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61.
  • Hakelius, Malin, et al. (författare)
  • Keratinocytes and Head and Neck Squamous Cell Carcinoma Cells Regulate Urokinase-type Plasminogen Activator and Plasminogen Activator Inhibitor-1 in Fibroblasts
  • 2013
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 33:8, s. 3113-3118
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Background: To investigate possible differences in the effects of soluble factors from oral squamous cell carcinoma (SCC) cells (UT-SCC-87) and normal oral keratinocytes (NOK) on fibroblast expression of genes involved in tumor stroma turnover. Materials and Methods: Transwell co-cultures with fibroblasts in collagen gels, and SCC cells or NOK in inserts were carried out. Fibroblast gene expression was measured with real-time polymerase chain reaction (PCR). Results: The expression of urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) was up-regulated in co-cultures with SCC cells but not with NOK. In contrast, both SCC cells and NOK regulated matrix metalloproteinase-1 (MMP1) and -3, and tissue inhibitor of metalloproteinases-2 (TIMP2) and -3 to a similar extent, while MMP2 and TIMP1 were largely unaffected. Interleukin 1 alpha (IL1 alpha) up-regulated both MMP1 and MMP3 and down-regulated PAI-1, TIMP2 and -3. Conclusion: SCC and NOK regulate fibroblast expression of genes involved in tumor stroma turnover differentially in vitro. These observations may contribute to a better understanding of the mechanisms behind extracellular matrix turnover in tumors.</p>
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62.
  • Hakelius, Malin, 1965-, et al. (författare)
  • Normal oral keratinocytes and head and neck squamous carcinoma cells induce an innate response in fibroblasts
  • 2016
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 36:5, s. 2131-2137
  • Tidskriftsartikel (övrigt vetenskapligt)abstract
    • <p>Background: Tumor stroma is similar to the connective tissue of chronic inflammation. The extracellular matrix of tumors is formed by cancer-associated fibroblasts that also modulate the inflammatory response. Materials and Methods: We studied the ability of oral keratinocytes (NOK) and oral squamous cell carcinoma cells (SCC) to induce an innate immune response in fibroblasts. Co-cultures with fibroblasts in collagen gels and keratinocytes in inserts were used. Pentraxin 3 (PTX3) was used as an indicator of an innate immune response. Results: SCC and NOK up-regulated fibroblast mRNA expression and protein release of PTX3. mRNA levels were more pronounced in cultures with malignant cells. The induction of PTX3 was abrogated by an interleukin-1 receptor antagonist Conclusion: Keratinocytes have the capacity to induce an interleukin-1-dependent innate immune response by fibroblasts in vitro. This could be important for subsequent fibroblast modulation of the inflammatory reaction in non-malignant and malignant disease processes.</p>
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63.
  • Hassan, Saadia Bashir, et al. (författare)
  • Alpha Terpineol : A Potential Anticancer Agent which Acts through Suppressing NF-kappa B Signalling
  • 2010
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 30:6, s. 1911-1919
  • Tidskriftsartikel (refereegranskat)abstract
    • <p><strong>Background:</strong></p> <p>Alpha terpineol is a bioactive component of Salvia libanotica essential oil extract and has shown antitumour activity.</p> <p><strong>Materials and Methods:</strong></p> <p>The cytotoxicity of alpha terpineol towards different tumour cell lines was evaluated in vitro. Mechanistic characterization was performed using analysis of drug activity in a cell line panel and drug-induced gene expression perturbation using the connectivity map approach.</p> <p><strong>Results:</strong></p> <p>The small cell lung carcinoma was the cell line most sensitive to alpha terpineol. The results proposed alpha terpineol as an NF-kappa B inhibitor, which was confirmed by the observed dose-dependent inhibition of NF-kappa B translocation and activity using two NF-kappa B assays, and by the down-regulation of the expression of several NE-kappa B-related genes such as IL-1 beta and IL1R1.</p> <p><strong>Conclusion: </strong></p> <p>The results suggest that alpha terpineol inhibits the growth of tumour cells through a mechanism that involves inhibition of the NF-kappa B pathway.</p>
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64.
