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Thematische Bibliographien / Sensitivity of the cancer cells

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Auswahl der wissenschaftlichen Literatur zum Thema „Sensitivity of the cancer cells“

Autor: Grafiati

Veröffentlicht am 28. Juni 2021

Zuletzt aktualisiert am 4. Februar 2022

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Zeitschriftenartikel zum Thema "Sensitivity of the cancer cells"

1

De Maria, R. „5 Drug sensitivity of cancer stem cells“. European Journal of Cancer Supplements 8, Nr. 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, Nr. 6 (11.09.2015): 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, Nr. 4 (28.12.2017): 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 und Fatemeh Kalalinia. „Crocin Increases Gastric Cancer Cells’ Sensitivity to Doxorubicin“. Asian Pacific Journal of Cancer Prevention 21, Nr. 7 (01.07.2020): 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 und Funda Meric-Bernstam. „Determinants of Rapamycin Sensitivity in Breast Cancer Cells“. Clinical Cancer Research 10, Nr. 3 (01.02.2004): 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 und David Morton Waisman. „Sensitivity of Cancer Cells to Truncated Diphtheria Toxin“. PLoS ONE 5, Nr. 5 (05.05.2010): 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 (Mai 2018): 13–30. http://dx.doi.org/10.1016/j.jbior.2018.02.002.

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Karagkounis, Georgios, Jennifer DeVecchio, Sylvain Ferrandon und Matthew F. Kalady. „Simvastatin enhances radiation sensitivity of colorectal cancer cells“. Surgical Endoscopy 32, Nr. 3 (15.09.2017): 1533–39. http://dx.doi.org/10.1007/s00464-017-5841-1.

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Liang, Zhiyu, und Chuan Li. „Downregulation of miR-24 Enhances Cisplatin Sensitivity in Breast Cancer Cells“. Journal of Biomaterials and Tissue Engineering 11, Nr. 8 (01.08.2021): 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, und Ruth J. Muschel. „Targeting tumor cells by enhancing radiation sensitivity“. Genes, Chromosomes and Cancer 38, Nr. 4 (14.10.2003): 330–38. http://dx.doi.org/10.1002/gcc.10296.

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Dissertationen zum Thema "Sensitivity of the cancer cells"

1

Tong, Zhimin. „The mechanisms of cellular sensitivity to photodynamic therapy /“. *McMaster only, 2001.

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Landry, Benjamin D. „Tumor-stroma interactions differentially alter drug sensitivity based on the origin of stromal cells“. eScholarship@UMMS, 2018. https://escholarship.umassmed.edu/gsbs_diss/1011.

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Tumor heterogeneity observed between patients has made it challenging to develop universal or broadly effective cancer therapies. Therefore, an ever-growing movement within cancer research aims to tailor cancer therapies to individual patients or specific tumor subtypes. Tumor stratification is generally dictated by the genomic mutation status of the tumor cells themselves. Importantly, non-genetic influences – such as interactions between tumor cells and other components of the tumor microenvironment – have largely been ignored. Therefore, in an effort to increase treatment predictability and efficacy, we investigated how tumor-stroma interactions contribute to drug sensitivity and drug resistance. I designed a high throughput co-culture screening platform to measure how tumor-stroma interactions alter drug mediated cell death. I identified tumor-stroma interactions that strongly desensitize or sensitize cancer cells to various drug treatments. The directionality of these observed phenotypes was dependent on the stromal cell tissue of origin. Further study revealed that interactions between tumor cells and fibroblasts modulate apoptotic priming in tumor cells to mediate sensitivity to chemotherapeutics. The principles uncovered in this study have important implications on the use of drugs that are designed to enhance apoptosis. For example, based on our screening data, I hypothesized and experimentally validated that the effectiveness of BH3 mimetic compounds would be strongly dependent on the fibroblast growth environment. Taken together, our study highlights the importance of understanding how environmental interactions alter the drug responses of cancer cells and reveals a mechanism by which stromal cells drive broad spectrum changes in tumor cell sensitivities to common chemotherapeutics.

