| 21. |
- El-Salhy, Magdy, 1951-
(författare)
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Comparison between triple therapy with octreotide, galanin and serotonin, 5-fluorouracil/leucovorin, and sequential treatment with both, on human colon cancer.
- 2004
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Ingår i: Oncology Reports. - 1021-335X .- 1791-2431. ; 11:6, s. 1161-1168
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Tidskriftsartikel (refereegranskat)abstract
- Human colon cancer cells were implanted s.c. in nude mice. After 6 days, the mice were divided into four groups, 10 in each. During the first 5 days, the first and second groups were injected i.p. with leucovorin (LV)/5-fluorouracil (FU), and the third and fourth groups with sterile saline solution. During the subsequent 14 days, groups 1 and 4 received continuous i.p. infusion with sterile saline solution, while groups 2 and 3 received octreotide, galanin and serotonin via an implanted osmotic pump. Tumour volumes diminished significantly in mice treated with both LV/FU and LV/FU-triple therapy, as compared with controls. Both volume and weight of the tumours in mice given LV/FU-triple therapy were less than in those received LV/FU. The volume and weight of the tumours in animals treated with triple therapy was reduced as compared with controls, though not statistically significantly. The proliferation index, and the number of tumour blood vessels were both reduced, while the apoptotic index was increased in the mice treated with both LV/FU-triple therapy, and with triple therapy only as compared with LV/FU-treated mice. The present study has shown that the anti-tumour efficacy and therapeutic efficacy of triple therapy with octreotide, galanin and serotonin is equivalent to LV/FU and that sequential treatment with both could be beneficial.
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| 22. |
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| 23. |
- El-Salhy, Magdy, 1951-
(författare)
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Effects of octreotide, galanin and serotonin on a human gastric cancer cell line.
- 2005
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Ingår i: Oncology Reports. - 1021-335X .- 1791-2431. ; 13:5, s. 787-791
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Tidskriftsartikel (refereegranskat)abstract
- Human gastric cancer cell line was exposed in vitro to octreotide, galanin and serotonin alone, or in double or triple combination, and the number of viable cells and proliferation index were measured after 3, 6 and 12 h. The tumour cells were also implanted subcutaneously in nude mice. After 8 days, the animals were randomly allocated to either of two groups, with 8 in each. The first group received a bolus intraperitoneal injection, twice daily with 100 microl sterile saline solution for 10 days, while the second group was given sterile saline solution containing 100 microg/kg body weight of octreotide, galanin and serotonin. In vitro exposure to octreotide, galanin and serotonin alone or in double or triple combination reduced the number of viable cells and proliferation index. Both the volume and weight of tumours in mice given triple therapy were less than in controls. There was no statistical difference between treated and control tumours regarding proliferation and apoptotic indices or the labelling index of epidermal growth factor (EGF). It was concluded that the reduction in tumour volume and weight following triple treatment in vivo experiments could be not explained by inhibition of proliferation, induction of apoptosis or decreased expression of EGF of the tumour cells, and that other mechanisms must be involved. The reduction of proliferation in vitro but not in vivo could not be explained by the difference in concentrations of octreotide, galanin and serotonin used in vitro and in vivo.
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| 24. |
- El-Salhy, Magdy, 1951-
(författare)
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Effects of triple therapy with octreotide, galanin and serotonin on a human colon cancer cell line.
- 2005
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Ingår i: Oncology Reports. - 1021-335X .- 1791-2431. ; 13:1, s. 45-49
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Tidskriftsartikel (refereegranskat)abstract
- Human colon cancer cells were implanted subcutaneously into nude mice. After 12 days, the animals were divided into two groups. The first group received 40 microg/kg body weight of octreotide, galanin and serotonin via an intraperitoneally implanted pump. The second group received sterile saline only. Treatment lasted for 14 days. The volume and weight of the tumours in treated mice tended to decrease, though not with statistical significance. The proliferation index and the number of tumour blood vessels was significantly reduced in the mice given triple therapy. The apoptotic index, as detected by TUNEL method and monoclonal anti-poly (ADP-ribose) polymerase, was significantly higher in the treated mice. Though the results of this investigation are promising, it is uncertain as to what use the present findings may imply for the treatment of patients with colorectal cancer.
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| 25. |
- El-Salhy, Magdy, 1951-, et al.
(författare)
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Effects of triple therapy with octreotide, galanin and serotonin on liver metastasis of human colon cancer in xenografts.
