Journal articles: 'Sensitivity of the cancer cells'

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De Maria, R. "5 Drug sensitivity of cancer stem cells." European Journal of Cancer Supplements 8, no. 7 (November 2010): 10. http://dx.doi.org/10.1016/s1359-6349(10)71708-0.

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Bikas, Athanasios, Kirk Jensen, Aneeta Patel, John Costello, Dennis McDaniel, Joanna Klubo-Gwiezdzinska, Olexander Larin, et al. "Glucose-deprivation increases thyroid cancer cells sensitivity to metformin." Endocrine-Related Cancer 22, no. 6 (September 11, 2015): 919–32. http://dx.doi.org/10.1530/erc-15-0402.

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Metformin inhibits thyroid cancer cell growth. We sought to determine if variable glucose concentrations in medium alter the anti-cancer efficacy of metformin. Thyroid cancer cells (FTC133 and BCPAP) were cultured in high-glucose (20 mM) and low-glucose (5 mM) medium before treatment with metformin. Cell viability and apoptosis assays were performed. Expression of glycolytic genes was examined by real-time PCR, western blot, and immunostaining. Metformin inhibited cellular proliferation in high-glucose medium and induced cell death in low-glucose medium. In low-, but not in high-glucose medium, metformin induced endoplasmic reticulum stress, autophagy, and oncosis. At micromolar concentrations, metformin induced phosphorylation of AMP-activated protein kinase and blocked p-pS6 in low-glucose medium. Metformin increased the rate of glucose consumption from the medium and prompted medium acidification. Medium supplementation with glucose reversed metformin-inducible morphological changes. Treatment with an inhibitor of glycolysis (2-deoxy-d-glucose (2-DG)) increased thyroid cancer cell sensitivity to metformin. The combination of 2-DG with metformin led to cell death. Thyroid cancer cell lines were characterized by over-expression of glycolytic genes, and metformin decreased the protein level of pyruvate kinase muscle 2 (PKM2). PKM2 expression was detected in recurrent thyroid cancer tissue samples. In conclusion, we have demonstrated that the glucose concentration in the cellular milieu is a factor modulating metformin's anti-cancer activity. These data suggest that the combination of metformin with inhibitors of glycolysis could represent a new strategy for the treatment of thyroid cancer.

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Wang, Ruiping, Yue Han, Zhangxiang Zhao, Fan Yang, Tingting Chen, Wenbin Zhou, Xianlong Wang, et al. "Link synthetic lethality to drug sensitivity of cancer cells." Briefings in Bioinformatics 20, no. 4 (December 28, 2017): 1295–307. http://dx.doi.org/10.1093/bib/bbx172.

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Abstract Synthetic lethal (SL) interactions occur when alterations in two genes lead to cell death but alteration in only one of them is not lethal. SL interactions provide a new strategy for molecular-targeted cancer therapy. Currently, there are few drugs targeting SL interactions that entered into clinical trials. Therefore, it is necessary to investigate the link between SL interactions and drug sensitivity of cancer cells systematically for drug development purpose. We identified SL interactions by integrating the high-throughput data from The Cancer Genome Atlas, small hairpin RNA data and genetic interactions of yeast. By integrating SL interactions from other studies, we tested whether the SL pairs that consist of drug target genes and the genes with genomic alterations are related with drug sensitivity of cancer cells. We found that only 6.26%∼34.61% of SL interactions showed the expected significant drug sensitivity using the pooled cancer cell line data from different tissues, but the proportion increased significantly to approximately 90% using the cancer cell line data for each specific tissue. From an independent pharmacogenomics data of 41 breast cancer cell lines, we found three SL interactions (ABL1–IFI16, ABL1–SLC50A1 and ABL1–SYT11) showed significantly better prognosis for the patients with both genes being altered than the patients with only one gene being altered, which partially supports the SL effect between the gene pairs. Our study not only provides a new way for unraveling the complex mechanisms of drug sensitivity but also suggests numerous potentially important drug targets for cancer therapy.

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Shariat Razavi, Seyedeh Mahya, Reyhaneh Mahmoudzadeh Vaziri, Gholamreza Karimi, Sepideh Arabzadeh, Vahideh Keyvani, Javad Behravan, and Fatemeh Kalalinia. "Crocin Increases Gastric Cancer Cells’ Sensitivity to Doxorubicin." Asian Pacific Journal of Cancer Prevention 21, no. 7 (July 1, 2020): 1959–67. http://dx.doi.org/10.31557/apjcp.2020.21.7.1959.

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Noh, Woo-Chul, Wallace H. Mondesire, Junying Peng, Weiguo Jian, Haixia Zhang, JinJiang Dong, Gordon B. Mills, Mien-Chie Hung, and Funda Meric-Bernstam. "Determinants of Rapamycin Sensitivity in Breast Cancer Cells." Clinical Cancer Research 10, no. 3 (February 1, 2004): 1013–23. http://dx.doi.org/10.1158/1078-0432.ccr-03-0043.

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Zhang, Yi, Wendy Schulte, Desmond Pink, Kyle Phipps, Andries Zijlstra, John D. Lewis, and David Morton Waisman. "Sensitivity of Cancer Cells to Truncated Diphtheria Toxin." PLoS ONE 5, no. 5 (May 5, 2010): e10498. http://dx.doi.org/10.1371/journal.pone.0010498.

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Candido, Saverio, Stephen L. Abrams, Linda Steelman, Kvin Lertpiriyapong, Alberto M. Martelli, Lucio Cocco, Stefano Ratti, et al. "Metformin influences drug sensitivity in pancreatic cancer cells." Advances in Biological Regulation 68 (May 2018): 13–30. http://dx.doi.org/10.1016/j.jbior.2018.02.002.

