Relevant bibliographies by topics / MCF-7 cell line

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Academic literature on the topic 'MCF-7 cell line'

Author: Grafiati
Published: 3 June 2025
Last updated: 23 June 2025

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Journal articles on the topic "MCF-7 cell line"

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Nguyen Phi, Hung, Toan Tran Quoc, Tuan Nguyen Anh, et al. "Human breast cancer cell inhibitory constituents from Tetradium ruticarpum." Journal of Science Natural Science 66, no. 1 (2021): 65–71. http://dx.doi.org/10.18173/2354-1059.2021-0008.

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Three alkaloids (named rutaecarpine (1), evodiamine (2), schinifoline (3) and one phenylpropanoid, integrifoliodiol (4)) have been isolated from the EtOAc extract of the fruits of Tetradium ruticarpum (A. Juss.) T. G. Hartley collected in Lang Son province. Their structures have been identified by using 1D and 2D NMR spectroscopies. All four compounds were tested for their cytotoxicity against the human breast cancer cell line (MCF-7) and tamoxifen-resistant breast cancer cell line (MCF\TAMR). The results showed that rutaecarpine (1) inhibited the growth of MCF7 and MCF\TAMR with its IC50 values of 41.2 and 64.6 µM, respectively. In addition, compounds 1, 2, and 4 showed moderate activity toward MCF-7 cell line.
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Men, Xin, Mengyang Su, Jun Ma, et al. "Overexpression of TMEM47 Induces Tamoxifen Resistance in Human Breast Cancer Cells." Technology in Cancer Research & Treatment 20 (January 1, 2021): 153303382110049. http://dx.doi.org/10.1177/15330338211004916.

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Background: Tamoxifen (TAM) is the eminent first-line drug for endocrine therapy of hormone receptor positive premenopausal breast cancer and reduces the risk of recurrence by ∼50%. However, many patients developed TAM resistance and their diseases recurred. Our previous study on transcriptome profile of TAM resistant breast cancer cells revealed that the TMEM47 is one of the most significantly differentially expressed genes. The mechanism of how TMEM47 is involved in TAM resistance was not known. Methods: We constructed a mammal breast cancer cell line, in which TMEM47 was stably overexpressed (TMEM47-OE/MCF-7), to further verify the role of TMEM47 in TAM resistance. siRNA targeting TMEM47 was transfected into TAMR / MCF-7 cells by Liposome. TMEM47 expression was validated on mRNA and protein level by qRT-PCR and western blotting. We tested the cytotoxicity of TAM in the cells. Apoptosis was detected by flow cytometry. Results: Compared to the MCF7 cells, TMEM47 mRNA was significantly up regulated more than 6 folds in the TAMR/MCF7 cells and so its protein. TMEM47 expression level in TMEM47-OE/MCF-7 was similar as in the TAMR/MCF-7 cells. The 50% inhibitory concentration (IC50) value (mean ± SD) of TAM in MCF-7, TAMR/MCF-7 and TMEM47-OE/MCF-7 cells was 1.58 ± 0.19, 2.74 ± 0.24 and 3.12 ± 0.32 µγ/mL, respectively. The apoptosis rates of TAMR/MCF-7 and TMEM47-OE/MCF-7 cell lines were significantly lower than that of MCF-7 cells. After 24 and 48 hours TAM treatments, cell viability was significantly inhibitied in TMEM47 knockdown TAMR/MCF7 cells (P < 0.01). Consistant with the decreased cell viability, the apoptosis rate in TMEM47 knockdown TAMR/MCF-7 cells was significantly increased. Conclusions: Our results suggest that overexpression of TMEM47 in MCF-7 cells acquired TAM resistance to those cells, and knockdown of TMEM47 in TAMR/MCF-7 cells reversed their resistance to TAM. TMEM47 might confer TAM resistance on MCF-7 cells through the inhibition of apoptosis.
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Lee, Jieun, Seung Yeon Joe, Ji-Sun Lee, Dong-Min Kim, and Ahwon Lee. "Abstract P3-10-02: Enhanced miR-579-3p by anti-estrogen treatment may affect capecitabine response in hormone receptor positive metastatic breast cancer." Cancer Research 82, no. 4_Supplement (2022): P3–10–02—P3–10–02. http://dx.doi.org/10.1158/1538-7445.sabcs21-p3-10-02.