- 2004
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Ingår i: Oncology Reports. - 1021-335X .- 1791-2431. ; 11:6, s. 1177-1182
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Tidskriftsartikel (refereegranskat)abstract
- Human colon cancer cells (SW 620) were implanted under the capsule of the left liver lobe of female nude (C57BL/6JBom-nu) mice. After 7 days, relaparatomy was performed and an ALZET osmotic pump was implanted intraperitoneally and left in situ for 14 days. The mice were divided into 2 groups, 10 in each. The first group received 40 micro g/kg body weight of octreotide, galanin and serotonin, and the second group received sterile saline. The number of metastases in the liver, and to the intra-abdominal lymph nodes was significantly greater in the controls. The incidence of metastases to the peritoneal cavity was lower in the treated animals (though not statistically significantly). Tumour volume, wet weight, proliferation index and number of tumour blood vessels decreased significantly in the treated animals. The apoptotic index was significantly higher in the treated mice. The decrease in the volume and weight of tumours following the triple therapy seemed to be caused by low proliferation, and increased apoptosis, and reduced vascularization of the tumours. The low invasion of cancer cells observed following this treatment could have been due to the low tumour burden, and to the reduced number of the blood and lymph vessels.
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| 26. |
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| 27. |
- Farnebo, Lovisa, et al.
(författare)
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Number of negative points : a novel method for predicting radiosensitivity in head and neck tumor cell lines.
- 2008
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Ingår i: Oncology Reports. - : Spandidos Publications. - 1021-335X .- 1791-2431. ; 20:2, s. 453-461
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Tidskriftsartikel (refereegranskat)abstract
- The present study was aimed at establishing a method that combines multiple factors of protein and genetic changes that enables prediction of radiosensitivity in the head and neck squamous cell carcinoma (HNSCC) cell lines. In nine HNSCC cell lines, the quantity of protein expression and the type of genetic alterations were translated into a point system, called the Number of Negative Points. The expression of 14 proteins involved in growth control and/or apoptosis was quantified using a densitometric assessment of Western blots. The blots were adjusted to actin and standardised to normal oral keratinocytes classifying them into four groups depending on the amount of protein expressed (0-3 points). Mutations of the p53 gene were classified into three groups and each mutation was given one point. Since the cell lines each had a known intrinsic radiosensitivity, a multivariate statistical calculation could then be performed to select for the combination of factors having the strongest correlation to radiosensitivity. The strongest correlation of the investigated factors was the combination of epidermal growth factor receptor, survivin and splice site/missense p53 mutations (R=0.990 and P<0.0001). No single factor had a significant correlation to the intrinsic radiosensitivity. Since a significant correlation to the intrinsic radiosensitivity was achieved only when two or more factors were combined, we conclude that a method such as the Number of Negative Points is necessary for prediction of treatment response. We present a novel method to combine factors which enables the prediction of radiosensitivity of HNSCC cell lines.
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| 28. |
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| 29. |
- Gabrielson, Marike, et al.
(författare)
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The mitochondrial transport protein SLC25A43 affects drug efficacy and drug-induced cell cycle arrest in breast cancer cell lines
- 2013
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Ingår i: Oncology Reports. - : Spandidos Publications. - 1021-335X .- 1791-2431. ; 29:4, s. 1268-
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Tidskriftsartikel (refereegranskat)abstract
- The mitochondria have been identified as key players of apoptosis, cell proliferation and cell cycle regulation. However, the role of mitochondria in breast cancer and treatment failure remains unclear. We have previously shown a common deletion of the gene SLC25A43 in human epidermal growth factor receptor 2 (HER2)-positive breast cancer. This gene is coding for a mitochondrial inner membrane transporter and, to date, little is known about the function of this protein. We have also found that low protein expression of SLC25A43 significantly correlates with a lower S phase fraction in HER2-positive breast cancer. The aim of this study was to investigate whether knockdown (KD) of SLC25A43 could have an effect on the cytotoxicity of different cytostatic drugs using MCF10A, MCF7 and BT-474 cells. Following siRNA-mediated KD of SLC25A43, one non-malignant and two breast cancer cell lines were exposed to the anthracycline epirubicin or the taxane paclitaxel. The HER2-positive breast cancer cells were also exposed to the targeted therapy trastuzumab and dual exposure to trastuzumab and paclitaxel. We found that KD of SLC25A43 resulted in a decreased cytotoxic effect of paclitaxel in the two cancer cell lines (P<0.05). Further analysis of cell cycle phase distribution showed that KD increased the paclitaxel-induced G2/M block in these two cell lines (P<0.05). KD of SLC25A43 also reduced the inhibitory effect of trastuzumab on cell proliferation in the HER2-positive cancer cell line BT-474 (P<0.05), and the drug-induced G0/G1 block (P<0.05). Moreover, SLC25A43 influenced the percentage of Ki-67-positive cells. Our findings demonstrate that the mitochondrial protein SLC25A43 affects drug efficacy and cell cycle regulation following drug exposure in breast cancer cell lines.
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| 30. |
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