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Karagkounis, Georgios, Jennifer DeVecchio, Sylvain Ferrandon, and Matthew F. Kalady. "Simvastatin enhances radiation sensitivity of colorectal cancer cells." Surgical Endoscopy 32, no. 3 (September 15, 2017): 1533–39. http://dx.doi.org/10.1007/s00464-017-5841-1.

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Liang, Zhiyu, and Chuan Li. "Downregulation of miR-24 Enhances Cisplatin Sensitivity in Breast Cancer Cells." Journal of Biomaterials and Tissue Engineering 11, no. 8 (August 1, 2021): 1643–48. http://dx.doi.org/10.1166/jbt.2021.2728.

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GSK-3β is a tumor suppressor gene in multiple cancers by phosphorylated degrading β-catenin. Several studies showed association of miR-24 with breast cancer. Bioinformatics analysis showed a relationship of miR-24 with GSK-3β. Our study assessed miR-24’s role in GSK-3β/β-catenin siganling and breast cancer cell cisplatin resistance. MiR-24, GSK-3β, β-catenin, and Bcl-2 expressions in MDA-MB-231 and MDA-MB-231/DDP cells were detected along cell proliferation and apoptosis. DDP resistance cells were assigned into miR-NC, miR-24 inhibitor, pIRES-blank, pIRES-GSK-3β, and miR-24 inhibitor+pIRES-GSK-3β groups and cell proliferation was determined. MiR-24 inhibited GSK-3β level. GSK-3β and cell apoptosis significantly downregulated, while miR-24, β-catenin, Bcl-2, and cell proliferation significantly elevated in DDP resistance cells. MiR-24 inhibitor and/or pIRES-GSK-3β significantly increased GSK-3β level, declined β-catenin and Bcl-2 expressions, attenuated cell proliferation, enhanced cell apoptosis, and weakened cisplatin resistance. MiR-24 upregulation was related to breast cancer cell cisplatin resistance. Inhibition of miR-24 upregulated GSK-3β, restrained Wnt/β-catenin signaling and cisplatin resistance in breast cancer cells.

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McKenna, W. Gillies, and Ruth J. Muschel. "Targeting tumor cells by enhancing radiation sensitivity." Genes, Chromosomes and Cancer 38, no. 4 (October 14, 2003): 330–38. http://dx.doi.org/10.1002/gcc.10296.

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Luty, Marcin, Katarzyna Piwowarczyk, Anna Łabędź-Masłowska, Tomasz Wróbel, Małgorzata Szczygieł, Jessica Catapano, Grażyna Drabik, et al. "Fenofibrate Augments the Sensitivity of Drug-Resistant Prostate Cancer Cells to Docetaxel." Cancers 11, no. 1 (January 11, 2019): 77. http://dx.doi.org/10.3390/cancers11010077.

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Metronomic agents reduce the effective doses and adverse effects of cytostatics in cancer chemotherapy. Therefore, they can enhance the treatment efficiency of drug-resistant cancers. Cytostatic and anti-angiogenic effects of fenofibrate (FF) suggest that it can be used for the metronomic chemotherapy of drug-resistant prostate tumors. To estimate the effect of FF on the drug-resistance of prostate cancer cells, we compared the reactions of naïve and drug-resistant cells to the combined treatment with docetaxel (DCX)/mitoxantrone (MTX) and FF. FF sensitized drug-resistant DU145 and PC3 cells to DCX and MTX, as illustrated by their reduced viability and invasive potential observed in the presence of DCX/MTX and FF. The synergy of the cytostatic activities of both agents was accompanied by the inactivation of P-gp-dependent efflux, dysfunction of the microtubular system, and induction of polyploidy in DCX-resistant cells. Chemical inhibition of PPARα- and reactive oxygen species (ROS)-dependent pathways by GW6471 and N-acetyl-L-cysteine, respectively, had no effect on cell sensitivity to combined DCX/FF treatment. Instead, we observed the signs of adenosine triphosphate (ATP) deficit and autophagy in DCX/FF-treated drug-resistant cells. Furthermore, the cells that had been permanently propagated under DCX- and DCX/FF-induced stress did not acquire DCX/FF-resistance. Instead, relatively slow proliferation of DCX-resistant cells was efficiently inhibited by FF. Collectively, our observations show that FF reduces the effective doses of DCX by interfering with the drug resistance and energy metabolism of prostate cancer cells. Concomitantly, it impairs the chemotherapy-induced microevolution and expansion of DCX/FF-resistant cells. Therefore, FF can be applied as a metronomic agent to enhance the efficiency of palliative chemotherapy of prostate cancer.

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Criscuolo, Daniela, Rosario Avolio, Giovanni Calice, Chiara Laezza, Simona Paladino, Giovanna Navarra, Francesca Maddalena, et al. "Cholesterol Homeostasis Modulates Platinum Sensitivity in Human Ovarian Cancer." Cells 9, no. 4 (March 30, 2020): 828. http://dx.doi.org/10.3390/cells9040828.

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Despite initial chemotherapy response, ovarian cancer is the deadliest gynecologic cancer, due to frequent relapse and onset of drug resistance. To date, there is no affordable diagnostic/prognostic biomarker for early detection of the disease. However, it has been recently shown that high grade serous ovarian cancers show peculiar oxidative metabolism, which is in turn responsible for inflammatory response and drug resistance. The molecular chaperone TRAP1 plays pivotal roles in such metabolic adaptations, due to the involvement in the regulation of mitochondrial respiration. Here, we show that platinum-resistant ovarian cancer cells also show reduced cholesterol biosynthesis, and mostly rely on the uptake of exogenous cholesterol for their needs. Expression of FDPS and OSC, enzymes involved in cholesterol synthesis, are decreased both in drug-resistant cells and upon TRAP1 silencing, whereas the expression of LDL receptor, the main mediator of extracellular cholesterol uptake, is increased. Strikingly, treatment with statins to inhibit cholesterol synthesis reduces cisplatin-induced apoptosis, whereas silencing of LIPG, an enzyme involved in lipid metabolism, or withdrawal of lipids from the culture medium, increases sensitivity to the drug. These results suggest caveats for the use of statins in ovarian cancer patients and highlights the importance of lipid metabolism in ovarian cancer treatment.