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Abstract Purpose Capecitabine is one of a treatment option in anthracycline and taxane pre-treated metastatic breast cancer (MBC) patients. We have performed miRNA microarray of durable and poor responders to capcitabine, and compared with cell line miRNA expression profile (MCF-7, tamoxifen-resistant MCF-7 [MCF-TAM] cell line treated with 5-FU. Methods Between Jan 2006 to Jan 2021, 66 patients treated with capecitabine after anthracycline and taxane failure were enrolled. Twenty-three archival tumor tissues (11 durables and 12 poor responders, each) were collected and went through nCounter miRNA expression assay. MCF-7, tamoxifen resistant MCF-7 (MCF-TAM) cell line was treated with tamoxifen or 5-FU for proliferation assay and also went through nCounter miRNA expression assay. Results HR positive patients who received anti-estrogen treatment before capecitabine showed longer PFS (median 7.7 vs. 4.03 months, P=0.006). MCF-7 treated with tamoxifen and 5-FU showed decreased proliferation compared to 5-FU treated MCF-7. There was significant difference of miR-579-3p expression between durable and poor responders (log2FC -3.02, P=0.004). Tamoxifen-treated MCF-7 cell line showed upregulation of miR-579-3p compared to MCF-7. Tamoxifen + 5-FU treated MCF-7 cell line showed decreased expression of miR-579-3p compared to 5-FU treated MCF-7 cell line. MCF-7 cell line was treated with 5-FU and miR-579-3p. Compared to 5-FU only treated cell line, 5-FU + miR-579-3p treated cell line showed trends for decreased cell proliferation, suggesting that miR-579-3p may have chemo-sensitizing role during systemic chemotherapy. Based on miRNA database, authors hypothesized that MDM2 may be target protein of miR-579-3p and planning to perform further analysis. Conclusions Anti-estrogen treatment before capecitabine administration was associated to better survival in HR positive MBC. Anti-estrogen potentiated the effect of 5-FU in MCF-7. MiR-579-3p was upregulated in durable responders and tamoxifen treated MCF-7 cell line. Further study is planned to analyze the role of miR-579-3p and its potential target, MDM2 in breast cancer. Citation Format: Jieun Lee, Seung Yeon Joe, Ji-Sun Lee, Dong-Min Kim, Ahwon Lee. Enhanced miR-579-3p by anti-estrogen treatment may affect capecitabine response in hormone receptor positive metastatic breast cancer [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P3-10-02.
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Alkreathy, Huda Mohammed, Noura Farraj AlShehri, Fatemah Omer Kamel, Ahmed Khalaf Alghamdi, Ahmed Esmat, and Shahid Karim. "Aged garlic extract potentiates doxorubicin cytotoxicity in human breast cancer cells." Tropical Journal of Pharmaceutical Research 19, no. 8 (2020): 1669–76. http://dx.doi.org/10.4314/tjpr.v19i8.15.

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Purpose: To investigate the potential chemo-sensitizing effect of aged garlic extract (AGE) on doxorubicin (DOX) in breast cancer cells (MCF-7), and the possible underlying mechanisms.Methods: Human breast cancer cell line (MCF-7) was treated with AGE and DOX. The cytotoxic effects of AGE and DOX were investigated via cell cycle analysis and apoptosis induction, using flow cytometry. Mechanistic studies involved the determination of cellular uptake of DOX and p-glycoprotein (P-gp) activity.Results: Combined treatment of MCF7 cells with AGE and DOX produced no significant effect at AGE dose of 10 mg/mL. However, co-treatment with AGE at doses of 50 and 93 mg/mL enhanced the cytotoxicity of DOX on MCF-7 cells, with IC50 values of 0.962 and 0.999 μM, respectively, whencompared with 1.85 μM DOX alone. Moreover, Annexin V-FITC and PI techniques showed that AGE significantly increased percentage of cells in late apoptosis. Besides, AGE-DOX treatment significantly increased cellular uptake of DOX and inhibited P-gp activity, when compared with DOX alone (p < 0.05).Conclusion: AGE enhances the cytotoxic effect of DOX on MCF-7 cells, most likely due to cell cycle distribution, stimulation of apoptosis, increased uptake of DOX by MCF7, and inhibition of P-gp activity.
 Keywords: Aged garlic extract, Doxorubicin, Breast cancer, MCF-7 cell line, P-glycoprotein, Apoptosis, Cell cycle
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Guo, Zhijun, Jianxun Lei, Allison Makovec, et al. "Abstract LB334: Mechanisms of endocrine resistance to letrozole, fulvestrant, and palbociclib are associated with increased sensitivity to hexyl-cuban-1-yl biguanide inhibitors of CYP3A4 mediated epoxyeicosatrienoic acid biosynthesis." Cancer Research 84, no. 7_Supplement (2024): LB334. http://dx.doi.org/10.1158/1538-7445.am2024-lb334.

