide polymorphism assays were used for the CCL4 rs10491121 polymorphism in 610 CRC patients and 409 healthy controls. RESULTS The CCL4 protein and messenger RNA expression levels were higher in CRC tissue than in normal paired tissue (90%, P < 0.001 and 45%, P < 0.05, respectively). CRC tissue from patients with localized disease had 2.8-fold higher protein expression levels than that from patients with disseminated disease. Low CCL4 protein expression levels in CRC tissue were associated with a 30% lower cancer-specific survival rate in patients (P < 0.01). The level of plasma CCL4 was 11% higher in CRC patients than in healthy controls (P < 0.05) and was positively correlated (r = 0.56, P < 0.01) with the CCL4 protein level in CRC tissue. The analysis of CCL4 gene polymorphism rs10491121 showed a difference (P < 0.05) between localized disease and disseminated disease in the right colon, with a dominance of allele A in localized disease. Moreover, the rate of the A allele was higher among CRC patients with mucinous cancer than among those with nonmucinous cancer. CONCLUSION The present study indicates that the CRC tissue levels of CCL4 and CCL4 gene polymorphism rs10491121, particularly in the right colon, are associated with clinical outcome in CRC patients.
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