2009
DOI: 10.1007/s00066-009-1993-9
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Radiation- and Chemoinduced Multidrug Resistance in Colon Carcinoma Cells

Abstract: Fractionated radiation can induce an MDR phenotype in SW620. However, long-term drug exposure establishes a more efficient selection. Various endpoints are not fully concordant regarding the extent of MDR. Posttranscriptional modifications, pleiotropic regulation, and alternative pathways may cause these discrepancies.

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Cited by 13 publications
(11 citation statements)
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“…Current cancer therapies may also be rendered inefficient by the selection or induction of cancer stem cells (CSCs) and the associated cellular heterogeneity (Hansen et al, 1997;Erenpreisa et al, 2008;Bartkowiak et al, 2009;McCord et al, 2009;Díaz-Carballo et al, 2010;Mo and Zhang, 2012;Mascre et al, 2012). The still evolving term CSC is based on both in vivo and in vitro tumor-initiating processes.…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…Current cancer therapies may also be rendered inefficient by the selection or induction of cancer stem cells (CSCs) and the associated cellular heterogeneity (Hansen et al, 1997;Erenpreisa et al, 2008;Bartkowiak et al, 2009;McCord et al, 2009;Díaz-Carballo et al, 2010;Mo and Zhang, 2012;Mascre et al, 2012). The still evolving term CSC is based on both in vivo and in vitro tumor-initiating processes.…”
Section: Introductionmentioning
confidence: 99%
“…The still evolving term CSC is based on both in vivo and in vitro tumor-initiating processes. It is assumed that CSCs derive from normal stem cells which undergo successive re-programming steps in response to physical, biological, or chemical stress, resulting in the generation of diverse cell phenotypes with a hierarchical structure (Walton et al, 2004;Spees et al, 2006;Lobo et al, 2007;Harris et al, 2008;Bartkowiak et al, 2009;Nakai et al, 2009;Sabisz and Skladanowski, 2009;Díaz-Carballo et al, 2010;Marques et al, 2010;Kitambi, 2011;Economopoulou et al, 2012;Mascre et al, 2012;Martin-Padura et al, 2012;Shyh-Chang et al, 2013;Zheng et al, 2013). While the presence of heterogeneity in tumors regardless of the therapy status is a well-documented fact, it should be emphasized that it can be increased by therapeutics.…”
Section: Introductionmentioning
confidence: 99%
“…3 among them, atPbinding cassette subfamily C member 4 (aBCC4) caught our attention, because there has been plenty of clinical and experimental research studies 4 performed to prove overexpression and amplification of aBCC4 contributing to poor prognosis in malignant tumors and resistance to anticancer and antiviral nucleotide analogues, such as methotrexate, 6-mercaptopurine, 6-thioguanine, irinotecan, 5 topotecan, camptothecins, tenofovir, lamivudine, and ganciclovir. however, it is unclear whether aBCC4 has an effect on radiation response, although fractionated irradiation can induce expression of functionally relevant members of the aBC transporter superfamily 6 and a multidrug resistance phenotype in colorectal carcinoma cell lines, 7 coupled with the potential for aBCC4 to mediate the transport of cyclic amP 8 and glutathione (GSH) conjugates. 9 Cyclic AMP and GSH play roles in sensitizing cancer cells to radiation, which implies that aBCC4 might be a useful molecular marker to predict radiosensitivity and a potential target for improving response to nRt.…”
mentioning
confidence: 99%
“…The cells were further incubated with EPA for 24 hours after irradiation and cultured for 11 days with the standard DMEM. The colonies formed were gently washed with PBS, fixed with ethanol, and stained with crystal violet [5]. The numbers of colonies containing more than 50 cells were counted, and the surviving fractions of cells were calculated.…”
Section: Experiments With Epa and Irradiationmentioning
confidence: 99%