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Abstract Introduction: Eicosanoid mediated mechanisms of hormone therapy resistance in ER+HER2- breast cancer are poorly understood. Cytochrome P450 arachidonic acid (AA) epoxygenase-derived epoxyeicosatrienoic acids (EETs) contribute to breast cancer progression by promoting mitochondrial oxidative phosphorylation (OXPHOS). However, it remains unclear how EETs contribute to hormonal therapy resistance. In this study, the well-known letrozole resistant (LR) MCF-7 AC1 cell line overexpressing aromatase was selected for fulvestrant resistance (FR). A clonal cell line resistant to letrozole and fulvestrant (LR/FR) also exhibited resistance to palbociclib (PR) (MCF-7 AC1 LR/FR/PR). Xenograft tumors of this cell line were resistant to letrozole, fulvestrant, and palbociclib. Structure activity studies and modeling led to the development of CYP3A4 AA epoxygenase inhibiting biguanides hexyl cuban-1-yl biguanide (HCB) and fluorinated hexyl derivatives C5F2-HCB and C6F3-HCB. Fluorination on the hexyl moiety led to broader inhibition of EET regioisomer biosynthesis. These agents were tested for inhibition of proliferation, signaling, and OXPHOS/glycolysis balance in the MCF-7 AC1 LR/FR/PR cell line. Results: In the MCF-7 AC1 LR/FR/PR clonal cell line cyclin D1 and estrogen receptor (ER) expression were undetectable, while cyclin E1, CDK4, CDK6, CYP3A4, and c-MYC were upregulated 11, 40, 13, 10, and 12- fold (n=3, p<0.001) compared to the MCF-7 cell line. LC-MS analysis demonstrated 1.8, 1.4, and 1.2- fold higher total cellular levels of (±)8,9, (±)11,12, and (±)14,15-EET in the MCF-7 AC1 LR/FR/PR cell line compared to the MCF-7 cell line (n=3, p<0.05). C6F3-HCB suppressed cellular levels of EETs: (±)8,9-EET by 55% (n=3, p<0.031), (±)11,12-EET by 53% (n=3, p<0.029), and (±)14,15-EET by 60% (n=3, P<0.0001). The MCF-7 AC1 LR/FR/PR cell line was more potently inhibited by hexyl-cuban-1-yl biguanides compared to the MCF-7 cell line, exhibiting lower IC50 values (MCF-7 AC1 LR/FR/PR IC50 vs. MCF-7 IC50; HCB 4.1 vs. 7.0 uM; for C5F2-HCB 10 vs. 25 uM; C6F3-HCB: 5.4 vs. 12 uM; P values all <0.05). Measurement of spare respiratory capacity revealed that the MCF-7 AC1 LR/FR/PR cell line had 4.2% spare respiratory capacity compared to 34% for MCF-7, indicating a lower OXPHOS reserve for the resistant cells. Additionally, the MCF-7 AC1 LR/FR/PR cell line displayed a 2.4-fold higher extracellular acidification rate (ECAR) than the MCF-7 cell line, indicating a higher glycolysis rate (Warburg effect) in the resistant cells. Conclusion: Selection for fulvestrant resistance of MCF-7 AC1 cells resulted in upregulation of CYP3A4 and biosynthesis of hormone therapy resistance associated EETs while correlating with greater sensitivity to fluorinated hexyl-cuban-1-yl biguanides that inhibit EET biosynthesis. Citation Format: Zhijun Guo, Jianxun Lei, Allison Makovec, Swaathi Jayaraman, John R. Hawse, Carol Lange, Elizabeth Ambrose, Gunda I. Georg, Tony D'Assoro, Goetz P. Matthew, David A. Potter. Mechanisms of endocrine resistance to letrozole, fulvestrant, and palbociclib are associated with increased sensitivity to hexyl-cuban-1-yl biguanide inhibitors of CYP3A4 mediated epoxyeicosatrienoic acid biosynthesis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 2 (Late-Breaking, Clinical Trial, and Invited Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(7_Suppl):Abstract nr LB334.
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Yazdi-Rouholamini, Sayedeh Elmira, Nasrin Motamed, Mohammad Tahmasb, and Kobra Omidfar. "Silibinin Cytotoxic Effect on MCF-7 Cell Line." Journal of Sabzevar University of Medical Sciences 23, no. 3 (2016): 386–91. http://dx.doi.org/10.21859/sums-2303386.

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Kaan, Dilek. "Expression and biochemical significance of Piwil2 in stem cell lines." Postępy Higieny i Medycyny Doświadczalnej 76, no. 1 (2022): 97–103. http://dx.doi.org/10.2478/ahem-2022-0009.

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Abstract Introduction P-element induced wimpy testis-like 2 (Piwil2) is in the Piwi gene family. Piwil2 has important roles in the self-renewal mechanism of stem cell induction and progression of numerous types of human malignancies such as lung, breast, colon, prostate, and cervical cancers. Glutathione S-transferase (GST) acts as detoxification in cancer metabolism. This study aimed to investigate the effects of the stem cell protein Piwil2 on MCF10A and MCF-7 at the GST activity levels. Materials/Methods MCF-7/Piwil2 and MCF10A/Piwil2, transfected with a plasmid carrying the Piwil2 gene, and non-transfected MCF-7 and MCF10A were cultured in a complete DMEM/F12 medium. GST A1 and P1 activity was determined in these cell lines using as substrates CDNB, EA respectively. Results According to experimental results, GST P1 activity decreased in the MCF-7/Piwil2 cells as compared with the non-transfected MCF-7 cells, however, MCF-7/Piwil2 cells demonstrated increases in GST A1 (total GST) activity. The statistically significant differences were found for the comparison of non-transfected MCF-7 and MCF-7/Piwil2 (p<0,0001), for GST enzyme activities by using CDNB and EA as substrates. These results were the same for the MCF10A cell line. Discussion It is shown for the first time that transfection studies may affect GST activity at the cellular mechanism level. The study contributes to determining the effect of transfection on GST isoenzymes and also how the Piwil2 gene may affect GST activity in the stem cell line.
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Arulnathan, Stephanie B., Kok H. Leong, Azhar Ariffin, Huda S. Kareem, and Kevin K. H. Cheah. "Activation of Intrinsic Apoptosis and G1 Cell Cycle Arrest by a Triazole Precursor, N-(4-chlorophenyl)-2-(4-(3,4,5-trimethoxybenzyloxy)benzoyl)-hydrazinecarbothioamide in Breast Cancer Cell Line." Anti-Cancer Agents in Medicinal Chemistry 20, no. 9 (2020): 1072–86. http://dx.doi.org/10.2174/1871520620666200318100051.