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Tao, Tao, Xiaomei Yang, Qiong Qin, Wen Shi, Qiqi Wang, Ying Yang, and Junqi He. "NHERF1 Enhances Cisplatin Sensitivity in Human Cervical Cancer Cells." International Journal of Molecular Sciences 18, no. 1 (January 12, 2017): 5. http://dx.doi.org/10.3390/ijms18010005.

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Ren, Juan, Yongli Chu, Hongbing Ma, Yuelang Zhang, Xiaozhi Zhang, Dongli Zhao, Zongfang Li, et al. "Epigenetic Interventions Increase the Radiation Sensitivity of Cancer Cells." Current Pharmaceutical Design 20, no. 11 (April 2014): 1857–65. http://dx.doi.org/10.2174/13816128113199990529.

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Niepel, Mario, Marc Hafner, Mirra Chung, and Peter K. Sorger. "Measuring Cancer Drug Sensitivity and Resistance in Cultured Cells." Current Protocols in Chemical Biology 9, no. 2 (January 2017): 55–74. http://dx.doi.org/10.1002/cpch.21.

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Liu, Chengfei, Yezi Zhu, Wei Lou, Nagalakshmi Nadiminty, Xinbin Chen, Qinghua Zhou, Xu Bao Shi, Ralph W. deVere White, and Allen C. Gao. "Functional p53 determines docetaxel sensitivity in prostate cancer cells." Prostate 73, no. 4 (September 19, 2012): 418–27. http://dx.doi.org/10.1002/pros.22583.

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Bigler, Dora, Daniel Gioeli, Mark R. Conaway, Michael J. Weber, and Dan Theodorescu. "Rap2 regulates androgen sensitivity in human prostate cancer cells." Prostate 67, no. 14 (August 17, 2007): 1590–99. http://dx.doi.org/10.1002/pros.20644.

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Wee, Shimei, Maria Niklasson, Voichita Dana Marinescu, Anna Segerman, Linnéa Schmidt, Annika Hermansson, Peter Dirks, et al. "Selective Calcium Sensitivity in Immature Glioma Cancer Stem Cells." PLoS ONE 9, no. 12 (December 22, 2014): e115698. http://dx.doi.org/10.1371/journal.pone.0115698.

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Gorsic, Lidija K., Amy L. Stark, Heather E. Wheeler, Shan S. Wong, Hae K. Im, and M. Eileen Dolan. "EPS8 Inhibition Increases Cisplatin Sensitivity in Lung Cancer Cells." PLoS ONE 8, no. 12 (December 19, 2013): e82220. http://dx.doi.org/10.1371/journal.pone.0082220.

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Sureechatchaiyan, Parichat, Alexandra Hamacher, Nicole Brockmann, Bjoern Stork, and Matthias U. Kassack. "Adenosine enhances cisplatin sensitivity in human ovarian cancer cells." Purinergic Signalling 14, no. 4 (August 4, 2018): 395–408. http://dx.doi.org/10.1007/s11302-018-9622-7.

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Lesko, Ewa, Anna Zebzda, Danuta Jarocha, and Marcin Majka. "Different Sensitivity of Normal and Malignant Cells to HSP90 Inhibitors." Blood 108, no. 11 (November 16, 2006): 4377. http://dx.doi.org/10.1182/blood.v108.11.4377.4377.

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Abstract Despite of great progress in cancer treatment over the past decades, there is still strong need for new, more efficient and specific therapeutics. Drugs that blocks activity of heat shock proteins, particularly heat shock protein 90 (HSP90), are the newcomers with potential to fulfill this expectation. HSP90 is a molecular chaperone crucial for correct protein folding, assembly and transportation across cellular compartments. Recent data show also essential role of HSP90 in facilitating malignant transformation. HSP90 serves as a biochemical buffer for the genetic instabilities characteristic of most cancers and enhances cancer cells survival under stress conditions. Thus, HSP90 inhibitors, like Geldanamycin (GA), seem to be attractive anticancer agents. One of the GA derivatives, 17-allylaminogeldanamycin (17AAG), has already entered clinical trials with promising preliminary results. Although HSP90 is highly expressed in most cells, geldanamycins seem to selectively kill cancer cells. However, the direct comparison of GA effect on normal and cancer cells has not been done yet. This prompted us to investigate the influence of GA and its analogs (17AAG, 17DMAG, 17AEP and 17DMAP) on normal, bone marrow populating cells and cancer cells. We choose normal bone marrow cells because one of the most life-threatening adverse effects of conventional chemotherapy and radiotherapy is damage of bone marrow cells and its environment. Thus, we asked if GA and its derivatives affect CD34+, mesenchymal and endothelial cells. We used in this study multiple myeloma (MM) cell lines and rhabdomyosarcoma cell lines (RMS). We found that GA and its analogs had negative influence on both MM and RMS cell lines. GA exhibited strong anticancer effect at concentrations ranging from 1 nM to 1000 nM, unfortunately causing also strong toxicity toward all normal cells tested. 17AAG, which is already in clinical trials, had surprisingly low inhibitory influence on proliferation of cancer cells (MM and RMS) at 100 nM concentration and lower, with strong inhibitory effect seen only at 1000 nM. However, at the same time 17AAG had little toxicity toward normal cells. New GA derivatives, 17DMAG, 17AEP and 17DMAP inhibited proliferation of cancer cells to almost the same extend as GA, and they exerted only mild negative effects on clonogenicity of CD34+, as measured by BFU-E and CFU-GM colony formation assay and proliferation of mesenchymal cells. Endothelial cells growth, important for tumor progression, was restrained by half with 100 nM of GA and its analogs except 17AAG. We also noticed that HSP90 inhibitors were able to block expression of genes responsible for angiogenesis (VEGF, HIF-1 a and IL-8). Finally, it is also worth stressing that 17DMAG, 17AEP and 17DMAP are water-soluble while GA and 17AAG must be dissolved in DMSO, agent known with neuronal side effects observed during bone marrow transplantation procedures. Different level of toxicity between normal and malignant cells could be due to different level of HSP90 expression in these cells. We performed western blot analysis of HSP90 expression in normal and cancer cells. We found lower expression of this protein in CD34+, endothelial and mesenchymal cells in comparison to MM and RMS cell lines. This could be one of the reasons for different sensitivity of normal and tumor cells to geldanamycins. Based on our results we postulate that GA derivatives, particularly 17AEP, have a potential to become specific, powerful drugs against various tumors with little unwanted side effects toward normal cells.