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Ferguson, Paul R. „The role of thymidylate synthase in modulating sensitivity to chemotherapeutic agents“. Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326399.

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Fung, Ka-lai. „Significance of MAD2 in mitotic checkpoint control and cisplatin sensitivity of testicular germ cell tumour cells“. View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38588912.

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Kanwal, Shahzina. „Effect of O-GlcNAcylation on tamoxifen sensitivity in breast cancer derived MCF-7 cells“. Phd thesis, Université René Descartes - Paris V, 2013. http://tel.archives-ouvertes.fr/tel-00912341.

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One of the hallmarks of cancer cells is to exhibit increased uptake and consumption of glucose.3-5% of the glucose entering into the cell leads to a minor pathway of the glucose metabolismknown as the hexosamine biosynthetic pathway (HBP). UDP-N-acetylglucosamine is the endproduct of HBP and is used as substrate by OGT (O-GlcNAc transferase) to modify diverserange of nuclear and cytoplasmic proteins with a recently characterized post-translationalmodification called O-GlcNAcylation. It corresponds to the addition of sugar moiety O-linked β-N-acetylglucosamine (O-GlcNAc) on serine or threonine residue of proteins. This process isantagonized by another enzyme called O-GlcNAcase (OGA). Recent studies indicated thepresence of increased O-GlcNAcylation level in several cancer cells. Moreover, inhibition ofOGT has been shown to reduce in vivo and in vitro tumor growth of breast cancer cells.However, the relationship between O-GlcNAcylation and the response to anti-cancer therapy hasnot been studied. Tamoxifen is the oldest and most prescribed selective-estrogen receptormodulator (SERM) for patients with estrogen receptor (ER)-positive breast cancer. Tamoxifen isknown to reduce tumor growth and invasion. Despite its beneficial effects de novo and acquiredresistance are great obstacles in its clinical effectiveness. We found that O-GlcNAc elevation inMCF-7 cells protected them from tamoxifen-induced cell death. Increased O-GlcNAc alsoincreased PI3-K/Akt signaling. However, the protective effect of PUGNAc+glucosamine fromtamoxifen-induced cell death is independent of PI3K/Akt pathway. Increased O-GlcNAcylationalso led to reduced ESR1 promoter activity and decreased expression of ERα at mRNA andprotein levels. The decrease in ERα expression is correlated with a reduced expression of twotamoxifen regulated genes i.e. early growth response 1 and p21 Waf1/Cip1. In conclusion, thisstudy showed for the first time the involvement of O-GlcNAcylation in reducing tamoxifen142sensitivity in MCF-7 cells. Thus, OGT can act as a novel therapeutic target for treatment oftamoxifen resistant cells.

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Sureechatchaiyan, Paichat [Verfasser]. „Role of Purinergic Ligands to Enhance Cisplatin Sensitivity in Ovarian Cancer Cells / Paichat Sureechatchaiyan“. Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2017. http://d-nb.info/1148066756/34.

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Fung, Ka-lai, und 馮家禮. „Significance of MAD2 in mitotic checkpoint control and cisplatin sensitivity of testicular germ cell tumour cells“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39357727.

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Zhang, Pingde, und 张萍德. „TAp73α enhances the cellular sensitivity to cisplatin in ovarian cancer cells via the JNK signaling pathway“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47752944.