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Background: Oxadiazoles, triazoles, and their respective precursors have been shown to exhibit various pharmacological properties, namely antitumour activities. Cytotoxic activity was reported for these compounds in various cancer cell lines. Aim and Objectives: In this study, we aim at investigating the mechanism of apoptosis by N-(4-chlorophenyl)-2-(4- (3,4,5-trimethoxybenzyloxy)benzoyl)-hydrazinecarbothioamide, a triazole precursor, henceforth termed compound P7a, in breast cancer cell line, MCF-7. We first screen a series of analogues containing (3,4,5-trimethoxybenzyloxy) phenyl moiety in breast cancer cell lines (MCF-7 and MDA-MB-231) to select the most cytotoxic compound and demonstrate a dose- and time-dependent cytotoxicity. Then, we unravel the mechanism of apoptosis of P7a in MCF-7 as well as its ability to cause cell cycle arrest. Methods: Synthesis was performed as previously described by Kareem and co-workers. Cytotoxicity of analogues containing (3,4,5-trimethoxybenzyloxy)phenyl moiety against MCF-7 and MDA-MB-231 cell lines was evaluated using the MTS assay. Flow cytometric analyses was done using Annexin V/PI staining, JC-1 staining and ROS assay. The activity of caspases using a chemoluminescence assay and western blot analysis was conducted to study the apoptotic pathway induced by the compound in MCF-7 cells. Lastly, cell cycle analysis was conducted using flow cytometry. Results: Upon 48 hours of treatment, compound P7a inhibited the proliferation of human breast cancer cells with IC50 values of 178.92 ± 12.51μM and 33.75 ± 1.20μM for MDA-MB-231 and MCF-7, respectively. Additionally, compound P7a showed selectivity towards the cancer cell line, MCF-7 compared to the normal breast cell line, hTERT-HME1, an advantage against current anticancer drugs (tamoxifen and vinblastine). Flow cytometric analyses using different assays indicated that compound P7a significantly increased the proportion of apoptotic cells, increased mitochondria membrane permeabilisation and caused generation of ROS in MCF-7. In addition, cell cycle analysis showed that cell proliferation was arrested at the G1 phase in the MCF-7 cell line. Furthermore, upon treatment, the MCF-7 cell line showed increased activity of caspase-3/7, and caspase-9. Lastly, the western blot analysis showed the up-regulation of pro-apoptotic proteins along with up-regulation of caspase-7 and caspase-9, indicating that an intrinsic pathway of apoptosis was induced. Conclusion: The results suggest that compound P7a could be a potential chemotherapeutic agent for breast cancer.
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Zhang, Ying, Haiyan Gao, and Haidong Gao. "BAG5 regulates PTEN stability in MCF-7 cell line." BMB Reports 46, no. 10 (2013): 490–94. http://dx.doi.org/10.5483/bmbrep.2013.46.10.268.

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Komorowska, Dominika, Agnieszka Gajewska, and Aleksandra Rodacka. "Radiosensitivity of human breast cancer cell line MCF-7." Acta Universitatis Lodziensis. Folia Biologica et Oecologica 17 (September 29, 2021): 12. http://dx.doi.org/10.18778/1730-2366.16.08.

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Dissertations / Theses on the topic "MCF-7 cell line"

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Demirel, Kars Meltem. "Molecular Mechanisms Of Vincristine And Paclitaxel Resistance In Mcf-7 Cell Line." Phd thesis, METU, 2008. http://etd.lib.metu.edu.tr/upload/3/12610241/index.pdf.

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Resistance to broad spectrum of chemotherapeutic agents in cancer cell lines and tumors has been called multiple drug resistance (MDR). In this study, the molecular mechanisms of resistance to two anticancer agents (paclitaxel and vincristine) in mammary carcinoma cell line MCF-7 were investigated. MCF-7 cells were selected in the presence of paclitaxel and vincristine by stepwise dose increments. The cell viability and growth profiles of resistant sublines were examined. As the resistance indices increased, the growth rates of sublines were found to decrease. Gene and protein expression levels of the basic drug resistance proteins P-gp and MRP1 were studied in sensitive and drug resistant MCF-7 cells. It was shown that P-gp overexpression is significantly contributing to the developed drug resistance phenotype. Mutation analysis of beta tubulin gene which encodes the target of paclitaxel and vincristine was performed. Single histidine to proline mutation was identified near GTP binding site of beta tubulin in vincristine resistant subline which was not reported before. Apoptosis related BCL-2 and BAX were examined at both gene and protein expression levels and they were not found to be significantly related to the developed resistance in the sublines. The reversal of drug resistance by various inhibitory agents of P-gp and MRP1 was investigated by using flow cytometry. Synthetic silicon compounds were found to be the most effective MDR reversal agents. The effects of various combinations of anticancer drugs and reversal agents on cell proliferation were examined by checkerboard microplate method. ALIS409-paclitaxel and paclitaxel-doxorubicin pairs seem to have highest antiproliferative effects on resistant sublines. The microarray expression profiling of sensitive and resistant MCF-7 cells was performed for a much detailed and comprehensive analysis of drug resistance. The results indicated that the upregulation of MDR1 gene is the dominating mechanism of paclitaxel and vincristine drug resistance. Additionally up regulation of the genes encoding the detoxifying enzymes (i.e. GSTP1) was observed. Significant down regulation of apoptotic genes (i.e. PDCD2/4/6/8) and alterations in expression levels of genes related to invasion and metastasis (MMPs, ADAMs, COL4A2, LAMA etc.) were detected. Upregulation of some oncogenes (i.e. ETS, RAS) and cell cycle regulatory genes (CDKN2A, CCNA2 etc.) was seen which may be in close relation to MDR in breast cancer. Further studies will demonstrate the relationship between the components contributing to drug resistance phenotype in breast cancer cells.
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Pfeiffer, Thomas J. "Phytoestrogens may inhibit proliferation of MCF-7 cells, an estrogen-responsive breast adenocarcinoma cell line." Link to electronic thesis, 2004. http://www.wpi.edu/Pubs/ETD/Available/etd-0430104-132238.

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Darcansoy, Iseri Ozlem. "Investigation Of Docetaxel And Doxorubicin Resistance In Mcf-7 Breast Carcinoma Cell Line." Phd thesis, METU, 2009. http://etd.lib.metu.edu.tr/upload/3/12610422/index.pdf.

