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  • 1
    Online-Ressource
    Online-Ressource
    Tumor-treating fields (TTFields) induce immunogenic cell death resulting in enhanced antitumor efficacy when combined with anti-PD-1 therapy
    Springer Science and Business Media LLC ; 2020
    In:  Cancer Immunology, Immunotherapy Vol. 69, No. 7 ( 2020-07), p. 1191-1204
    Details
    In: Cancer Immunology, Immunotherapy, Springer Science and Business Media LLC, Vol. 69, No. 7 ( 2020-07), p. 1191-1204
    Kurzfassung: Tumor-treating fields (TTFields) are alternating electric fields in a specific frequency range (100–300 kHz) delivered to the human body through transducer arrays. In this study, we evaluated whether TTFields-mediated cell death can elicit antitumoral immunity and hence would be effectively combined with anti-PD-1 therapy. We demonstrate that in TTFields-treated cancer cells, damage-associated molecular patterns including high-mobility group B1 and adenosine triphosphate are released and calreticulin is exposed on the cell surface. Moreover, we show that TTFields treatment promotes the engulfment of cancer cells by dendritic cells (DCs) and DCs maturation in vitro, as well as recruitment of immune cells in vivo. Additionally, our study demonstrates that the combination of TTFields with anti-PD-1 therapy results in a significant decline of tumor volume and increase in the percentage of tumor-infiltrating leukocytes in two tumor models. In orthotopic lung tumors, these infiltrating leukocytes, specifically macrophages and DCs, showed elevated expression of PD-L1. Compatibly, cytotoxic T-cells isolated from these tumors demonstrated increased production of IFN-γ. In colon cancer tumors, T-cells infiltration was significantly increased following long treatment duration with TTFields plus anti-PD-1. Collectively, our results suggest that TTFields therapy can induce anticancer immune response. Furthermore, we demonstrate robust efficacy of concomitant application of TTFields and anti-PD-1 therapy. These data suggest that integrating TTFields with anti-PD-1 therapy may further enhance antitumor immunity, hence achieve better tumor control.
    Materialart: Online-Ressource
    ISSN: 0340-7004 , 1432-0851
    URL: Article
    DOI: 10.1007/s00262-020-02534-7
    Sprache: Englisch
    Verlag: Springer Science and Business Media LLC
    Publikationsdatum: 2020
    ZDB Id: 1458489-X
    ZDB Id: 195342-4
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
    Online-Ressource
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    Tumor Treating Fields (TTFields) downregulate the Fanconi Anemia-BRCA pathway and increase the efficacy of chemotherapy in malignant pleural mesothelioma preclinical models
    Elsevier BV ; 2021
    In:  Lung Cancer Vol. 160 ( 2021-10), p. 99-110
    Details
    In: Lung Cancer, Elsevier BV, Vol. 160 ( 2021-10), p. 99-110
    Materialart: Online-Ressource
    ISSN: 0169-5002
    URL: Article
    DOI: 10.1016/j.lungcan.2021.08.011
    Sprache: Englisch
    Verlag: Elsevier BV
    Publikationsdatum: 2021
    ZDB Id: 2025812-4
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
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    Tumor treating fields (TTFields) in combination with sorafenib inhibit hepatocellular carcinoma in vitro and in vivo.
