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

Author: Grafiati

Published: 28 June 2021

Last updated: 29 July 2025

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1

Kozak, T. P. "MODIFICATION OF BREAST CANCER CELLS' SENSITIVITY TO METFORMIN DUE TO CO-CULTIVATION WITH B. ANIMALIS." Biotechnologia Acta 18, no. 2 (2025): 54–56. https://doi.org/10.15407/biotech18.02.054.

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Glucose metabolism (GM) disturbances are well-known risk factors for the development of breast cancer (BC). The GM regulator metformin is used as an adjunctive therapy for BC. Another potent modulator of GM in BC cells is the microbiota, particularly bifidobacteria. The combined action of these factors may lead to unpredictable effects on the sensitivity of malignant cells to antitumor agents. Aim. To investigate the effect of Bifidobacterium animalis on the sensitivity of BC cells to the cytotoxic/cytostatic effects of metformin. Materials and Methods. The impact of B. animalis on GM in BC ce

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

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3

Chang, Yu-Yao, Tsung-Ying Yang, and Gwo-Tarng Sheu. "Association of Wild-Type TP53 with Downregulation of Lovastatin Sensitivity in Human Non-Small Cell Lung Cancer Cells." Current Issues in Molecular Biology 46, no. 9 (2024): 10130–39. http://dx.doi.org/10.3390/cimb46090604.

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Statins inhibit 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), the rate-limiting enzyme of the mevalonate pathway, and reduce cholesterol synthesis. They also have been demonstrated to improve prognosis in patients with various cancers, suggesting a potential anti-cancer effect of statins. However, there is no consensus on the molecular targets of statins for their anti-cancer effects. Docetaxel (DOC) is a microtubule-stabilizing agent currently used as a chemotherapeutic drug in several cancers, including lung cancer. Interestingly, the anti-cancer effects of either drug that are related t

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Pummarin, Siwanut, Natcha Madared, Sotida Kayem, et al. "Different Doxorubicin Sensitivity Across Various Human Cancer Cell Lines." Trends in Sciences 21, no. 12 (2024): 8566. http://dx.doi.org/10.48048/tis.2024.8566.

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Doxorubicin (Dox) is a highly potent chemotherapeutic agent, approved by FDA since 1974, for treating a broad spectrum of cancers. However, development of severe side effects and drug resistance are main issues that limit the clinical use of Dox. Herein, we aimed to investigate the sensitivity of Dox in a variety of human cancer cell lines. Eleven cell lines were tested in this study including 2 hepatocellular carcinoma (HCC) cell lines (HepG2 and Huh7), 4 bladder cancer (BlCa) cell lines (UMUC-3, VMCUB-1, TCCSUP and BFTC-905), a lung cancer cell line (A549), a cervical carcinoma cell line (He

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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 (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-fluor

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Noh, Woo-Chul, Wallace H. Mondesire, Junying Peng, et al. "Determinants of Rapamycin Sensitivity in Breast Cancer Cells." Clinical Cancer Research 10, no. 3 (2004): 1013–23. http://dx.doi.org/10.1158/1078-0432.ccr-03-0043.

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Zhang, Yi, Wendy Schulte, Desmond Pink, et al. "Sensitivity of Cancer Cells to Truncated Diphtheria Toxin." PLoS ONE 5, no. 5 (2010): e10498. http://dx.doi.org/10.1371/journal.pone.0010498.

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8

Candido, Saverio, Stephen L. Abrams, Linda Steelman, 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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9

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

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10

Shariat Razavi, Seyedeh Mahya, Reyhaneh Mahmoudzadeh Vaziri, Gholamreza Karimi, et al. "Crocin Increases Gastric Cancer Cells’ Sensitivity to Doxorubicin." Asian Pacific Journal of Cancer Prevention 21, no. 7 (2020): 1959–67. http://dx.doi.org/10.31557/apjcp.2020.21.7.1959.

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11

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 (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

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12

Bikas, Athanasios, Kirk Jensen, Aneeta Patel, et al. "Glucose-deprivation increases thyroid cancer cells sensitivity to metformin." Endocrine-Related Cancer 22, no. 6 (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

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13

Wang, Ruiping, Yue Han, Zhangxiang Zhao, et al. "Link synthetic lethality to drug sensitivity of cancer cells." Briefings in Bioinformatics 20, no. 4 (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 a

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Jansen, Aaron P., Corinne E. Camalier, Cristi Stark, and Nancy H. Colburn. "Characterization of programmed cell death 4 in multiple human cancers reveals a novel enhancer of drug sensitivity." Molecular Cancer Therapeutics 3, no. 2 (2004): 103–10. http://dx.doi.org/10.1158/1535-7163.103.3.2.