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Multidrug resistance phenotype of tumor cells describes resistance to wide range of structurally unrelated anticancer agents and is a serious limitation to effective chemotherapy. It is a multifactor yet not fully elucidated phenomenon by the involvement of diverse cellular pathways. Aim of this study was to investigate the resistance mechanisms developed against docetaxel and doxorubicin that are widely used in the treatment of breast cancer in model cell line MCF-7. Resistant sublines were developed by application of drugs in dose increments and effect of docetaxel and doxorubicin on drug applied cells were investigated by cell viability assays. Expression analysis of P-gp, MRP1, BCRP, Bcl-2, Bax and &amp<br>#946<br>-tubulin isotypes were performed by RT-PCR, qPCR, Western blot and immunocytochemistry. Genome-wide expression analysis was also performed by cDNA microarray. According to cell viability assays, drug applied cells developed varying degree of resistance to docetaxel and doxorubicin. Gene expression analysis demonstrated that de novo expression of P-gp contributed significantly to drug resistance. Expression levels of class II, III and V &amp<br>#946<br>-tubulin isotypes increased in docetaxel resistant sublines. According to microarray analysis, a variety of genes showed significantly altered expression levels particularly drug metabolizing and detoxification enzymes (i.e. increased GPX1 and GSTP1 with decreased POR), survival proteins (e.g. decreased TRAIL together with increased decoy receptors and CD40), extracellular matrix components (e.g. increased integrin signaling), growth factors and cytokines (e.g. EGFR1, FGFR1, CTGF, IL6, IL8 and IL18 overexpression), epithelial-mesenchymal transition proteins (i.e. increased vimentin and N-cadherin with decreased E-cadherin and occludin) and microtubule dynamics related proteins (e.g. increased MAP1B and decreased MAP7). Development of cross-resistance and combined drug effects on resistant sublines were also studied. Results demonstrated that docetaxel and doxorubicin resistant cells developed cross-resistance to paclitaxel, vincristine, ATRA, tamoxifen and irradiation. Finally, modulatory effects of verapamil and promethazine in combined drug applications were investigated and verapamil and promethazine were shown to decrease MDR1 expression level thus reverse the MDR. They also showed synergic and additive effects in combined docetaxel and doxorubicin applications. Identification of resistance mechanisms may personalize chemotherapy potentially increasing efficacy of chemotherapy and life quality of patients.
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Kaplan, Esra. "Development And Investigation Of Etoposide Resistance In Mcf-7 Breast Cancer Cell Line." Master's thesis, METU, 2010. http://etd.lib.metu.edu.tr/upload/12612781/index.pdf.

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Failure of chemotherapy in cancer patients because of development of drug resistance is a major problem. Alterations of DNA repair mechanisms and drug targets are among the important resistance mechanisms which are developed against topoisomerase II inhibitors etoposide and doxorubicin. Modifications in the expression levels of mismatch repair (MMR) genes due to resistance to topoisomerase II inhibitors are involved in breast cancer. In this study, etoposide resistant sublines were developed from MCF7 breast cancer cell line (MCF7/S) and the expression levels of TOP2A and two important MMR genes MSH2 and MLH1 were examined by real time qPCR. Previously developed doxorubicin resistant cells were also studied for comparison. Etoposide resistant sublines MCF7/1000E, MCF7/1250E and MCF7/2000E were approximately 2, 3 and 4 fold resistant relative to parental MCF7/S cells, respectively. MLH1, MSH2 and TOP2A expressions decreased in both etoposide and doxorubicin resistant sublines relative to MCF7/S cells. Expression levels of TOP2A in resistant sublines differ between 10-95 percent of the expression levels in the parental cells. In the sublines MCF7/200E, MCF7/500E, MCF7/750E and MCF7/1000E a decrease in TOP2A gene expression was determined. In sublines MCF7/1250E and MCF7/2000E fluctuations in the expression levels were observed. Among the doxorubicin resistant sublines (MCF7/600D and MCF7/1000D), in MCF7/1000D which is more resistant to doxorubicin, TOP2A expression level was higher. Expression levels of MSH2 decreased regularly as the resistance increased. However, in MCF7/1250E significant increase relative to MCF7/1000E was observed. In MCF7/2000E, expression levels of MSH2 again significantly decreased to 41 percent of the levels in parental cell line. Expression levels of MLH1 decreased significantly (18-58 percent) in etoposide resistant sublines relative to MCF7/S cells. In doxorubicin resistant sublines, a decrease in MLH1 gene expression was observed in MCF7/1000D. It can be concluded from the results that decrease in the expression levels of TOP2A, MSH2 and MLH1 genes may contribute to resistance together. Above a certain resistance level, sublines may develop new strategies for acquiring higher resistance. Whenever a strategy becomes limited, new strategies emerge. New approaches developed to overcome resistance in cancer chemotherapy should consider the molecular basis of resistance in different stages of the disease.
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Sener, Emine Cigdem. "Reversal Of Paclitaxel Resistance In Mcf-7 Cell Line By A Chemical Modulator Elacridar." Master's thesis, METU, 2012. http://etd.lib.metu.edu.tr/upload/12614644/index.pdf.