    American Society of Clinical Oncology (ASCO) ; 2022
    In:  Journal of Clinical Oncology Vol. 40, No. 4_suppl ( 2022-02-01), p. 464-464
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 40, No. 4_suppl ( 2022-02-01), p. 464-464
    Kurzfassung: 464 Background: Hepatocellular carcinoma (HCC) is a highly malignant liver cancer and a leading cause of cancer related mortality. Sorafenib was the first approved systemic treatment for HCC, and remains one of few front-line treatments for this malignancy. Tumor treating fields (TTFields) are low intensity (1-3 V/cm), intermediate frequency (100-500 kHz), alternating electric fields that exert antimitotic effects on cancerous cells. Results of the phase 2 HEPANOVA study of TTFields (150 kHz) plus sorafenib for advanced HCC support investigation of TTFields in a randomized controlled phase 3 study. The current research aimed to describe the in vitro and in vivo efficacy of this combination and to elucidate details regarding the underlying mechanism of action. Methods: In vitro examinations were performed in HepG2 and Huh-7D12 human HCC cell lines, to which TTFields at a frequency of 150 kHz were applied using the inovitro system. Autophagy was examined by western blot and fluorescence detection of microtubule-associated protein light chain 3 (LC3) levels, an accepted autophagy marker. The effect of TTFields in combination with sorafenib was evaluated using cytotoxic, clonogenic, and apoptotic assays. In vivo, SD rats were inoculated orthotopically into the left hepatic lobe with N1S1 HCC cells. 7 days later, TTFields or sham (heat) were applied to the abdominal region of the rats, continuously for 6 days. Daily intraperitoneal injections of sorafenib (10 mg/kg/day) or vehicle were performed during this time. To determine tumor volume growth, MRI images were acquired before and after treatment. Levels of autophagy and apoptosis were examined in tumor sections by immunohistochemistry for LC3 and cleaved PARP, respectively. Results: Application of TTFields induced autophagy in HCC cells. TTFields delivery was cytotoxic to the cells, reduced their colony forming ability, and induced apoptosis while combination with sorafenib elevated these effects. In vivo, tumor volume increased 6-fold in control animals vs 1.6-fold in animals treated with TTFields plus sorafenib. This effect was accompanied by significantly elevated levels of cleaved PARP and LC3 within the tumors of treated relative to control rats. Conclusions: The results demonstrate induction of autophagy and apoptosis in HCC following treatment with TTFields. Concomitant application of TTFields with sorafenib enhanced efficacy via a mechanism that may involve overwhelming autophagy, in vitro and in vivo.
    Materialart: Online-Ressource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2022.40.4_suppl.464
    RVK:
    XA 52760
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Society of Clinical Oncology (ASCO)
    Publikationsdatum: 2022
    ZDB Id: 2005181-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
    Online-Ressource
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    Meta-analysis of cancer cell lines genomes based on their response to ttfields.
    American Society of Clinical Oncology (ASCO) ; 2013
    In:  Journal of Clinical Oncology Vol. 31, No. 15_suppl ( 2013-05-20), p. e22125-e22125
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 31, No. 15_suppl ( 2013-05-20), p. e22125-e22125
    Kurzfassung: e22125 Background: Tumor Treating Fields (TTFields) therapy is an established anti-mitotic treatment modality. The inhibitory effect of TTFields was demonstrated in numerous cancer cell lines with some cell lines exhibiting higher treatment sensitivity than others. The goal of the present study is to compare genomic characteristics of cell lines based on their response pattern to TTFields. Methods: Fifteen different human cancerous cell lines were treated using TTFields at their optimal frequency with the same nominal intensity (1.8 V/cm). The distribution of the response to TTFields was found to be bimodal with inhibitions of 30-40% and 50-60% compared to controls. Cell lines were divided into regular and high sensitivity groups according to their response to TTFields. Both groups were characterized based upon the distribution of mutated genes using the Cancer Cell Line Encyclopedia (CCLE) database. Results: Based on the distribution of mutated genes we identified 1 gene with significantly higher probability (P=0.017) to be present in the regular than the high sensitivity group. This gene (NEK3) is a never-in-mitosis (NIMA) related kinase 3 responsible for deacetylation of microtubules. In addition, 2 genes were found with significantly higher probability (P 〈 0.05) to be present in the high- than the regular sensitivity group; ASPH, an aspartate beta-hydroxylase involved in negative regulation of cell proliferation through modulation of calcium homeostasis and TEC, a protein tyrosine kinase involved in immunological signaling pathways. Conclusions: The possible involvement of NEK3 mutations in determining sensitivity to TTFields is interesting in view of the known interference of TTFields with spindle microtubule assembly. ASPH mutations could release cells from negative regulation of proliferation, increasing their replication rate, and thus increasing their sensitivity to TTFields. In order to further test this hypothesis, a comparison of the effect of TTFields needs to be performed on wild type and knockout cell lines for these genes. A comparison of the mutation of these genes in tissue samples from patients whose tumors show high sensitivity to TTFields, may lead to a personalized approach to the use of TTFields clinically.
    Materialart: Online-Ressource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2013.31.15_suppl.e22125
    RVK:
    XA 52760
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Society of Clinical Oncology (ASCO)
    Publikationsdatum: 2013
    ZDB Id: 2005181-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 5
    Online-Ressource
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    Immunomodulatory effects of tumor treating fields (TTFields) on colon cancer models.