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Chandimali, Nisansala, Hyebin Koh, Jihwan Kim, Jaihyung Lee, Yang Park, Hu-Nan Sun, and Taeho Kwon. "BRM270 targets cancer stem cells and augments chemo‑sensitivity in cancer (Review)." Oncology Letters 20, no. 4 (August 7, 2020): 1. http://dx.doi.org/10.3892/ol.2020.11964.

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Watanabe, Takayuki, Takaaki Oba, Keiji Tanimoto, Tomohiro Shibata, Shinobu Kamijo, and Ken-ichi Ito. "Tamoxifen resistance alters sensitivity to 5-fluorouracil in a subset of estrogen receptor-positive breast cancer." PLOS ONE 16, no. 6 (June 8, 2021): e0252822. http://dx.doi.org/10.1371/journal.pone.0252822.

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Sequential treatment with endocrine or chemotherapy is generally used in the treatment of estrogen receptor (ER)-positive recurrent breast cancer. To date, few studies have investigated the effect of long-term endocrine therapy on the response to subsequent chemotherapy in ER-positive breast cancer. We examined whether a preceding endocrine therapy affects the sensitivity to subsequent chemotherapy in ER-positive breast cancer cells. Three ER-positive breast cancer cell lines (T47D, MCF7, BT474) and tamoxifen-resistant sublines (T47D/T, MCF7/T, BT474/T) were analyzed for sensitivity to 5-fluorouracil, paclitaxel, and doxorubicin. The mRNA levels of factors related to drug sensitivity were analyzed by RT-PCR. MCF7/T cells became more sensitive to 5-fluorouracil than wild-type (wt)-MCF7 cells. In addition, the apoptosis induced by 5-fluorouracil was significantly increased in MCF7/T cells. However, no difference in sensitivity to chemotherapeutic agents was observed in T47D/T and BT474/T cells compared with their wt cells. Dihydropyrimidine dehydrogenase (DPYD) mRNA expression was significantly decreased in MCF7/T cells compared with wt-MCF7 cells. The expression of DPYD mRNA was restored with 5-azacytidine treatment in MCF7/T cells. In addition, DPYD 3′-UTR luciferase activity was significantly reduced in MCF7/T cells. These data indicated that the expression of DPYD mRNA was repressed by methylation of the DPYD promoter region and post-transcriptional regulation by miRNA in MCF7/T cells. In the mouse xenograft model, capecitabine significantly reduced the tumor volume in MCF7/T compared with MCF7. The results of this study indicate that endocrine therapy could alter the sensitivity to chemotherapeutic agents in a subset of breast cancers, and 5-fluorouracil may be effective in tamoxifen-resistant breast cancers.

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Lee, Namgyu, Anne E. Carlisle, Austin Peppers, Sung Jin Park, Mihir B. Doshi, Meghan E. Spears, and Dohoon Kim. "xCT-Driven Expression of GPX4 Determines Sensitivity of Breast Cancer Cells to Ferroptosis Inducers." Antioxidants 10, no. 2 (February 20, 2021): 317. http://dx.doi.org/10.3390/antiox10020317.

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Inducers of ferroptosis such as the glutathione depleting agent Erastin and the GPX4 inhibitor Rsl-3 are being actively explored as potential therapeutics in various cancers, but the factors that determine their sensitivity are poorly understood. Here, we show that expression levels of both subunits of the cystine/glutamate antiporter xCT determine the expression of GPX4 in breast cancer, and that upregulation of the xCT/selenocysteine biosynthesis/GPX4 production axis paradoxically renders the cancer cells more sensitive to certain types of ferroptotic stimuli. We find that GPX4 is strongly upregulated in a subset of breast cancer tissues compared to matched normal samples, and that this is tightly correlated with the increased expression of the xCT subunits SLC7A11 and SLC3A2. Erastin depletes levels of the antioxidant selenoproteins GPX4 and GPX1 in breast cancer cells by inhibiting xCT-dependent extracellular reduction which is required for selenium uptake and selenocysteine biosynthesis. Unexpectedly, while breast cancer cells are resistant compared to nontransformed cells against oxidative stress inducing drugs, at the same time they are hypersensitive to lipid peroxidation and ferroptosis induced by Erastin or Rsl-3, indicating that they are ‘addicted’ to the xCT/GPX4 axis. Our findings provide a strategic basis for targeting the anti-ferroptotic machinery of breast cancer cells depending on their xCT status, which can be further explored.

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Colombatti, Marco, Massimo Bisconti, Lorena Dell'Arciprete, Massimo A. Gerosa, and Giuseppe Tridente. "Sensitivity of human glioma cells to cytotoxic heteroconjugates." International Journal of Cancer 42, no. 3 (September 15, 1988): 441–48. http://dx.doi.org/10.1002/ijc.2910420322.

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Beksac, Meral, Emin Kansu, Ayse Kars, Zahide Ibrahimoglu, and Dincer Firat. "A rapid drug sensitivity assay for neoplasmatic cells." Medical Oncology and Tumor Pharmacotherapy 5, no. 4 (December 1988): 253–57. http://dx.doi.org/10.1007/bf03003193.