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The phenomenon called multi drug resistance (MDR) is the resistance of cancer cells to anticancer drugs before or during chemotherapy. One of the mechanisms causing MDR is the upregulation of efflux pumps. The overexpression of MDR1 and MRP1 results in increased efflux of anticancer agents. The aim of this study was to reverse MDR1-mediated paclitaxel resistance in MCF7 breast cancer cell line by a chemical MDR modulator elacridar. In this study, cytotoxicity and the reversal effect of elacridar on sensitive and paclitaxel resistant cells were investigated. The effect of elacridar on MDR1 and MRP1 gene expressions were also determined. Results indicated MDR1 gene was highly overexpressed (208 fold) in MCF7/Pac cells compared to MCF7/S cells. Elacridar was not found to be cytotoxic in MCF7/Pac cells up to 30&micro<br>M. XTT results demonstrated 0.5&micro<br>M elacridar concentration was able to restore the antiproliferative effect of paclitaxel by 94% in MCF7/Pac cells. Complete MDR reversal was achieved at 5&micro<br>M elacridar concentration. qPCR results revealed dose dependent upregulations in MDR1 and MRP1 gene expression levels after elacridar treatment which did not prevent reversal of MDR by elacridar. Elacridar was shown to be very effective against paclitaxel resistance in MCF7/Pac cells at low concentrations. Therefore, it can be a suitable candidate for therapeutic applications in patients who developed paclitaxel resistance. Nevertheless, dose dependent upregulations in MDR1 and MRP1 gene expressions should be taken into consideration and overdose elacridar administration should be avoided.
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Urfali, Cagri. "Reversal Of Breast Cancer Resistance Protein Mediated Multidrug Resistance In Mcf-7 Breast Adenocarcinoma Cell Line." Master's thesis, METU, 2012. http://etd.lib.metu.edu.tr/upload/12614062/index.pdf.

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Resistance to various chemotherapeutic agents is a major problem in success of cancer chemotherapy. One of the primary reasons of development of multidrug resistance (MDR) is the overexpression of ATP binding cassette (ABC) transporter proteins. Breast cancer resistance protein (BCRP) belongs to ABC transporter family and encoded by ABCG2 gene. BCRP is mainly expressed in MDR1 (P-glycoprotein) lacking breast cancer cells. Overexpression of BCRP leads to efflux of chemotherapeutic agents at higher rates, therefore, decreased levels of intracellular drug accumulation. Despite the fact that several chemical modulators claim to restore BCRP-mediated increased drug efflux, these modulators were shown to display various side effects, precluding their clinical use. Therefore, to reverse BCRPmediated MDR phenotype by a modulator with minimum cytotoxicity may increase clinical benefits and minimize side effects.
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Kim, Ju Young. "Transcriptional regulation of glycosyltransferase genes in MCF-7 human breast cancer cell line following drug treatment." Master's thesis, University of Cape Town, 2018. http://hdl.handle.net/11427/29866.

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Bioinformatics is a subfield in computational science that is principally focused on developing methods and performing data analytics in the areas of proteomics and genomics. In this thesis I draw a link between proteomics and genomics by focusing on the regulation patterns of glycosyltransferase (GT) genes in breast cancer cell line following the treatment with a large set of Food and Drug Administration (FDA) approved drugs. This is based on the understanding that aberrant glycosylation in breast cancer tumours stem from altered GT gene expression. A major goal of genomic research is the identification of genes that have been differentially expressed under abnormal conditions. A gene expression profile provides a snapshot of the transcriptional level of a cell. A comparative gene expression profile between a diseased and normal-state can be used to map out the regulatory mechanisms of disease. In this thesis, the results of Microarray experiments on MCF-7 human breast cancer cell-lines are analysed using statistical and computational tools to identify differentially expressed genes. Here a bioinformatics analysis of the regulation of GT gene expressions was performed to identify a set of glycosylation related genes with the aim of making an inference about their biological functions. A set of raw gene expression profiles from MCF-7 human breast cancer cell-line treated with different therapeutic drugs were obtained from the Connectivity Map (CMap) database. Initially 7,000 gene expression profiles were used and these were treated by 1,309 different FDA-approved drugs. The number of genes initially was counted up to 22,000. Using the Bioconductor open source software in R statistical programming environment a statistical differential expression analysis followed by several data filtering and pre-processing steps were performed to identify up and down regulated GT genes using. Using non-parametric rank sum meta-analysis three cancer drugs and two non-cancer drugs were identified as effective agents able to control the transcriptional regulatory state of GT genes. The study concluded by employing co-expression gene module analysis using the Weighted Gene Co-Expression Network Analysis (WGCNA) package on each of the cancer and non-cancer drug treatments. The gene modules discovered from the analysis were used to perform gene ontology enrichment analysis to identify the biological functions where they were significantly enriched in. The co-expression modules where GT genes have been down regulated by the drugs, were involved in processes such as Wnt signalling and cell surface pattern recognition receptor signalling important for cancer development. Immune response and apoptotic processes in the cell were identified from co-expression modules where GT genes were up regulated. This key finding that the GT gene expressions are markers for treatment analysis points to their use in drug development studies. The second more direct finding is that non-breast cancer specific FDA-approved drugs may have a role in treating breast cancer and may be the subject of future drug repurposing strategies.
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Gilhooly, Elaine Marie. "The cloning and characterization of an oestrogen-inducible mRNA from the MCF-7 breast cancer cell line." Thesis, University of Liverpool, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337142.

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Van, den Heever Martine. "A comparison of the effect of curcumin treatment on apoptosis, necrosis and autophagy in a MCF-7 mammary adenocarcinoma and a MCF-12A healthy mammary epithelial cell line." Thesis, Stellenbosch : University of Stellenbosch, 2009. http://hdl.handle.net/10019.1/2970.