    American Society of Clinical Oncology (ASCO) ; 2020
    In:  Journal of Clinical Oncology Vol. 38, No. 4_suppl ( 2020-02-01), p. 136-136
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 38, No. 4_suppl ( 2020-02-01), p. 136-136
    Kurzfassung: 136 Background: Tumor Treating Fields (TTFields) are clinically approved in glioblastoma and malignant pleural mesothelioma as an anti-mitotic treatment modality delivered via noninvasive application of low intensity (1-3 V/cm), intermediate frequency (100-500 kHz), alternating electric fields. We evaluated whether TTFields (150 kHz) induced colon cancer cell death can be perceived as immunogenic and suitable for combination with anti-programmed cell death protein 1 (anti-PD-1; immune checkpoint inhibitor) therapy. Methods: Murine colorectal carcinoma cells (CT-26) were treated with TTFields using the inovitro system. Immunogenic cell death was evaluated by assessing changes in the levels of calreticulin (CRT) on the surface of treated cells, phosphorylation of eukaryotic translation initiation factor alpha (eIF2α), and secretion of ATP and high-mobility group box 1 (HMGB1). For in-vivo studies, CT-26 cells were subcutaneously implanted in BALB/c mice. The mice were treated with TTFields (150 kHz), anti-PD-1 (200 μg/mouse), or a combination of the 2 modalities. Tumor volume was monitored and flow cytometry analyses performed for phenotypic characterization of infiltrating immune cells. Results: We demonstrate that cancer cell death under TTFields application exhibited release of HMGB1, ATP secretion from cells, and ER stress leading to CRT translocation to the cell surface, all of which are signs of immunogenic cell death. The combined treatment of colon tumor-bearing mice with TTFields plus anti-PD-1 led to a significant decrease in tumor volume compared to anti-PD-1 alone or to the control group. Significant increases in CD45+ tumor infiltrating cells were observed in the TTFields plus anti-PD-1 group. We demonstrate significant increases in both CD8 and CD4 T-cells in tumors treated with combination therapy, and in CD8 in tumors treated with anti-PD-1 alone. Conclusions: Our results establish the potential of TTFields therapy to induce immunogenic cell death. We also demonstrate efficacy of concurrent application of TTFields and anti PD-1 therapy in mouse cancer models. These data suggest that TTFields plus anti-PD-1 combination treatment may achieve tumor control by further enhancing anti-tumor immunity.
    Materialart: Online-Ressource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2020.38.4_suppl.136
    RVK:
    XA 52760
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Society of Clinical Oncology (ASCO)
    Publikationsdatum: 2020
    ZDB Id: 2005181-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 6
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    Tumor treating fields (TTFields; 150 kHz) and FOLFOX combination treatment effects on gastric cancer in vitro .
    American Society of Clinical Oncology (ASCO) ; 2020
    In:  Journal of Clinical Oncology Vol. 38, No. 4_suppl ( 2020-02-01), p. 406-406
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 38, No. 4_suppl ( 2020-02-01), p. 406-406
    Kurzfassung: 406 Background: Gastric cancer is the third most common cause of cancer mortality worldwide, yet long-term survival in gastric cancer remains poor despite systemic therapeutic advances. FOLFOX (oxaliplatin, fluorouracil [5-FU], and leucovorin) is an approved chemotherapy regimen for gastric cancer treatment. Tumor Treating Fields (TTFields) are an antimitotic, loco-regional anticancer treatment delivered via non-invasive application of low intensity (1-3V/cm), intermediate frequency (100-500 kHz), alternating electrical fields. TTFields targets rapidly dividing cancer cells by disrupting microtubules leading to mitotic catastrophe, abnormal chromosome segregation, and apoptosis induction. We investigated the potential use of TTFields alone and in combination with FOLFOX for gastric carcinomas. Methods: Gastric cells (AGS and KATO III) were treated for 72 hours with TTFields (1.1 and 1.7 V/cm, respectively) at frequencies of 100-400 kHz using the inovitro system. Efficacy of TTFields and FOLFOX and its individual components was tested by applying TTFields at the optimal frequency in combination with various drug concentrations. Cell counts, apoptosis induction, clonogenic potential, and overall effect were determined. Results: The optimal TTFields frequency that led to the greatest cell count reduction (AGS, 55%; KATO III, 52%) was 150 kHz. The clonogenic potential was reduced by 〉 70% in both cell lines. TTFields combined with each FOLFOX component (oxaliplatin, 5-FU, or leucovorin) led to a significant reduction in AGS and KATO III cell survival (2-way ANOVA, P 〈 0.001 for each cell line) versus each treatment alone. In AGS, TTFields plus FOLFOX combination treatment led to a further reduction in the overall effect (cytotoxic and clonogenic; 79%) versus TTFields alone (65%) and FOLFOX alone (34%). Similar results were observed in KATO III cells. Conclusions: These results suggest that TTFields (150 kHz; optimal frequency) are an effective gastric cancer treatment; and combining TTFields with FOLFOX may further enhance efficacy. There is a strong rational to continue exploring the use of TTFields in combination with standard of care for gastric cancer treatment in the clinical settings.
