Application of the ATP-Cell Viability Assay for Assessment of in vitro Radiation Treatment Response in Gynecologic Cancer Cell Lines

1994 ◽  
pp. 156-165
Author(s):  
Michael Rodriguez ◽  
Albert J. Steren
Keyword(s):  
Cell Viability ◽  
Treatment Response ◽  
Cell Lines ◽  
Cancer Cell ◽  
Radiation Treatment ◽  
Gynecologic Cancer ◽  
Cancer Cell Lines ◽  
Cell Viability Assay ◽  
Viability Assay

Characteristics of the combination paclitaxel plus doxorubicin in breast cancer cell lines analyzed with the ATP-Cell Viability Assay

1993 ◽  
Vol 28 (1) ◽  
pp. 21-27 ◽  
Author(s):  
Ossi R. Koechli ◽  
Bernd-Uwe Sevin ◽  
James P. Perras ◽  
Ting Chao Chou ◽  
Roberto Angioli ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Viability ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Cell Viability Assay ◽  
Viability Assay

Comparison of paclitaxel and docetaxel (Taxotere) in gynecologic and breast cancer cell lines with the ATP–cell viability assay

1994 ◽  
Vol 5 (1) ◽  
pp. 24-30 ◽  
Author(s):  
Michael Untch ◽  
Andrea Untch ◽  
Bernd-Uwe Sevin ◽  
Roberto Angioli ◽  
James P Perras ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Viability ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Cell Viability Assay ◽  
Viability Assay

scholarly journals In vitro study of combined cilengitide and radiation treatment in breast cancer cell lines

2013 ◽  
Vol 8 (1) ◽  
Author(s):  
Tim Lautenschlaeger ◽  
James Perry ◽  
David Peereboom ◽  
Bin Li ◽  
Ahmed Ibrahim ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Radiation Treatment ◽  
In Vitro Study ◽  
Cancer Cell Lines ◽  
Vitro Study ◽  
Breast Cancer Cell Lines

In Vitro Evaluation of the Novel Chemotherapeutic Agents U-73, 975, U-77, 779, and U-80, 244 in Gynecologic Cancer Cell Lines

1993 ◽  
Vol 11 (3) ◽  
pp. 276-282 ◽  
Author(s):  
Randall D. Hightower ◽  
Bernd-Uwe Sevin ◽  
James Perras ◽  
Hoa Nguyen ◽  
Roberto Angioli ◽  
...  
Keyword(s):  
Cell Lines ◽  
Cancer Cell ◽  
Gynecologic Cancer ◽  
Cancer Cell Lines ◽  
Chemotherapeutic Agents ◽  
The Novel ◽  
In Vitro Evaluation

Sensitivity of Oncogenic KRAS-Expressing Cells to CDK9 Inhibition

2021 ◽  
pp. 247255522110088
Author(s):  
Lick Pui Lai ◽  
Viviane Brel ◽  
Kanika Sharma ◽  
Julia Frappier ◽  
Nadia Le-Henanf ◽  
...  
Keyword(s):  
Cell Viability ◽  
Cell Lines ◽  
Specific Activity ◽  
Mammalian Target Of Rapamycin ◽  
Mouse Embryonic Fibroblast ◽  
Wild Type ◽  
Compound Library ◽  
Cell Viability Assay ◽  
Viability Assay