  • Hassan, Saadia B., et al. (författare)
  • CHS 828 kill tumour cells by inhibiting the nuclear factor-kappa B translocation but unlikely through down-regulation of proteasome
  • 2006
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 26:6B, s. 4431-4436
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>CHS 828 (N-(6-chlorophenoxyhexyl)-N'cyano-N"-4-pyridylguanidine) has shown promising activity in many preclinical systems and in phase I/II clinical trials. The nuclear transcription factor kappa B (NF-κB) has been identified as a target for CHS 828. The aim of this study was to confirm the inhibitory effect of CHS 828 on NF-κB translocation and to explore its possible effect on the proteasome using 7 cell lines. Translocation of NF-κB from the cytoplasm to the nucleus was analysed using a quantitative cytometric system, ArrayScan®. The activity of the proteasome was assayed by monitoring the hydrolysis of a fluorogenic substrate. In parallel, the in vitro cytotoxic effect of CHS 828 was analyzed using a 72-h microtiter plate-based cytotoxicity assay (FMCA). CHS 828 inhibited NF-κB translocation in the cell lines where it was able to inhibit the tumour cell growth. However, the results did not prove any effect of CHS 828 on proteasome activity when compared to a proteasome inhibitor activity.</p>
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65.
  • Hassan, Saadia Bashir, et al. (författare)
  • The Nanoparticulate Quillaja Saponin BBE Is Selectively Active Towards Renal Cell Carcinoma
  • 2013
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 33:1, s. 143-151
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Aim: To characterize the cytotoxic effect of BBE, the particulate of desacyl-saponin, in model systems of solid tumours. Materials and Methods: Cytotoxic activity of BBE was investigated in solid human tumour cell lines, in tumour cells from patients with renal cell carcinoma, in normal human renal cells and in peripheral blood mononuclear cells. The BBE mode of cell death was assessed in vitro. In vivo effect of BBE was evaluated in xenograft-bearing mice. Results: BBE was selectively active against renal cell carcinoma, with no or little effect on normal cells. BBE induced caspase activity and apoptosis. An inhibitory activity of BBE on xenograft tumour growth, with no apparent signs of haematological toxicity was shown. In the non-proliferative model of patient tumour cells, BBE was active on only 1/5 patient samples, suggesting association of BBE effect with cell proliferation. Conclusion: BBE has interesting activities against renal cell carcinoma and should be further explored as a drug against this resistant tumour type.</p>
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66.
  • Hedman, Mattias, et al. (författare)
  • Fractionated Irradiation of Five Human Lung Cancer Cell Lines and Prediction of Survival According to a Radiobiology Model
  • 2011
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 31:4, s. 1125-1130
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Background: This study evaluates a predictive radiobiology model by measurements of surviving fraction (SF) by the clonogenic assay or the extrapolation method and the proliferation rate in vitro. It is hypothesized that incorporating proliferation to intrinsic radiosensitivity, measured by SF, to predict radiation responsiveness after fractionated irradiation adds to the model's accuracy. Materials and Methods. Five lung cancer cell lines with known SF after 1 Gy (SF1), and also SF2 and SF5, were irradiated with three different fractionation regimes; 10x1 Gy, 5x2 Gy or 2x5 Gy during the same total time to achieve empirical SF. In addition, the SF1, SF2 and SF5 after fractionated irradiation was calculated for each cell line based on the already known single fraction SF and with or without a proliferation factor. The results were compared to the empirical data. Results and Discussion: By using the clonogenic assay to measure radiosensitivity, prediction of radiosensitivity was improved after fractionated radiotherapy when proliferation was used in the radiobiology model. However, this was not the case in the cell lines where the extrapolation method was used to calculate SF. Thus, a radiobiology model including intrinsic radiosensitivity, measured by the clonogenic assay, as well as proliferation, is better at predicting survival after fractionated radiotherapy, compared to the use of intrinsic radiosensitivity alone.</p>
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67.