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Jingjing, Lin, Wang Wangyue, Xu Qiaoqiao, and Ye Jietong. "MiR-218 increases sensitivity to cisplatin in esophageal cancer cells via targeting survivin expression." Open Medicine 11, no. 1 (January 1, 2016): 31–35. http://dx.doi.org/10.1515/med-2016-0007.

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AbstractObjectivesIncreasing evidence showed that microRNAs (miRNAs) were implicated in the chemical resistance of human cancers. We intended to investigate the role of miR-218 in cisplatin sensitivity of esophageal cancer cells.MethodsQuantitative real-time polymerase chain reaction (qRT-PCR) was carried out to analyze miR-218 expression in human esophageal cancer cell line Eca9706 and a cisplatin-resistant subline (ECa9706-CisR cells). The effects of miR-218 transfection on ECa9706 and ECa9706-CisR cell viability, including cell viability and apoptosis rate were confirmed using MTT assay, or flow cytometry, respectively. qRT-PCR was used to validate survivin as a direct target gene of miR-218 in our system.ResultsWe found that miR-218 was significantly decreased in ECa9706-CisR cells compared with parent Eca9706 cells. Overexpression of miR-218 by mimics transfection would enhance cisplatin sensitivity evaluated by cell viability inhibition and apoptosis promotion. We validated here survivin as a direct target of miR-218 in ECa9706 cells, which might contribute to the chemoresistance of esophageal cancer cells to cisplatin.ConclusionsIn summary, our data suggest that miR-218 might represent as a promising sensitizer of cisplatin therapy in clinical esophageal cancer patients.

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Sengupta, Prattusha, Sudeshna Gangopadhyay, Saubhik Sengupta, Ujjal Kanti Ray, and Ashis Mukhopadhyay. "Ovarian cancer stem cells (OCSCs): Therapy for advanced chemoresistant ovarian cancer." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e16542-e16542. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e16542.

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e16542 Background: Invasive and mesenchymal property of Ovarian Cancer Stem Cells (OCSCs)with CD44+/CD133+has made them promising target for targeted treatment. Chemotherapy treatment uses medicine to weaken and destroy cancer cells in body, including cells at original cancer site and any cancer cells that may have spread to another part of body. Chemotherapeutic drugs for advanced chemo-resistant ovarian cancer are yet to be well defined. Combination of drugs is also not fully known. Our objective is to define chemotherapeutic drugs and its action in OCSC which is the major reason for chemo resistance in case of advanced chemo-resistant ovarian cancer patients. Methods: A total of twenty biopsy proven advanced chemo-resistant ovarian cancer patients in the age group of 22-36 years were selected randomly and tested for CD44/CD133 via flow cytometry. Isolated OCSCs were cultured for ex vivo drug sensitivity towards platinum, anthracyclin, docetaxel, rapamycin, sunitinib, sorafenib and gefitinib. Correlation was drawn between cell differentiations, % of stem cells and drug response. Accordingly chemotherapy was designed for a particular patient. Results: We detected OCSCs in 90% of cases. Among positive samples ex vivo drug sensitivity was seen in 4(20%) to rapamycin, 1(5%) to sunitinib, 1(5%) to sorafenib, 1(5%) to gefitinib, 3(15%) to platinum, 1(5%) to anthracyclin, 1(5%) to docetaxel and rest showed no sensitivity to any drug. Conclusions: Thus primary aim to target OCSCs at onset of tumors in ovarian cancer patients to control metastasis and relapse of disease was somewhat obtained. Most interestingly, we found that the chemotherapeutic drugs which were less prescribed for ovarian cancer showed greater sensitivity in comparison to the widely used ones. We like to do animal model study followed by phase I, II and III human clinical trial to establish our hypothesis for better management of chemo-resistant ovarian cancer.

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Ma, Changpo, Xuejun Shi, Wenchao Guo, Jianxin Niu, and Guangshun Wang. "miR-107 enhances the sensitivity of breast cancer cells to paclitaxel." Open Medicine 14, no. 1 (June 1, 2019): 456–66. http://dx.doi.org/10.1515/med-2019-0049.

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AbstractBreast cancer remains the most commonly diagnosed cancer in Chinese women. Paclitaxel (PTX) is a chemotherapy medication used to treat breast cancer patients. However, a side effect of paclitaxel is the severe drug resistance. Previous studies demonstrated that dysregulation of microRNAs could regulate sensitivity to paclitaxel in breast cancer. Here, the present study aimed to lucubrate the underlying mechanisms of miR-107 in regulating the sensitivity of breast cancer cells to PTX. The results demonstrated that miR-107 was down-regulated in breast cancer tumor tissues, while TPD52 was significantly up-regulated compared with the non-tumor adjacent tissues. After confirming that TPD52 may be a major target of miR-107 via a dual-luciferase reporter assay, the western blot and RT-qPCR assays further demonstrated that miR-107 may reduce the expression level of TPD52 as well. In addition, miR-107 may prominently enhance PTX induced reduction of cell viability and the promotion of cell apoptosis in breast cancer, and the variation could be reversed by co-transfected with pcDNA3.1-TPD52. Finally, miR-107 could further reduce the decreased expression of TPD52, Wnt1, β-catenin and cyclin D1 that was induced by PTX in both mRNA and protein levels, which were rescued by pcDNA3.1-TPD52 indicating that miR-107 regulated breast cancer cell sensitivity to PTX may be targeting TPD52 through Wnt/β-catenin signaling pathway.

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Srinivasan, Ajay, Dadasaheb B. Akolkar, Pradip Fulmali, Pooja Fulmali, Navin Srivastava, Darshana Patil, Revati Patil, et al. "Circulating ensembles of tumor-associated cells in genitourinary cancers." Journal of Clinical Oncology 38, no. 6_suppl (February 20, 2020): 718. http://dx.doi.org/10.1200/jco.2020.38.6_suppl.718.