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Thesis (MSc (Physiological Sciences))--University of Stellenbosch, 2009.<br>Breast cancer is currently the primary cause of cancer-related death in women worldwide. Conventional treatments such as radiation and chemotherapy have many deleterious and long lasting side-effects, some of which are permanent, such as infertility. As certain tumour cells can also acquire resistance to chemotherapy, the need for the development of a less severe, yet more effective, targeted anti-cancer treatment exists. Curcumin, a plant polyphenol from Curcuma longa, has long been thought to possess antitumour, antioxidant, anti-arthritic, anti-amyloid, anti-ischemic and anti-inflammatory properties. Numerous studies conducted over the past sixty years confirm this. We aimed at examining the effect of curcumin on cell viability and the different modes of cell death, namely apoptosis, necrosis and autophagy, in the MCF-12A (non-tumorigenic mammary epithelial) and MCF-7 (mammary adenocarcinoma) cell lines. Cells were incubated with different doses of curcumin to evaluate the dose response through a MTT assay. Thereafter, cells were incubated with 200 μM curcumin for 48 hrs and stained with markers and DNA stains for apoptosis (Hoechst, Caspase-3, PARP), necrosis (Propidium Iodide) and autophagy (LC3B and Beclin-1). Cells were examined via fluorescence microscopy, Western Blot- and FACS analyses. MTT results showed no significant decrease in viability in the MCF-12A cell line after curcumin treatment. However, a significant decrease in viability was observed in MCF-7 cells after treatment with 200 μM curcumin (p < 0.05). Treated MCF-7 cells also show clear LC3B expression. FACS results show a significant difference in Hoechst mean fluorescence intensity in MCF-7 cells after curcumin treatment (p < 0.05). This study provides evidence that MCF-7 cells respond to a 200 μM dose of curcumin treatment through metabolic change and induction of the autophagic pathway. The model system used in this study provides groundwork for further cell culture based studies regarding breast cancer and curcumin.
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Sun, Wei [Verfasser]. "Genome-wide analyses of transcriptional regulation mediated by estrogen receptor alpha in human breast cancer cell line MCF-7 / Wei Sun." Berlin : Freie Universität Berlin, 2012. http://d-nb.info/102730835X/34.

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Books on the topic "MCF-7 cell line"

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Dew, William Albert. The use of a Secreted Embryonic Alkaline Phosphatase-based reporter plasmid assay and Electrophoretic Mobility Shift Assays to investigate differences in signal transduction between a chemosensitive cell line (MCF-7) and two chemoresistant cell lines (MCF-7 tax, and MCF-7 dox). Laurentian University, School of Graduate Studies, 2006.

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Wijesuriya, Kanchana. Limiting glucose concentrations in human breast cancer cell lines, MCF-7/WT and MCF-7/ADR. Laurentian University, 1998.

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Eng, Jamei R. Pharmacogenomics of paclitaxel and doxorubicin resistance in human MCF-7 breast cancer cell lines. Laurentian University, 2004.

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Turnbull, Heather. Biochemical and physiological characterization of newly established drug-resistant MCF-7 breast tumour cell lines. Laurentian University, 2000.

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Wei, Khor Heng, Yeoh Bee Yoong, and Toh Li Fang. Attempts to transfect the prion protein in human cancer cell lines: Attempts to stably transfect the prion protein into SH-SY5Y cancer cell line and MCF-7 cancer cell line. LAP Lambert Academic Publishing, 2011.

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Book chapters on the topic "MCF-7 cell line"

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Prévost, Grégoire, Nathalie Veber, Lucien Israël, and Philippe Planchon. "Growth Hormone Releasing Hormone Receptor in Human Breast Cancer Cell Line MCF-7." In Growth Hormone Secretagogues. Springer New York, 1996. http://dx.doi.org/10.1007/978-1-4612-2396-2_9.

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Buck, C., A. Wawer, W. Mach, et al. "Synergism of Lymphotoxin and Interferon-γ in the Growth Inhibition of Breast Cancer Cell Line MCF-7." In Cytokines in Hemopoiesis, Oncology, and AIDS. Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75510-1_28.

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Nguyen-Thi, Lam-Huyen, Sinh Truong Nguyen, Thao Phuong Tran, Chinh-Nhan Phan-Lu, Phuc Van Pham, and Trung The Van. "Anti-cancer Effect of Xao Tam Phan Paramignya trimera Methanol Root Extract on Human Breast Cancer Cell Line MCF-7 in 3D Model." In Advances in Experimental Medicine and Biology. Springer International Publishing, 2018. http://dx.doi.org/10.1007/5584_2018_148.

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Akim, A. M., E. E. Tung, P. P. Chong, M. Y. Hamzah, and K. Z. M. Dahlan. "Nanoparticle-Encapsulated Tamoxifen Inducing Cytotoxic Effect on Mcf-7 Breast Cancer Cell Lines." In IFMBE Proceedings. Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-32183-2_58.

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Arsianti, Ade, Maya Dorothea, Naura Syafira, Ananda Tony, and Anton Bahtiar. "In Vitro Cytotoxicity of Gallic Acid Derivatives (Alkyl gallates) Against Breast MCF-7 Cancer Cells." In Proceedings of the 4th International Conference on Life Sciences and Biotechnology (ICOLIB 2021). Atlantis Press International BV, 2022. http://dx.doi.org/10.2991/978-94-6463-062-6_26.

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Leone, Anna, and John Wilkinson. "The Effects of Melatonin and Melatonin Analogues on the P388, DLD-1 and MCF-7 Tumour Cell Lines." In Role of Melatonin and Pineal Peptides in Neuroimmunomodulation. Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3756-4_27.

