Lower proliferation was observed in tumours treated with paclitaxel and ABT 737

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 Lower proliferation was observed in tumours treated with paclitaxel and ABT 737 Empty Lower proliferation was observed in tumours treated with paclitaxel and ABT 737

Post  huwan123456 on Wed Aug 06, 2014 7:15 am

Irinotecan decreases the expression of HIF 1 and VEGF under both normoxic and hypoxic conditions, which could be why there JNJ-7706621 ic50 is no difference in effect in some cell lines, here U 937. Melphalan is an alkylating agent with an enhanced effect in hypoxia and in HIF 1 inhibited cells. Al though the correlation between hypoxia and melphalan resistance was not distinct, both A2780 and ACHN were clearly less sensitive and U 937 more sensitive, in oxygen deprived cells. Sorafenib inhibits vascular endothelial growth factor receptor and platelet derived growth factor receptor signaling, thus one might hypothesize that sorafenib would be more potent under hypoxic conditions. With respect to the cell lines used in this report, we have found no information on SCLC cell line NCI H69 expression or dependence on VEGF signaling.

The renal cell adenocarcinoma ACHN has a low normal baseline secretion of VEGF to cell growth medium, a secretion that may be inhibited by sorafenib, and to which ACHN is sensitive. The breast cancer cell line MCF 7 has been described Lenalidomide Revlimid with a survival system by which VEGF can act as an internal autocrine survival factor through its binding to VEGFR 1, and cell line is sensitive to treatment with sorafenib, which also appear to down regulate hypoxia induced HIF 1 expression. The ovarian carcinoma cell line A2780 expresses VEGFR 1, but its sensitivity to sorafenib has not been described previously. In this study sorafenib was less effective in hypoxic and anoxic ACHN, MCF 7 and U 937 cells, which may be related to the mono culture assay with no communicating stroma cells.

In the LY2228820 溶解度 study presented herein we have emphasized to isolate hypoxia as the variable in the experiments, all other factors were standardized, and all arms of each replicate were analyzed simultaneously. There are several environmental factors in solid tumors that may be studied, e. g. the low nutrient supply, interaction with stroma cells, acidity, as well as proliferation of the tumor cells. These factors may be studied individually, or by assays including several aspects, for example by the use of spheroid cultures or prolonged incubation times beyond confluency. Furthermore, since different drugs act on cancer cells in different ways resulting in cytostatic or cytotoxic effects, different readouts would probably yield different results.

The FMCA based IC50 value used in this report is based on survival indices at the end of the experiment, and is thus the result of both antiproliferative and toxic effects. Conclusion Our results show that impaired chemosensitivity is not universal, in contrast different cell lines behave different and some drugs appear even less effective in normoxia. Part of the results obtained with this method, as prob ably with any model of oxygen deficiency, can be directly explained by decreased proliferation when cells are deprived of oxygen. However, this is clearly not the only variable, as some cells appeared to increase their prolif eration and sensitivity under low oxygen pressure.


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