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718 Background: Detection of genitourinary cancers is based on histopathological analysis of tumor tissue obtained by invasive biopsies following manifestation of clinical or radiological symptoms. There is presently no non-invasive blood-based test with high specificity and sensitivity for detection of genitourinary cancers. Considering that unprovoked thromboembolism is a significant risk in multiple cancers, we hypothesized that tumor derived circulating emboli in peripheral blood could comprise cancer cells and would serve as a reliable biomarker for detection of genitourinary cancers. These Circulating Ensembles of Tumor Associated Cells (C-ETACs) are defined as clusters of 3 or more cells of tumorigenic origin (EpCAM+, CK+ and CD45±). Methods: We obtained 15ml of blood from 8828 individuals, including 103 cases of Renal cancer, 79 cases of bladder cancer, 153 cases of prostate cancers as well as from 8493 asymptomatic individuals with age related elevated risk and were negative in various screening investigations (CEA, AFP, CA19-9, CA125, PSA, LDCT, Mammography, PAP Smear). PBMC were isolated by centrifugation. C-ETACs were enriched, harvested and characterized by immunofluorescence staining for EpCAM, CK, CD45 as well as organ specific markers for renal, bladder and prostate cancers. Results: C-ETACs were detected in 87 (84.5%) of 103 renal cancers, 71 (89.9%) of 79 bladder cancers and 138 (90.2%) of 153 prostate cancers respectively irrespective of extent (stage / metastatic status) of disease and prior treatments. Overall sensitivity among 335 cancer patients was 88.4%. Among the 8493 asymptomatic individuals, C-ETACs were detected in 255 individuals (97% specificity). Conclusions: C-ETACs were ubiquitously detected in cancers of Kidney, Bladder and Prostate regardless of stage and treatment status, and pose significant latent risk of metastasis/recurrence. The relative undetectability of C-ETACs in the asymptomatic cohort indicates causative connection with malignancies and are hence suitable for screening for these cancers.

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Schoeler, D., C. Weber, A. Tornack, F. Schriever, and F. Ringel. "Differential sensitivity of B-CLL cells and normal B cells to hyperthermia." Journal of Clinical Oncology 23, no. 16_suppl (June 2005): 6693. http://dx.doi.org/10.1200/jco.2005.23.16_suppl.6693.

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Akolkar, Dadasaheb, Darshana Patil, Raymond Page, Timothy Crook, Sewanti Limaye, Vineet Datta, Stefan Schuster, et al. "Circulating ensembles of tumor-associated cells in gastrointestinal cancers." Journal of Clinical Oncology 38, no. 4_suppl (February 1, 2020): 808. http://dx.doi.org/10.1200/jco.2020.38.4_suppl.808.

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808 Background: CEA and CA19-9 are non-specific markers for Gastrointestinal (GI) cancers. Molecular analysis of fecal blood is of limited utility in colorectal cancers. A non-invasive pan-GI-cancer blood-based test with high specificity and sensitivity is an unmet medical need. Considering that unprovoked thromboembolism is a significant risk in multiple cancers, we hypothesized that circulating thrombotic emboli in peripheral blood could comprise cancer cells and would serve as a reliable biomarker for detection of GI cancers. Methods: We obtained 15ml of blood from 7481 individuals, including 181 cases of Esophageal cancer, 125 cases of Gastric cancer, 448 cases of colorectal cancer and from 6727 asymptomatic individuals with age related elevated risk who underwent evaluation of serum CA19-9 and AFP. Peripheral blood mononuclear cells (PBMC) were isolated by centrifugation and further processes for negative enrichment and harvesting of circulating tumor cell clusters which were characterized by immunostaining. Circulating Ensembles of Tumor Associated Cells (C-ETACs) were defined as clusters of 3 or more cells which were positive for EpCAM and CK, irrespective of CD45 status. Results: C-ETACs were detected in 86.7% of esophageal cancers, 94.4% of gastric cancers and 91.3% of colorectal cancers respectively irrespective of extent (stage / metastatic status) of disease and prior treatments. Overall sensitivity among 754 cancer patients was 90.7%. Among the asymptomatic individuals, C-ETACs were detected in 31 / 366 (8.5%) individuals with elevated CEA and 10 / 152 (6.2%) individuals with elevated CA19-9. C-ETACs were detected in 160 / 5333 (2.9%) of the asymptomatic individuals who had no abnormal findings in any of the said markers. Conclusions: C-ETACs were ubiquitously detected in cancers of Oesophagus, Stomach and Colorectum regardless of stage and treatment status, and pose significant latent risk of thromboembolism and metastasis/recurrence. The relative undetectability of C-ETACs in the asymptomatic cohort indicates causative connection with malignancies and are suitable for screening for these cancers.

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Kenmotsu, Hirotsugu, Masahito Hosokawa, Yasuhiro Koh, Tomoko Yoshino, Takayuki Yoshikawa, Tateaki Naito, Toshiaki Takahashi, et al. "Sensitivity of microcavity array system for circulating tumor cells in lung cancer patients." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): e21007-e21007. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e21007.