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Ovarian cancer is the most lethal gynecological malignancy. Most of ovarian cancer patients relapse and subsequently die due to the development of resistance to chemotherapy. P73 belongs to the tumor suppressor p53 family. Like p53, the transcriptionally active TAp73 can bind specifically to p53 responsive elements and transactivates some of the p53 target genes, and finally leads to cell cycle arrest and apoptosis. TAp73 can be induced by DNA damage to enhance cellular sensitivity to anticancer agents in human cancer cells. However, the functions of TAp73 in ovarian cancer cells and the role in the regulation of cellular response to commonly used chemotherapeutic agents cisplatin are still poorly understood. The aims of this study were to examine the functions of TAp73 in ovarian cancer cells and its role in cellular response to cisplatin, as well as the relationship between TAp73 and p53 in ovarian cancer cells. Functional studies showed that over-expression of TAp73alpha (TAp73α) inhibited cell proliferation, colony formation ability and anchorage-independent growth of ovarian cancer cells, and this was irrespective of p53 expression status. In addition, TAp73α inhibited cell growth by arresting cell cycle at G2/M phase and up-regulating the expressions of G2/M regulators of p21, 14-3-3sigma and GADD45α. TAp73α enhanced the cellular sensitivity to cisplatin through the activation of JNK signaling pathway, at least partially, in ovarian cancer cells. TAp73α activated the JNK pathway through the up-regulation of its target gene GADD45α and subsequent activation of MKK4, the JNK up-stream kinase. Inhibition of JNK activity by a specific inhibitor (SP600125) or small interfering RNAs (siRNAs) significantly abrogated TAp73-mediated apoptosis induced by cisplatin. Moreover, the activations of MKK4, JNK and c-Jun were abolished when GADD45α was knocked down by siRNAs, and the JNK-dependent apoptosis was not observed. Collectively, these results supported that TAp73α was able to mediate apoptotic response to cisplatin through the GADD45α/MKK4/JNK signaling pathway, which was respective of p53 expression status. Further investigation on the relationship between TAp73α and p53 demonstrated that TAp73α increased p53 protein, but not mRNA expression by attenuating p53 protein degradation in wild-type p53 ovarian cancer cells. TAp73α could directly interact with p53 protein, which might interfere with the binding ability of MDM2 to p53, and consequently block the p53 protein degradation. In addition, TAp73α inactivated the Akt and ERK pathways and activated the p38 pathway in response to cisplatin in wild-type p53 OVCA433, but not in null-p53 SKOV3 cells, suggesting that the effect of TAp73α on these pathways might be p53-dependent. These results indicated that a functional cooperation of TAp73α and p53, to some extent, existed in ovarian cancer cells. In conclusion, this study demonstrated that TAp73α acted as a tumor suppressor in ovarian carcinogenesis. It promoted the cellular sensitivity to cisplatin via, at least partially, the activation of JNK signaling pathway. These TAp73α functions were irrespective of p53 expression. In addition, TAp73α was able to bind to p53 and increase p53 expression.
published_or_final_version
Obstetrics and Gynaecology
Doctoral
Doctor of Philosophy

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Newbury, Golnar. „A Numerical Study of a Delay Differential Equation Model for Breast Cancer“. Thesis, Virginia Tech, 2007. http://hdl.handle.net/10919/34420.

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In this thesis we construct a new model of the immune response to the growth of breast cancer cells and investigate the impact of certain drug therapies on the cancer. We use delay differential equations to model the interaction of breast cancer cells with the immune system. The new model is constructed by combining two previous models. The first model accounts for different cell cycles and includes terms to evaluate drug treatments, but ignores quiescent tumor cells. The second model includes quiescent cells, but ignores the immune response and drug treatments. The new model is obtained by combining and modifying these two models to account for quiescent cells, immune cells and includes drug intervention terms. This new model is used to evaluate the effects of pulsed applications of the drug Paclitaxel for models with and without quiescent cells. We use sensitivity equation methods to analyze the sensitivity of the model with respect to the initial number of immune cytotoxic T-cells. Numerical experiments are conducted to compare the model predictions to observed behavior.
Master of Science

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Dilruba, Shahana [Verfasser]. „Impact of ERK signaling and its spatial regulation on cisplatin sensitivity in ovarian cancer cells / Shahana Dilruba“. Bonn : Universitäts- und Landesbibliothek Bonn, 2019. http://d-nb.info/1220912638/34.

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Bücher zum Thema "Sensitivity of the cancer cells"

1

Steinberg, Ken. Effects of structural domains of Raf-1 on the sensitivity of MCF-7 breast cancer cells to Taxol (Paclitaxel). Sudbury, Ont: Laurentian University, School of Graduate Studies, 2005.

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Cancer stem cells. Hauppauge, N.Y: Nova Science Publishers, 2010.