Oncogenic forms of KRAS proteins are known to be drivers of pancreatic, colorectal, and lung cancers. The goal of this study is to identify chemical leads that inhibit oncogenic KRAS signaling. We first developed an isogenic panel of mouse embryonic fibroblast (MEF) cell lines that carry wild-type RAS, oncogenic KRAS, and oncogenic BRAF. We validated these cell lines by screening against a tool compound library of 1402 annotated inhibitors in an adenosine triphosphate (ATP)-based cell viability assay. Subsequently, this MEF panel was used to conduct a high-throughput phenotypic screen in a cell viability assay with a proprietary compound library. All 126 compounds that exhibited a selective activity against mutant KRAS were selected and prioritized based on their activities in secondary assays. Finally, five chemical clusters were chosen. They had specific activity against SW620 and LS513 over Colo320 colorectal cancer cell lines. In addition, they had no effects on BRAFV600E, MEK1, extracellular signal-regulated kinase 2 (ERK2), phosphoinositide 3-kinase alpha (PI3Kα), AKT1, or mammalian target of rapamycin (mTOR) as tested in in vitro enzymatic activity assays. Biophysical assays demonstrated that these compounds did not bind directly to KRAS. We further identified the mechanism of action and showed that three of them have CDK9 inhibitory activity. In conclusion, we have developed and validated an isogenic MEF panel that was used successfully to identify RAS oncogenic or wild-type allele-specific vulnerabilities. Furthermore, we identified sensitivity of oncogenic KRAS-expressing cells to CDK9 inhibitors, which warrants future studies of treating KRAS-driven cancers with CDK9 inhibitors.

scholarly journals CBMT-09. THERAPEUTIC EFFECT OF INDUCTION OF POLYGLUTAMYLATION IN HIGH-DOSE METHOTREXATE THERAPY TO PRIMARY CENTRAL NERVOUS SYSTEM LYMPHOMA

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi34-vi34
Author(s):  
Kenji Fujimoto ◽  
Naoki Shinojima ◽  
Keishi Makino ◽  
Koichi Ichimura ◽  
Akitake Mukasa
Keyword(s):  
Cell Viability ◽  
Tumor Cells ◽  
Cell Lines ◽  
Therapeutic Response ◽  
Combined Effect ◽  
Occurrence Rate ◽  
High Dose ◽  
Cell Viability Assay ◽  
Viability Assay

Abstract BACKGROUND Polyglutamylation is a reversible protein modification with a high occurrence rate in tumor cells. Methotrexate (MTX) incorporated into cells is polyglutamylated and strongly binds to dihydrofolate reductase without competitive inhibition by leucovorin (LV). Tumor cells with high polyglutamylation levels are selectively killed, whereas normal cells with lower polyglutamylation are rescued by LV. In this study, we investigated the therapeutic response of PCNSL to HD-MTX therapy with LV rescue based on polyglutamylation status and evaluated the combined effect of MTX and the drugs which upregulated polyglutamylation of MTX. METHODS Among 113 consecutive PCNSL patients who underwent HD-MTX therapy in our department between 2001 and 2014, polyglutamylation was evaluated by immunostaining in 82 cases, with relationships between polyglutamylation and therapeutic response retrospectively examined. Human malignant lymphoma cell lines were used for in vitro and in vivo experiments. The association of polyglutamylation and the response to MTX with LV rescue was assessed in these cell lines. Histone-deacetylase inhibitor (HDACI) has been reported to induce polyglutamylation by elevating folpolyglutamate synthetase (FPGS) expression, so the effects of HDACIs on polyglutamylation were evaluated. Combined effects of MTX and HDACI were evaluated by cell viability assay and xenograft mouse models. RESULTS The complete response rate was significantly higher in the group with polyglutamylation than in the non-polyglutamylation group [58.1% (25/43) and 33.3% (13/39), respectively] (p < 0.05), and progression-free survival was also significantly increased in the group with polyglutamylation (p < 0.01). The combined effect of MTX and HDACI was significantly enhanced in cell viability assay in vitro (p< 0.05), in subcutaneous (p< 0.001) and intracranial tumor xenografts (p< 0.001). CONCLUSION These findings suggested that polyglutamylation could be a predictor of therapeutic response to HD-MTX therapy with LV rescue in PCNSL. Combined therapy with HD-MTX and HDACIs might represent a promising treatment for HD-MTX resistant intractable PCNSL.

scholarly journals A Warp-Knitted Light-Emitting Fabric-Based Device for In Vitro Photodynamic Therapy: Description, Characterization, and Application on Human Cancer Cell Lines