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Abstract Programmed cell death 4 (Pdcd4), originally identified as an inhibitor of murine cellular transformation, inhibits protein synthesis by directly interacting with eukaryotic initiation factor 4A (eIF4A) of the translation initiation complex. The relevance of Pdcd4 to a broad range of human cancers derived from multiple tissue sites is unknown. Protein expression patterns from the National Cancer Institute drug-screening panel of 60 human cancer cells (NCI60) were analyzed by Western blot methods and revealed frequent reduction of Pdcd4 protein levels in renal-, lung-, and glia-derived

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Hámori, Lilla, Gyöngyi Kudlik, Kornélia Szebényi, et al. "Establishment and Characterization of a Brca1−/−, p53−/− Mouse Mammary Tumor Cell Line." International Journal of Molecular Sciences 21, no. 4 (2020): 1185. http://dx.doi.org/10.3390/ijms21041185.

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Breast cancer is the most commonly occurring cancer in women and the second most common cancer overall. By the age of 80, the estimated risk for breast cancer for women with germline BRCA1 or BRCA2 mutations is around 80%. Genetically engineered BRCA1-deficient mouse models offer a unique opportunity to study the pathogenesis and therapy of triple negative breast cancer. Here we present a newly established Brca1−/−, p53−/− mouse mammary tumor cell line, designated as CST. CST shows prominent features of BRCA1-mutated triple-negative breast cancers including increased motility, high proliferati

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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 (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 charac

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17

Kim, Young-Ho, Hyun-Kyoung Kim, Hee Yeon Kim, et al. "FAK-Copy-Gain Is a Predictive Marker for Sensitivity to FAK Inhibition in Breast Cancer." Cancers 11, no. 9 (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 sensit

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18

Criscuolo, Daniela, Rosario Avolio, Giovanni Calice, et al. "Cholesterol Homeostasis Modulates Platinum Sensitivity in Human Ovarian Cancer." Cells 9, no. 4 (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 th

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19

Zhang, Fang, Jian-ying Cui, Hai-feng Gao, et al. "Cancer-associated fibroblasts induce epithelial-mesenchymal transition and cisplatin resistance in ovarian cancer via CXCL12/CXCR4 axis." Future Oncology 16, no. 32 (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 CXC

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20

Rigopoulos, Christos, Ilias Georgakopoulos-Soares, and Apostolos Zaravinos. "A Multi-Omics Analysis of an Exhausted T Cells’ Molecular Signature in Pan-Cancer." Journal of Personalized Medicine 14, no. 7 (2024): 765. http://dx.doi.org/10.3390/jpm14070765.

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T cells are essential tumor suppressors in cancer immunology, but their dysfunction induced by cancer cells can result in T cell exhaustion. Exhausted T cells (Tex) significantly influence the tumor immune environment, and thus, there is a need for their thorough investigation across different types of cancer. Here, we address the role of Tex cells in pan-cancer, focusing on the expression, mutations, methylation, immune infiltration, and drug sensitivity of a molecular signature comprising of the genes HAVCR2, CXCL13, LAG3, LAYN, TIGIT, and PDCD1across multiple cancer types, using bioinformat

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21

Luty, Marcin, Katarzyna Piwowarczyk, Anna Łabędź-Masłowska, et al. "Fenofibrate Augments the Sensitivity of Drug-Resistant Prostate Cancer Cells to Docetaxel." Cancers 11, no. 1 (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 t

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22

Fraser, Cameron, Xingping Qin, Kenichi Shimada, et al. "Abstract 6130: Cancer sensitivity to therapy is constrained by apoptosis regulation in cells of origin." Cancer Research 83, no. 7_Supplement (2023): 6130. http://dx.doi.org/10.1158/1538-7445.am2023-6130.

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Abstract Many chemotherapeutic agents target cellular components or processes that are present in all cancers, yet clinical responses to these agents vary greatly between cancer types and even patient age - the basis for these broad-scale differences are unclear. The vast majority of targeted and cytotoxic cancer therapies including ionizing radiation produce pro-apoptotic signaling in exposed cells, suggesting that the mitochondrial apoptosis sensitivity of cancer cells could act as a central signaling “node” to broadly impact therapy outcomes. To test this, we used BH3 profiling and compleme

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23

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

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24

Guler, Gulfem D., Giuliana P. Mognol, Yuhong Ning, et al. "Abstract A057: Cancer-induced epigenomic changes in circulating immune cells enable breast, colorectal and lung cancer detection." Clinical Cancer Research 30, no. 21_Supplement (2024): A057. http://dx.doi.org/10.1158/1557-3265.liqbiop24-a057.