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Yu, John S., Hrsg. Cancer Stem Cells. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-280-9.

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Rajasekhar, Vinagolu K., Hrsg. Cancer Stem Cells. Hoboken, NJ: John Wiley & Sons, 2014. http://dx.doi.org/10.1002/9781118356203.

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Bapat, Sharmila, Hrsg. Cancer Stem Cells. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2008. http://dx.doi.org/10.1002/9780470391594.

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Wiestler, O. D., B. Haendler und D. Mumberg, Hrsg. Cancer Stem Cells. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-70853-7.

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Papaccio, Gianpaolo, und Vincenzo Desiderio, Hrsg. Cancer Stem Cells. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7401-6.

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Farrar, William L., Hrsg. Cancer Stem Cells. Cambridge: Cambridge University Press, 2009. http://dx.doi.org/10.1017/cbo9780511605536.

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Okudela, Koji. Cancer stem cells in lung cancer. Hauppauge, N.Y: Nova Science Publishers, 2010.

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Salter, Russell D., und Michael R. Shurin, Hrsg. Dendritic Cells in Cancer. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-88611-4.

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Buchteile zum Thema "Sensitivity of the cancer cells"

1

Saeed, Mohamed, Henry Johannes Greten und Thomas Efferth. „Collateral Sensitivity in Drug-Resistant Tumor Cells“. In Resistance to Targeted Anti-Cancer Therapeutics, 187–211. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7070-0_10.

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Lebert-Ghali, Charles-Etienne, Joanne Margaret Ramsey, Alexander Thompson und Janetta Bijl. „Sensitivity of Hematopoietic and Leukemic Stem Cells to Hoxa Gene Levels“. In Stem Cells and Cancer Stem Cells, Volume 4, 19–29. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2828-8_2.

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Yoshida, Tatsushi, und Toshiyuki Sakai. „Agents that Regulate DR5 and Sensitivity to TRAIL“. In Sensitization of Cancer Cells for Chemo/Immuno/Radio-therapy, 41–49. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-474-2_4.

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Stahl, Sebastian, Fabian Mueller, Ira Pastan und Ulrich Brinkmann. „Factors that Determine Sensitivity and Resistances of Tumor Cells Towards Antibody-Targeted Protein Toxins“. In Resistance to Targeted Anti-Cancer Therapeutics, 57–73. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17275-0_3.

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Brown, J. Martin, und Bradly G. Wouters. „Does Apoptosis Contribute to Tumor Cell Sensitivity to Anticancer Agents?“ In Apoptosis and Cancer Chemotherapy, 1–19. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-720-8_1.

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Quinones, Addison, und Anne Le. „The Multifaceted Glioblastoma: From Genomic Alterations to Metabolic Adaptations“. In The Heterogeneity of Cancer Metabolism, 59–76. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_4.

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AbstractGlioblastoma multiforme (GBM) develops on glial cells and is the most common as well as the deadliest form of brain cancer. As in other cancers, distinct combinations of genetic alterations in GBM subtypes induce a diversity of metabolic phenotypes, which explains the variability of GBM sensitivity to current therapies targeting its reprogrammed metabolism. Therefore, it is becoming imperative for cancer researchers to account for the temporal and spatial heterogeneity within this cancer type before making generalized conclusions about a particular treatment’s efficacy. Standard therapies for GBM have shown little success as the disease is almost always lethal; however, researchers are making progress and learning how to combine therapeutic strategies most effectively. GBMs can be classified initially into two subsets consisting of primary and secondary GBMs, and this categorization stems from cancer development. GBM is the highest grade of gliomas, which includes glioma I (low proliferative potential), glioma II (low proliferative potential with some capacity for infiltration and recurrence), glioma III (evidence of malignancy), and glioma IV (GBM) (malignant with features of necrosis and microvascular proliferation). Secondary GBM develops from a low-grade glioma to an advanced-stage cancer, while primary GBM provides no signs of progression and is identified as an advanced-stage glioma from the onset. The differences in prognosis and histology correlated with each classification are generally negligible, but the demographics of individuals affected and the accompanying genetic/metabolic properties show distinct differentiation [3].