Cancers ◽  
2021 ◽  
Vol 13 (16) ◽  
pp. 4109
Author(s):  
Elise Thécua ◽  
Laurine Ziane ◽  
Guillaume Paul Grolez ◽  
Alexandre Fagart ◽  
Abhishek Kumar ◽  
...  
Keyword(s):  
Photodynamic Therapy ◽  
Cell Viability ◽  
Cell Lines ◽  
Cancer Cell ◽  
Human Cancer ◽  
Cancer Cell Lines ◽  
Human Cancer Cell ◽  
Light Emitting ◽  
Human Cancer Cell Lines

Photodynamic therapy (PDT) appears to be a promising strategy in biomedical applications. However, the complexity of its parameters prevents wide acceptance. This work presents and characterizes a novel optical device based on knitted light-emitting fabrics and dedicated to in vitro PDT involving low irradiance over a long illumination period. Technical characterization of this device, called CELL-LEF, is performed. A cytotoxic study of 5-ALA-mediated PDT on human cancer cell lines is provided as a proof of concept. The target of delivering an irradiance of 1 mW/cm2 over 750 cm2 is achieved (mean: 0.99 mW/cm2; standard deviation: 0.13 mW/cm2). The device can maintain a stable temperature with the mean thermal distribution of 35.1 °C (min: 30.7 °C; max: 38.4 °C). In vitro outcomes show that 5-ALA PDT using CELL-LEF consistently and effectively induced a decrease in tumor cell viability: Almost all the HepG2 cells died after 80 min of illumination, while less than 60% of U87 cell viability remained. CELL-LEF is suitable for in vitro PDT involving low irradiance over a long illumination period.

scholarly journals Pathway profiling of a novel SRC inhibitor, AZD0424, in combination with MEK inhibitors

2021 ◽  
Author(s):  
John C Dawson ◽  
Alison Munro ◽  
Kenneth Macleod ◽  
Morwenna Muir ◽  
Paul Timpson ◽  
...  
Keyword(s):  
Cell Viability ◽  
Cell Lines ◽  
Cancer Cell ◽  
Mek Inhibitor ◽  
Cancer Cell Lines ◽  
Drug Induced ◽  
Combination Strategies ◽  
Src Inhibitor

AbstractA more comprehensive understanding of how cells respond to drug intervention, the likely immediate signalling responses and how resistance may develop within different microenvironments allows us anticipate how cells adapt to targeted therapy enabling more informed prediction of rational drug combinations. The non-receptor tyrosine kinase SRC regulates many cellular signalling processes and pharmacological inhibition has long been a target of drug discovery projects for the treatment of cancer. Here we describe the in vitro and in vivo characterisation of the small molecule SRC inhibitor, AZD0424. We show that AZD0424 potently inhibits the phosphorylation of tyrosine-416 of SRC (IC50 ∼ 100 nM) in many cancer cell lines; however inhibition of cell viability, via a G1 cell cycle arrest, was observed only in a sub-set of cancer cell lines in the low (on target) micromolar range. We profiled the changes in intracellular pathway signalling in cancer cells following exposure to AZD0424 and other targeted therapies using Reverse Phase Protein Array analysis. We demonstrate that SRC is activated in response to MEK inhibitor (trametinib or AZD6244)-treatment of KRAS mutant colorectal cell lines (HCT116 and DLD1) and that AZD0424 abrogates this. Cell lines treated with trametinib or AZD6244 in combination with AZD0424 revealed reduction of EGFR, FAK and SRC compensatory activation, and, synergistically inhibits cell viability in vitro. In vivo, trametinib-treatment of mice bearing HCT116 tumours increased phosphorylation of SRC on Tyr416, and when combined with AZD0424, inhibition of tumour growth is greater than trametinib alone. We also demonstrate that drug-induced resistance to trametinib is not re-sensitised by AZD0424 treatment in vitro, likely as a result of multiple compensatory signalling mechanisms; however inhibition of SRC remains an effective way to block invasion of trametinib resistant tumour cells. These data imply that inhibiting SRC may offer a useful addition to MEK inhibitor combination strategies.

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