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e21007 Background: Epithelial Cell Adhesion Molecule (EpCAM)-based enumeration of circulating tumor cells (CTCs) has prognostic value in solid tumors such as advanced breast, colon and prostate cancers. However, poor sensitivity has been reported in non-small cell lung cancer (NSCLC). We have developed a microcavity array (MCA) system integrated with a microfluidic device for recovery and enumeration of CTsC, regardless of EpCAM expression level. This system can isolate tumor cells on the basis of differences in size and deformability between tumor and hematologic cells. Methods: Paired peripheral blood samples were collected from metastatic lung cancer patients. CTCs were enumerated by EpCAM-based immunomagnetic capture (CellSearch, Veridex) and by the MCA system. In the MCA system, trapped cells were stained with Hoechst 33342, FITC-labeled anti-pan cytokeratin antibodies and PE-labeled anti-CD45 antibodies for subsequent imaging analysis. CTCs were defined as cells with round to oval morphology, a visible nucleus, positive staining for pan-cytokeratin and negative staining for CD45. We evaluated the sensitivity of the MCA system for detecting CTCs in lung cancer patients compared with the CellSearch system. Results: Twenty-two metastatic NSCLC patients and 13 small-cell lung cancer (SCLC) patients were enrolled into this study between April 2011 and January 2012. CTCs were detected using the MCA system in 17 of 22 NSCLC patients (count ≥1 per 7.5 ml) compared with 9 of 22 patients using CellSearch (p=0.013). On the other hand, CTCs were detected using MCA in all 13 SCLC patients compared with just 9 of 13 patients using CellSearch (p=0.012). More CTCs from NSCLC patients were detected by the MCA system (median 13, range 0-313 cells/7.5ml) than by the CellSearch system (median 0, range 0-37 cells/7.5ml) demonstrating statistical superiority (p=0.002, Wilcoxon test). Conclusions: Our results suggest that the MCA system is potentially superior to the CellSearch system for detecting CTCs in lung cancer patients and further clinical development should be considered.

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Zhang, Fang, Jian-ying Cui, Hai-feng Gao, Hao Yu, Fu-feng Gao, Jin-long Chen, and Liang Chen. "Cancer-associated fibroblasts induce epithelial-mesenchymal transition and cisplatin resistance in ovarian cancer via CXCL12/CXCR4 axis." Future Oncology 16, no. 32 (November 2020): 2619–33. http://dx.doi.org/10.2217/fon-2020-0095.

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Aim: Cancer-associated fibroblasts (CAFs) are closely related to epithelial-mesenchymal transition (EMT) and chemoresistance in various cancers. Patients & methods: Experiments in vivo and retrospective studies were applied to explore the role of CAFs in epithelial ovarian cancer (EOC). Results: We found that CXCL12 expression was significantly increased in interstitial CAFs by immunofluorescence. CAF-derived CXCL12 induced EMT though CXCR4/Wnt/β-catenin pathway in EOC cells. Inhibited EMT led to increased apoptosis and cisplatin sensitivity. Multivariate regression analysis shows that CXCL12 expression in the stromal cells and cytoreduction satisfaction are independent prognostic markers of platinum-containing chemotherapy sensitivity in 296 EOC patients. Conclusion: CAFs may activate the Wnt/β-catenin pathway in EOC cells via CXCL12/CXCR4 axis, and then induce EMT and cisplatin resistance.

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Kim, Young-Ho, Hyun-Kyoung Kim, Hee Yeon Kim, HyeRan Gawk, Seung-Hyun Bae, Hye Won Sim, Eun-Kyung Kang, Ju-Young Seoh, Hyonchol Jang, and Kyeong-Man Hong. "FAK-Copy-Gain Is a Predictive Marker for Sensitivity to FAK Inhibition in Breast Cancer." Cancers 11, no. 9 (September 2, 2019): 1288. http://dx.doi.org/10.3390/cancers11091288.

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Background: Cancers with copy-gain drug-target genes are excellent candidates for targeted therapy. In order to search for new predictive marker genes, we investigated the correlation between sensitivity to targeted drugs and the copy gain of candidate target genes in NCI-60 cells. Methods: For eight candidate genes showing copy gains in NCI-60 cells identified in our previous study, sensitivity to corresponding target drugs was tested on cells showing copy gains of the candidate genes. Results: Breast cancer cells with Focal Adhesion Kinase (FAK)-copy-gain showed a significantly higher sensitivity to the target inhibitor, FAK inhibitor 14 (F14). In addition, treatment of F14 or FAK-knockdown showed a specific apoptotic effect only in breast cancer cells showing FAK-copy-gain. Expression-profiling analyses on inducible FAK shRNA-transfected cells showed that FAK/AKT signaling might be important to the apoptotic effect by target inhibition. An animal experiment employing a mouse xenograft model also showed a significant growth-inhibitory effect of F14 on breast cancer cells showing FAK-copy-gain, but not on those without FAK-copy-gain. Conclusion: FAK-copy-gain may be a predictive marker for FAK inhibition therapy in breast cancer.

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Maj, M., E. Nalejska, A. Bajek, T. Kloskowski, and T. Drewa. "C67: Do mesenchymal stem cells influence genitourinary tract cancer cells sensitivity to ciprofloxacin?" European Urology Supplements 13, no. 6 (November 2014): e1258. http://dx.doi.org/10.1016/s1569-9056(14)61459-7.

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Kumar, Balawant, Rizwan Ahmad, Swagat Sharma, Saiprasad Gowrikumar, Mark Primeaux, Sandeep Rana, Amarnath Natarajan, et al. "PIK3C3 Inhibition Promotes Sensitivity to Colon Cancer Therapy by Inhibiting Cancer Stem Cells." Cancers 13, no. 9 (April 30, 2021): 2168. http://dx.doi.org/10.3390/cancers13092168.