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Abstract Background: Epigenomic changes via the measurement of 5-hydroxymethylation cytosine (5hmC) in DNA have been shown to enable detection in a variety of cancers including pancreatic and ovarian cancer in plasma-derived cell-free DNA (cfDNA). Here, we investigated whether blood-based 5hmC profiling of genomic DNA (gDNA) derived from cells of the buffy coat (BC) possess signals that enable the detection of breast, colorectal and lung cancers. Method: Blood samples collected in Streck tubes from cancer patients or non-cancer controls were processed to obtain buffy coat and plasma samples. g

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25

Lee, Namgyu, Anne E. Carlisle, Austin Peppers, et al. "xCT-Driven Expression of GPX4 Determines Sensitivity of Breast Cancer Cells to Ferroptosis Inducers." Antioxidants 10, no. 2 (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 u

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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 (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

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Rose, Madison M., Veronica L. Espinoza, Katelyn J. Hoff, et al. "BCL2L11 Induction Mediates Sensitivity to Src and MEK1/2 Inhibition in Thyroid Cancer." Cancers 15, no. 2 (2023): 378. http://dx.doi.org/10.3390/cancers15020378.

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Patients with advanced thyroid cancer, including advanced papillary thyroid cancer and anaplastic thyroid cancer (ATC), have low survival rates because of the lack of efficient therapies available that can combat their aggressiveness. A total of 90% of thyroid cancers have identifiable driver mutations, which often are components of the MAPK pathway, including BRAF, RAS, and RET-fusions. In addition, Src is a non-receptor tyrosine kinase that is overexpressed and activated in thyroid cancer, which we and others have shown is a clinically relevant target. We have previously demonstrated that co

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Marzano, Flaviana, Mariano Francesco Caratozzolo, Graziano Pesole, Elisabetta Sbisà, and Apollonia Tullo. "TRIM Proteins in Colorectal Cancer: TRIM8 as a Promising Therapeutic Target in Chemo Resistance." Biomedicines 9, no. 3 (2021): 241. http://dx.doi.org/10.3390/biomedicines9030241.

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Colorectal cancer (CRC) represents one of the most widespread forms of cancer in the population and, as all malignant tumors, often develops resistance to chemotherapies with consequent tumor growth and spreading leading to the patient’s premature death. For this reason, a great challenge is to identify new therapeutic targets, able to restore the drugs sensitivity of cancer cells. In this review, we discuss the role of TRIpartite Motifs (TRIM) proteins in cancers and in CRC chemoresistance, focusing on the tumor-suppressor role of TRIM8 protein in the reactivation of the CRC cells sensitivity

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29

Tao, Tao, Xiaomei Yang, Qiong Qin, et al. "NHERF1 Enhances Cisplatin Sensitivity in Human Cervical Cancer Cells." International Journal of Molecular Sciences 18, no. 1 (2017): 5. http://dx.doi.org/10.3390/ijms18010005.

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30

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

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31

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

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32

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 (2013): e82220. http://dx.doi.org/10.1371/journal.pone.0082220.

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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 (2007): 1590–99. http://dx.doi.org/10.1002/pros.20644.

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34

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 (2017): 55–74. http://dx.doi.org/10.1002/cpch.21.

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35

Liu, Chengfei, Yezi Zhu, Wei Lou, et al. "Functional p53 determines docetaxel sensitivity in prostate cancer cells." Prostate 73, no. 4 (2012): 418–27. http://dx.doi.org/10.1002/pros.22583.

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36

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 (2018): 395–408. http://dx.doi.org/10.1007/s11302-018-9622-7.

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Yao, Jiahui, and Mingshuai Han. "Effect of the blood cells, inflammatory cytokines, antibodies, circulating metabolome, and immune cells on skin cancers: A bidirectional 2-sample Mendelian randomization study and mediation analysis." Medicine 104, no. 28 (2025): e43233. https://doi.org/10.1097/md.0000000000043233.