    Materialart: Online-Ressource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2020.38.4_suppl.406
    RVK:
    XA 52760
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Society of Clinical Oncology (ASCO)
    Publikationsdatum: 2020
    ZDB Id: 2005181-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 7
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    The effect of alternating electric fields (TTFields) on inhibition of repair of DNA damage induced by ionizing radiation and sensitization of glioma and non-small cell lung cancer cells to radiation.
    American Society of Clinical Oncology (ASCO) ; 2014
    In:  Journal of Clinical Oncology Vol. 32, No. 15_suppl ( 2014-05-20), p. e22239-e22239
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 32, No. 15_suppl ( 2014-05-20), p. e22239-e22239
    Materialart: Online-Ressource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2014.32.15_suppl.e22239
    RVK:
    XA 52760
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Society of Clinical Oncology (ASCO)
    Publikationsdatum: 2014
    ZDB Id: 2005181-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 8
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    The combined treatment of 150 kHz tumor treating fields (TTFields) and sorafenib inhibits hepatocellular carcinoma in vitro and in vivo.
    American Society of Clinical Oncology (ASCO) ; 2019
    In:  Journal of Clinical Oncology Vol. 37, No. 15_suppl ( 2019-05-20), p. e15653-e15653
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 37, No. 15_suppl ( 2019-05-20), p. e15653-e15653
    Kurzfassung: e15653 Background: Hepatocellular carcinoma (HCC) is the third cause of cancer related mortality and the primary cause of cancer death. Tumor Treating Fields (TTFields) therapy is an effective anti-neoplastic treatment modality delivered via noninvasive application of low intensity, intermediate frequency, alternating electric fields. Sorafenib, an oral multikinase inhibitor is approved for patients with advanced HCC, yet its survival benefit is still limited. In this work we explored the potential of the use of TTFields alone and in combination with Sorafenib as a treatment for HCC. Methods: HepG2 and Huh-7D12 cells were treated with various TTFields frequencies for 72 hours using the inovitro system. Efficacy of the combined treatment of TTFields and Sorafenib (36-3000 nM) was tested by applying TTFields at the optimal frequency together with various drug concentrations. Cell counts, induction of apoptosis, cell cycle and clonogenic potential were determined. TTFields (1.2 V/cm) and Sorafenib (10 mg/kg) were applied for 6 days to rats injected to the liver with N1S1 HCC cells. Tumor growth was followed using MRI. Results: The optimal TTFields frequency was 150 kHz for both cell lines. TTFields application (1.0 - 1.7 V/cm, 72 hours) at 150 kHz led to 36-40% reduction in cell counts and to additional reduction of over 70% in the clonogenic potential. The combined treatment of TTFields and Sorafenib led to a significant reduction in the number of cells (p 〈 0.001) as compared to each treatment alone. The averaged tumor volume fold increase of the combination treatment group was significantly lower than the one observed in the: control group, the TTFields group and the Sorafenib group. Conclusions: The results presented in this work demonstrate that TTFields can be an effective treatment against HCC cells and that the combination with Sorafenib may further enhance treatment efficacy.
    Materialart: Online-Ressource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2019.37.15_suppl.e15653
    RVK:
    XA 52760
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Society of Clinical Oncology (ASCO)
    Publikationsdatum: 2019
    ZDB Id: 2005181-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 9
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    Efficacy of tumor treatment field (TTF) therapy alone and in combination with chemotherapyin pancreatic cancer preclinical models.