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Sujatha, K., B. Deepa lakshmi, B. Rajeswary Hari, D. Sangeetha, and B. Selvapriya. "Image Processing Technique for Effective Analysis of the Cytotoxic Activity in Human Breast Cancer Cell Lines – MCF-7." In Advances in Intelligent Systems and Computing. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-51859-2_5.

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"Growth inhibition of Euphorbia extract on breast cancer cell line MCF-7." In Biotechnology, Agriculture, Environment and Energy. CRC Press, 2014. http://dx.doi.org/10.1201/b17720-31.

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VILLACAMPA, M. J., R. MORO, J. NAVAL, et al. "Evidence for Alpha-Fetoprotein Receptors in the MCF-7 Human Breast Cancer Cell Line." In Protides of the Biological Fluids. Elsevier, 1985. http://dx.doi.org/10.1016/b978-0-08-031739-7.50144-0.

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Thirumurugan, Alagu, Vijayakumar Blessy, and Muthu Karthikeyan. "Comparative Study on Doxorubicin Loaded Metallic Nanoparticles in Drug Delivery Against MCF-7 Cell Line." In Applications of Nanomaterials. Elsevier, 2018. http://dx.doi.org/10.1016/b978-0-08-101971-9.00011-9.

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Conference papers on the topic "MCF-7 cell line"

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Chaubey, Shivam Kumar, Mohit Rathor, Rupen Tamang, Biplob Koch, and Rakesh Kumar Singh. "Enhanced live cell imaging through polarization digital holographic microscope." In JSAP-Optica Joint Symposia. Optica Publishing Group, 2024. https://doi.org/10.1364/jsapo.2024.16p_a37_2.

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Polarization is significant in understanding complex optical behaviors and revealing properties that conventional methods often miss. However, traditional polarization measurement techniques typically involve multiple captures, which are not ideal for live cell imaging. This study presents our advancements in developing a polarization digital holographic microscope (PDHM) tailored for spatially resolved, label-free imaging. Our approach focuses on single-shot polarization imaging, which significantly enhances the feasibility of real-time observations [1]. We demonstrate the practical application of PDHM in imaging live cancer cells, specifically (MCF-7 breast cancer cells), showcasing its ability to capture detailed cellular structures without the need for external staining agents.
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den Hollander, P., I. Osadchey, O. Hampton, et al. "Evolution of Genomic Diversity in the Breast Cancer Cell Line MCF-7." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-3171.

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"The Effects of Valproic Acid on Viability of MCF-7 Cell Line." In International Conference on Cellular & Molecular Biology and Medical Sciences. Universal Researchers (UAE), 2016. http://dx.doi.org/10.17758/uruae.ae0916406.

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Mathew, Jasmine, and Vandana Rathod. "Mechanistic action of AgNps (silver nanoparticles) in apoptosis of MCF-7- cell line." In Proceedings of the International Conference on Nanotechnology for Better Living. Research Publishing Services, 2016. http://dx.doi.org/10.3850/978-981-09-7519-7nbl16-rps-330.

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Tabakoğlu, H. Özgür. "Transmittance of MCF-7 breast tumor cell line through visible and near infrared spectrum." In SPIE BiOS, edited by E. Duco Jansen. SPIE, 2016. http://dx.doi.org/10.1117/12.2212647.

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"Analysis of hypoxia signature in TCGA-BRCA dataset and in mcf-7 cell line." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-221.

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Agarwal, Rakhee, Nawab Ali, and Olga Tarasenko. "INOSITOL HEXAKISPHOSPHATE MEDIATES APOPTOSIS IN HUMAN BREAST ADENOCARCINOMA MCF-7 CELL LINE VIA INTRINSIC PATHWAY." In BIOLOGY, NANOTECHNOLOGY, TOXICOLOGY AND APPLICATIONS: 4th BioNanoTox (Biology, Nanotechnology, Toxicology) and Applications. AIP, 2010. http://dx.doi.org/10.1063/1.3419682.

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Mfouo-Tynga, Ivan, Nicolette N. Houreld, and Heidi Abrahamse. "Photodynamic effects of gold nanoparticles in a breast cancer cell line (MCF-7)in vitro." In European Conferences on Biomedical Optics, edited by Lothar D. Lilge and Ronald Sroka. SPIE, 2015. http://dx.doi.org/10.1117/12.2184043.

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Yang, Hui, Natalia Volfovsky, Alison Rattray, Xiongfong Chen, Hisashi Tanaka, and Strathern Jeffrey. "Abstract LB-233: Identification of DNA palindromes in the MCF-7 breast cancer cell line." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-lb-233.

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Kutlu, HM, E. Çömlekçi, H. Izgördü, C. Vejselova Sezer, and G. Kuş. "PO-070 Evaluation the cytotoxic effect of carmofur on MCF-7 human breast cancer cell line." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.113.

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Reports on the topic "MCF-7 cell line"

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Melkoumian, Zaroui. Regulation of C-myc Gene Expression by Potassium Channel Blocker Quindine in MCF-7 Human Breast Cancer Cell Line. Defense Technical Information Center, 2000. http://dx.doi.org/10.21236/ada384096.

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Catalano, Jennifer G., James J. Valdes, Darrel Menking, Kyle Hubbard, and Averell L. Gnatt. Standardization of the 3-(4,5-Dimethylthiazol-2-yl)-5-(3-Carboxymethoxyphenyl)-2-(4-Sulfophenyl)-2H-Tetrazolium, Inner Salt (MTS) Assay for the SK-N-SH, KYSE-30, MCF-7, and HeLa Cell Lines. Defense Technical Information Center, 2006. http://dx.doi.org/10.21236/ada452182.

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