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Previous research has highlighted the involvement of several human blood cells in skin cancer, but large-scale studies are lacking to explore their relationship and avoid confounding factors. Here, we comprehensively investigated the causal effect of blood cells on skin cancer subtypes across 4 different human microenvironments through 2-sample Mendelian randomization (MR) analysis and mediation analysis. Summary statistics of 91 human blood cells, 233 circulating metabolites, 731 immune cells, 46 antibody immune responses, 91 inflammatory cytokines, and 4 skin cancer traits (including cutaneo

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Akolkar, Dadasaheb, Darshana Patil, Raymond Page, et al. "Circulating ensembles of tumor-associated cells in gastrointestinal cancers." Journal of Clinical Oncology 38, no. 4_suppl (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, includi

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Lee, Carol, Weixue Mu, Xi July Chen, et al. "Oncogenic Activity and Sorafenib Sensitivity of ARAF p.S214C Mutation in Lung Cancer." Cancers 17, no. 13 (2025): 2246. https://doi.org/10.3390/cancers17132246.

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Background/Objectives: RAF pathway aberrations are one of the hallmarks of lung cancer. Sorafenib is a multi-kinase inhibitor targeting the RAF pathway and is FDA-approved for several cancers, yet its efficacy in lung cancer is controversial. Previous clinical research showed that a ARAF p.S214C mutation exhibited exceptional responsiveness to sorafenib in lung adenocarcinoma. Methods: Considering this promising clinical potential, the oncogenic potential and sorafenib response of the ARAF p.S214C mutation were investigated using lung cancer models. ARAF p.S214C mutant, ARAF wild-type (WT), an

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Asih, Tri Sri Noor, Fajar Adi-Kusumo, Ario Wiraya, and Jonathan Forde. "Numerical Bifurcations and Sensitivity Analysis of an SIVPC Cervical Cancer Model." Communication in Biomathematical Sciences 7, no. 2 (2024): 281–90. https://doi.org/10.5614/cbms.2024.7.2.8.

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We consider a mathematical model of cervical cancer based on the Natural History of Cervical Cancer. The model is a five dimensional system of the first order of ordinary differential equations that represents the interaction between the free Human Papilloma Virus (HPV) population and four cells sub-populations, i.e., the normal cells, infected cells by HPV, precancerous cells, and cancer cells. We focus our analysis to determine the existence conditions of the nontrivial equilibrium point, the bifurcations, and the sensitivity of the parameters that play important roles in metastasis. Based o

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Ziegler, Yvonne, Valeria Sanabria Guillen, Sung Hoon Kim, John A. Katzenellenbogen, and Benita S. Katzenellenbogen. "Transcription Regulation and Genome Rewiring Governing Sensitivity and Resistance to FOXM1 Inhibition in Breast Cancer." Cancers 13, no. 24 (2021): 6282. http://dx.doi.org/10.3390/cancers13246282.

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Forkhead box M1 (FOXM1), an oncogenic transcription factor associated with aggressiveness and highly expressed in many cancers, is an emerging therapeutic target. Using novel 1,1-diarylethylene-diammonium small molecule FOXM1 inhibitors, we undertook transcriptomic, protein, and functional analyses to identify mechanisms by which these compounds impact breast cancer growth and survival, and the changes that occur in estrogen receptor (ERα)-positive and triple negative breast cancer cells that acquire resistance upon long-term treatment with the inhibitors. In sensitive cells, these compounds r

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Park, Jaewoo, Min Sung Joo, JaeYung Lee, et al. "Abstract 386: High CRBN expression in neuroendocrine cancer creates a vulnerability to GSPT1 molecular glue degraders: Target indication selection for CYRS1542 development." Cancer Research 85, no. 8_Supplement_1 (2025): 386. https://doi.org/10.1158/1538-7445.am2025-386.

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Abstract Multiple companies have been developing GSPT1-targeted molecular glue degraders (MGDs) for neuroendocrine (NE) cancers, a rare and aggressive cancer type. CYRS1542, a potent and orally bioavailable GSPT1 MGD with a superior therapeutic index, was identified and derived from CYRS381 (originally known as SJ6986) in our previous work (Joo et al., AACR 2024). In this study, we investigated the mechanistic basis of GSPT1 MGD sensitivity in NE cancers, using CYRS381 as a tool compound to assess selective susceptibilities. We found that CYRS381-induced GSPT1 degradation was selectively effec

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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 (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 r

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Voutsadakis, Ioannis A. "Molecular Alterations and Putative Therapeutic Targeting of Planar Cell Polarity Proteins in Breast Cancer." Journal of Clinical Medicine 12, no. 2 (2023): 411. http://dx.doi.org/10.3390/jcm12020411.