    American Society of Clinical Oncology (ASCO) ; 2012
    In:  Journal of Clinical Oncology Vol. 30, No. 15_suppl ( 2012-05-20), p. e14616-e14616
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 30, No. 15_suppl ( 2012-05-20), p. e14616-e14616
    Kurzfassung: e14616 Background: TTF therapy is a novel, non-invasive treatment modality for solid tumors and was recently approved by the FDA for recurrent glioblastoma. It utilizes alternating electric fields to inhibit tumor growth, by mitotic spindle disruption and destruction of plasma membrane integrity during cytokinesis. TTF inhibits the growth of many solid tumor cell lines in vitro and in vivo. The optimal treatment for pancreas cancer remains elusive, thus we sought to evaluate the efficacy of TTF in pre-clinical pancreatic cancer models. Methods: Cultures of hamster and human pancreatic adenocarcinoma cell lines (PC1-0 and AsPC-1, respectively) were treated with TTF (frequencies ranging from 75 to 300 kHz), using two pairs of perpendicularly oriented insulated transducer arrays. Once determining optimal frequency, TTF was combined with chemotherapy (gemcitabine or 5-Fluorouracil, 5-FU). Hamsters bearing syngeneic, orthotopic pancreatic tumors were treated with either TTF alone or in combination with gemcitabine or 5-FU. Results: TTF treatment had significant inhibitory effect on proliferation of pancreatic cancer cultures. The maximal inhibitory effect for PC1-0 and ASPC-1 was observed when TTF frequencies of 100 and 150 kHz were applied (respectively). The application of TTF to cultures treated with either gemcitabine or 5-FU resulted in an additive inhibitory effect. In-vivo, TTF therapy, either alone or in combination with chemotherapy, resulted in a significant decrease in tumor weight and volume. Compared to chemotherapy alone, TTF increased tumor response to both gemcitabine and 5-FU. Histological analysis demonstrated higher mitotic index in TTF-treated tumors, consistent with the mitotic arrest previously shown in TTF treated cultures. Conclusions: TTF therapy demonstrated efficacy in pancreatic adenocarcinoma in both in vitro and in vivo models. These results support the evaluation of this novel treatment modality in combination with standard chemotherapy in pancreatic cancer patients. A pilot study is in development to test the clinical benefit of combined TTF and gemcitabine in patients with advanced pancreatic adenocarcinoma.
    Materialart: Online-Ressource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2012.30.15_suppl.e14616
    RVK:
    XA 52760
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Society of Clinical Oncology (ASCO)
    Publikationsdatum: 2012
    ZDB Id: 2005181-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 10
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    Online-Ressource
    Overcoming cell size escape from tumor treating fields using a varying frequency treatment paradigm in vitro.
    American Society of Clinical Oncology (ASCO) ; 2013
    In:  Journal of Clinical Oncology Vol. 31, No. 15_suppl ( 2013-05-20), p. e22134-e22134
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 31, No. 15_suppl ( 2013-05-20), p. e22134-e22134
    Kurzfassung: e22134 Background: TTFields Therapy at 200 kHz received FDA approval for the treatment of patients with recurrent glioblastoma (GBM) based on the results of a phase III clinical trial. Radiological responses were observed in 14% of the treated patients. The lack of radiological response in the remaining patients suggests that GBM cells may escape the effect of TTFields over time. The goals of the present study were to identify possible routes by which cancer cells can escape the antimitotic effect of TTFields and to explore ways to overcome such escape mechanisms. Methods: Measurements of cell size before and after 72 hours TTFields application revealed a significant volume increase in 10 cancer cell lines (17% - 101%). A2780 ovarian cancer cultures (cell volume 2.0+0.2 pL) exhibit maximal inhibition by TTFields at 200 kHz. Twenty four hour application of 200 kHz TTFields led to a 70+29% increase in average cell volume (p 〈 0.05). FACS analysis showed that TTFields application to A2780 cells led to a 44% increase in the G2 population due to the antimitotic effect of TTFields. However, the increase in the G2 proportion is not sufficient to explain the increase in cell volume seen after TTFields application. Furthermore, after an additional 24 hours of treatment, the fraction of cells in the G2 population returned to its original percentage (30%), while the increase in cell volume remained high (67+26%). Results: Previous publications demonstrated an inverse relationship exists between cell size and optimal TTFields frequency. Thus an increase in cell size may allow cells to avoid the maximal TTFields effect. To attempt to overcome such cell size escape we decreased the frequency of the TTFields from 200 to 150 kHz after 24 hours treatment to coincide with the increase in cell volume. We found that varying the frequency from 200 to 150 kHz increased the inhibitory effect of TTFields compared to continuous treatment at 200Khz (37+10% and 57+16% decrease in cell count, respectively; p=0.043). Conclusions: This is the first evidence of an escape mechanism from the antimitotic effect of TTFields. The results presented provide a simple way to restore treatment efficacy by varying TTFields frequency in parallel to the change in cell volume.
    Materialart: Online-Ressource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2013.31.15_suppl.e22134
    RVK:
    XA 52760
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Society of Clinical Oncology (ASCO)
    Publikationsdatum: 2013
    ZDB Id: 2005181-5
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
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