  • Heedman, Per-Anders, et al. (författare)
  • Symptom assessment in advanced palliative home care for cancer patients using the ESAS : Clinical aspects
  • 2001
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 21:6 A, s. 4077-4082
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Four hundred and thirty-one cancer patients were assessed with the ESAS and a VAS-QoL at admission to Hospital-based home care (HBHC) and subsequently. Results: Pain and nausea were well-controlled (mean 2.5 and 1.8) whereas patients were less satisfied with appetite, activity and sense of well-being. Dyspnoea and anxiety (lung cancer, p<0.001 and p<0.01) and pain (prostate cancer, p<0.01), were related to diagnosis while activity, drowsiness, appetite and well-being to survival (p<0.05 to p<0.001). The correlations between individual symptoms and well-being were low (0.2-0.5), whereas the correlation between well-being and the Symptom Distress Score (SDS) was 0.76. "Well-being" was a better word to use than QoL. Discussion: ESAS is useful in HBHC and data show that symptoms other than merely pain and nausea are of importance. As the global measurement (one VAS) of well-being has a high correlation with SDS, this single measurement may be clinically adequate for quality assurance of symptom control in dying cancer patients.</p>
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68.
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69.
  • Hellberg, Dan, et al. (författare)
  • Differences in expression of tumor markers between pre- and postmenopausal women with invasive cervical cancer
  • 2008
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 28:3B, s. 1793-1795
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>The aim of the present study was to investigate the differences in the expression of tumor markers in squamous cell and in adenomatous carcinomas in pre- and postmenopausal women, respectively. Patients and Methods: The study population comprised 53 premenopausal and 107 postmenopausal women. Thirty-four tumors were adenomatous (n=31) or adenosquamous carcinomas (n=3), distributed between 13 premenopausal and 21 postmenopausal women. The remaining 126 squamous cell carcinomas were diagnosed in 40 pre- and 86 postmenopausal women. Expression of ten tumor markers of possible clinical importance in cervical cancer was evaluated. Results: Expression of three tumor markers, p53 (&gt; ;0% vs. 0%), p27 (&gt; , 20% vs. &lt; ;20%) and cyclooxygenase-2 (COX-2) (high intensity vs. moderate/none) differed significantly between pre- compared to postmenopausal women with squamous cell (p27, 54% vs. 72%, p=0.009) or adenomatous carcinomas (p53, 8% vs. 63%, p=0.006 and COX-2, 46% vs. 20%, p=0.03). All results were adjusted for clinical cancer stage. Conclusion: The unusual age-specific incidence curve in cervical cancer has rarely been related to expression of tumor markers. Age-related differences in expression of tumor markers could reflect some age-related different biological mechanisms in cervical cancer.</p>
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70.
  • Hellberg, Dan (författare)
  • Sex Steroids and Cervical Cancer
  • 2012
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 32:8, s. 3045-3054
  • Forskningsöversikt (refereegranskat)abstract
    • <p>During the 19th century, studies indicated that reproductive events were involved in cervical cancer. Human papillomavirus (HPV) infection is a prerequisite for development of cancer, but co-factors, among them the action of sexual steroid hormones, are necessary. Childbirth has been an important risk factor but now probably plays a minor role in the industrialized world, where parity is low. Longterm oral contraceptive use has been thoroughly studied epidemiologically, and correlates to cervical cancer in most studies. In vitro studies on cervical cell lines transfected with HPV and animal studies indicate that sex steroid hormones are capable to induce cancer. In in vivo cervical cancer tissue studies there have been observations that endogenous progesterone in serum correlates to a negative pattern of expression of cellular and extracellular proteins, tumor markers. Immune response could be another mechanism. Estradiol might be associated with a positive pattern and high estradiol and low progesterone levels increase duration of survival in cervical cancer. Studies where treatment of compounds that influence sex steroid hormones have been given are rare and have been disappointing.</p>
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