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Background: Despite recent advances in therapies, resistance to chemotherapy remains a critical problem in the clinical management of colorectal cancer (CRC). Cancer stem cells (CSCs) play a central role in therapy resistance. Thus, elimination of CSCs is crucial for effective CRC therapy; however, such strategies are limited. Autophagy promotes resistance to cancer therapy; however, whether autophagy protects CSCs to promote resistance to CRC-therapy is not well understood. Moreover, specific and potent autophagy inhibitors are warranted as clinical trials with hydroxychloroquine have not been successful. Methods: Colon cancer cells and tumoroids were used. Fluorescent reporter-based analysis of autophagy flux, spheroid and side population (SP) culture, and qPCR were done. We synthesized 36-077, a potent inhibitor of PIK3C3/VPS34 kinase, to inhibit autophagy. Combination treatments were done using 5-fluorouracil (5-FU) and 36-077. Results: The 5-FU treatment induced autophagy only in a subset of the treated colon cancer. These autophagy-enriched cells also showed increased expression of CSC markers. Co-treatment with 36-077 significantly improved efficacy of the 5-FU treatment. Mechanistic studies revealed that combination therapy inhibited GSK-3β/Wnt/β-catenin signaling to inhibit CSC population. Conclusion: Autophagy promotes resistance to CRC-therapy by specifically promoting GSK-3β/Wnt/β-catenin signaling to promote CSC survival, and 36-077, a PIK3C3/VPS34 inhibitor, helps promote efficacy of CRC therapy.

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An, Zhengzhe, Xianguang Liu, Hyejin Song, Chihwan Choi, Won-Dong Kim, Jae-Ran Yu, and Woo-Yoon Park. "Effect of troglitazone on radiation sensitivity in cervix cancer cells." Radiation Oncology Journal 30, no. 2 (2012): 78. http://dx.doi.org/10.3857/roj.2012.30.2.78.

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Eskandari, N. "Cytokine-mediated modulation of cisplatin sensitivity in ovarian cancer cells." Obstetrics & Gynecology 97, no. 5 (May 2001): S2. http://dx.doi.org/10.1016/s0029-7844(01)01132-2.

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Eyler, Christine E., Wen-Chi Foo, Katherine M. LaFiura, Roger E. McLendon, Anita B. Hjelmeland, and Jeremy N. Rich. "Brain Cancer Stem Cells Display Preferential Sensitivity to Akt Inhibition." STEM CELLS 26, no. 12 (September 18, 2008): 3027–36. http://dx.doi.org/10.1634/stemcells.2007-1073.

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Ohnishi, Ken, Zorica Scuric, Robert H. Schiestl, Noritomo Okamoto, Akihisa Takahashi, and Takeo Ohnishi. "siRNA TargetingNBS1orXIAPIncreases Radiation Sensitivity of Human Cancer Cells Independent ofTP53Status." Radiation Research 166, no. 3 (September 2006): 454–62. http://dx.doi.org/10.1667/rr3606.1.

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Efferth, Thomas, Mohamed E. M. Saeed, Onat Kadioglu, Ean-Jeong Seo, Samira Shirooie, Armelle T. Mbaveng, Seyed Mohammad Nabavi, and Victor Kuete. "Collateral sensitivity of natural products in drug-resistant cancer cells." Biotechnology Advances 38 (January 2020): 107342. http://dx.doi.org/10.1016/j.biotechadv.2019.01.009.

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Chen, Jun-Jie, Steen Knudsen, Wiktor Mazin, Jesper Dahlgaard, and Baolin Zhang. "A 71-Gene Signature of TRAIL Sensitivity in Cancer Cells." Molecular Cancer Therapeutics 11, no. 1 (October 25, 2011): 34–44. http://dx.doi.org/10.1158/1535-7163.mct-11-0620.

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Lam, S., K. Lodder, A. F. A. S. Teunisse, M. J. W. E. Rabelink, M. Schutte, and A. G. Jochemsen. "Role of Mdm4 in drug sensitivity of breast cancer cells." Oncogene 29, no. 16 (February 8, 2010): 2415–26. http://dx.doi.org/10.1038/onc.2009.522.

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Eskandari, Niloofar, Julia Gage, Michael T. Johnson, and Otoniel Martinez-Maza. "Cytokine-Mediated Modulation of Cisplatin Sensitivity in Ovarian Cancer Cells." Obstetrics & Gynecology 97, Supplement (April 2001): 2S. http://dx.doi.org/10.1097/00006250-200104001-00001.

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Zwacka, Ralf M., Lesley Stark, and Malcolm G. Dunlop. "NF-?B kinetics predetermine TNF-? sensitivity of colorectal cancer cells." Journal of Gene Medicine 2, no. 5 (2000): 334–43. http://dx.doi.org/10.1002/1521-2254(200009/10)2:5<334::aid-jgm129>3.0.co;2-q.

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Li, Jin‐Li, Jian‐Ping Wang, Hong Chang, Sheng‐Ming Deng, Jia‐Hui Du, Xiao‐Xiao Wang, He‐Juan Hu, et al. "FEN1 inhibitor increases sensitivity of radiotherapy in cervical cancer cells." Cancer Medicine 8, no. 18 (October 31, 2019): 7774–80. http://dx.doi.org/10.1002/cam4.2615.

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Xiao, Xia, Shaorong Yu, Shuchun Li, Jianzhong Wu, Rong Ma, Haixia Cao, Yanliang Zhu, and Jifeng Feng. "Exosomes: Decreased Sensitivity of Lung Cancer A549 Cells to Cisplatin." PLoS ONE 9, no. 2 (February 21, 2014): e89534. http://dx.doi.org/10.1371/journal.pone.0089534.

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Yamaguchi, Takahiro, Tomoko Kurita, Kazuto Nishio, Junichi Tsukada, Toru Hachisuga, Yasuo Morimoto, Yoshiko Iwai, and Hiroto Izumi. "Expression of BAF57 in ovarian cancer cells and drug sensitivity." Cancer Science 106, no. 4 (February 25, 2015): 359–66. http://dx.doi.org/10.1111/cas.12612.

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CHEN, C., Y. WANG, J. F. MEI, S. S. LI, H. X. XU, H. P. XIONG, X. H. WANG, and X. HE. "Targeting RAD50 increases sensitivity to radiotherapy in colorectal cancer cells." Neoplasma 65, no. 01 (2018): 75–80. http://dx.doi.org/10.4149/neo_2018_170219n128.

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Journal articles on the topic 'Sensitivity of the cancer cells'

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