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Background: Treatment and outcomes of breast cancer, one of the most prevalent female cancers, have improved in recent decades. However, metastatic breast cancer remains incurable in most cases, and new therapies are needed to ameliorate prognosis. Planar cell polarity (PCP) is a characteristic of epithelial cells that form layers and is integral to the communication of these cells with neighboring cells. Dysfunction of PCP is observed in cancers and may confer a targetable vulnerability. Methods: The breast cancer cohorts from The Cancer Genome Atlas (TCGA) and the METABRIC study were interro

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Chandimali, Nisansala, Hyebin Koh, Jihwan Kim, et al. "BRM270 targets cancer stem cells and augments chemo‑sensitivity in cancer (Review)." Oncology Letters 20, no. 4 (2020): 1. http://dx.doi.org/10.3892/ol.2020.11964.

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Srinivasan, Ajay, Dadasaheb B. Akolkar, Pradip Fulmali, et al. "Circulating ensembles of tumor-associated cells in genitourinary cancers." Journal of Clinical Oncology 38, no. 6_suppl (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. The

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Ou, Mengting, Shun Li, and Liling Tang. "PRDM14: A Potential Target for Cancer Therapy." Current Cancer Drug Targets 18, no. 10 (2018): 945–56. http://dx.doi.org/10.2174/1568009618666180430143055.

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PRDM14 belongs to the PR domain-containing (PRDM) family. Although a precise understanding focused on the function of PRDM14 to maintain stemness and pluripotency in embryonic stem cells via epigenetic mechanisms, growing experimental evidence has been linked PRDM14 to human cancers. In adults, PRDM14 has low expression in human tissues. Aberrant PRDM14 expression is connected with various malignant histological types and solid cancers, where PRDM14 can act as a driver of oncogenic processes. Overexpression of RPDM14 enhanced cancer cells growth and reduced cancer cells sensitive to chemothera

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Abali, Fikri, Narges Baghi, Lisanne Mout, Joska J. Broekmaat, Arjan G. J. Tibbe, and Leon W. M. M. Terstappen. "Measurement of the Drug Sensitivity of Single Prostate Cancer Cells." Cancers 13, no. 23 (2021): 6083. http://dx.doi.org/10.3390/cancers13236083.

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The treatment of cancer faces a serious challenge as cancer cells within patients are heterogeneous and frequently resistant to therapeutic drugs. Here, we introduce a technology enabling the assessment of single cancer cells exposed to different drugs. PCa cells were individually sorted in self-seeding microwells, cultured for 24 h, and then exposed to several drugs to induce (R1881) or inhibit (Enzalutamide/Abiraterone) the secretion of a protein (PSA). Cell viability and PSA secretion of each individual prostate cell were monitored over a 3-day period. The PSA protein secreted by each cell

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Williams, King, Emmanson Godswill, Chiamaka Mercy, et al. "Study of Gynecological Cancer Heterogeneity in Breast and Ovarian Cancer Models Using Induced Pluripotent Stem Cells." Journal of Cancer and Tumor International 14, no. 4 (2024): 1–17. http://dx.doi.org/10.9734/jcti/2024/v14i4262.

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Gynecological cancers, notably breast and ovarian cancers, exhibit significant heterogeneity, complicating treatment strategies and impacting patient outcomes. Traditional cancer models often fail to capture the complexity and diversity of these tumors. Induced pluripotent stem cells (iPSCs) offer a promising alternative for modeling cancer due to their ability to differentiate into various cell types. This study aims to establish and characterize iPSC-derived models of breast and ovarian cancers to explore their heterogeneity and therapeutic responses. We cultured iPSCs and differentiated the

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Hou, Guiqin, Yiru Bai, Ang Jia, et al. "Inhibition of autophagy improves resistance and enhances sensitivity of gastric cancer cells to cisplatin." Canadian Journal of Physiology and Pharmacology 98, no. 7 (2020): 449–58. http://dx.doi.org/10.1139/cjpp-2019-0477.

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Autophagy plays critical roles in tumorigenesis, while the effects of autophagy on chemoresistance of cancer cells had great disparity. This study aims to explore the impacts of autophagy on the sensitivity and resistance of gastric cancer cells to cisplatin (DDP). We firstly demonstrated that there was stronger autophagy activity in gastric cancer SGC-7901 cells than that in DDP-resisting SGC-7901/DDP cells. Then, we discovered that inhibiting autophagy by chloroquine (CQ) significantly enhanced the proliferation-inhibiting and apoptosis-inducing effects of DDP to SGC-7901 and SGC-7901/DDP ce

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