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Crescimanno, M., N. Borsellino, V. Leonardi, L. Rausa und N. D’Alessandro. „Effects of Tumor Necrosis Factor-Alpha on Growth and Doxorubicin Sensitivity of Multidrug Resistant Tumor Cell Lines“. In Cancer Therapy, 201–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84613-7_16.

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Derweesh, Ithaar H., Luis Molto, Charles Tannenbaum, Patricia Rayman, Christina Moon, Cynthia Combs, Thomas Olencki, Paul Elson, Ronald M. Bukowski und James H. Finke. „Alterations in T-Cell Signaling Pathways and Increased Sensitivity to Apoptosis“. In Cancer Immunotherapy at the Crossroads, 119–44. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-743-7_7.

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Wong, Yong-Chuan, Xiao-Meng Zhang, Ming-Tak Ling und Xiang-Hong Wang. „Inactivation of ID-1 Gene Induces Sensitivity of Prostate Cancer Cells to Chemotherapeutic Drugs“. In Hormonal Carcinogenesis V, 565–72. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-69080-3_58.

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Bose, Mayil Vahanan, und Thangarajan Rajkumar. „Assessment of the Radiation Sensitivity of Cervical Cancer Cell Lines“. In Methods in Molecular Biology, 351–62. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2013-6_26.

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Konferenzberichte zum Thema "Sensitivity of the cancer cells"

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Tang, Xin, Tony Cappa, Theresa B. Kuhlenschmidt, Mark S. Kuhlenschmidt und Taher A. Saif. „Studying the Mechanical Sensitivity of Human Colon Cancer Cells Through a Novel Bio-MEMS Force Sensor“. In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13237.

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Cancer deaths are primarily caused by metastases, not by the parent tumor. During the metastasis, malignant cancer cells detach from the parent tumor, and spread through the patient’s circulatory system to invade new tissues and organs [1]. To study the role played by the mechanical microenvironment on the cancer cell growth and malignancy promotion, we cultured human colon carcinoma (HCT-8) cells in vitro on substrates with varied mechanical stiffness, from the physiologically relevant 1 kPa, 20 kPa to very stiff 3.5 GPa. A novel and versatile micro-electromechanical systems (Bio-MEMS) force sensor [2] is developed to quantify the strength of non-specific adhesion between living cancer cells membrane and probe, an important hallmark of cancer cell malignancy level. Immunoflurescent staining and Confocal microscopy imaging are used to visualize the cellular organelle organization and cooperate to explore the underlying mechanism.

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Song, Ji-Hong, Woo-Young Kim und Yong-Yeon Cho. „Abstract 356: Mutaome-based magnolin sensitivity in ovarian cancer cells“. In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-356.

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Fan, Z. Hugh, Weian Sheng, Thomas George und Chen Liu. „Abstract IA21: Enumeration of circulating tumor cells for studying cancer drug sensitivity“. In Abstracts: AACR Precision Medicine Series: Drug Sensitivity and Resistance: Improving Cancer Therapy; June 18-21, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.pms14-ia21.

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4

Kulsum, Safeena, Sindhu VG, Ramanan Somasundara Pandian, Debashish Das, Binay Panda, Wesley Hicks, Mukund Seshadri, Moni Abraham Kuriakose und Amritha Suresh. „Abstract A08: Cancer stem cell-like cells in drug resistance of head and neck squamous cell carcinoma“. In Abstracts: AACR Precision Medicine Series: Drug Sensitivity and Resistance: Improving Cancer Therapy; June 18-21, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.pms14-a08.

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5

Liu, Jingchun, Darryl T. Martin, Marcia A. Wheeler und Robert M. Weiss. „Abstract B21: Chemoresistant bladder cancer cells induces epithelial mesenchymal transition“. In Abstracts: AACR Precision Medicine Series: Drug Sensitivity and Resistance: Improving Cancer Therapy; June 18-21, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.pms14-b21.

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6

Pelosof, Lorraine, Sashidhar Yerram, Nilofer Azad und James Herman. „Abstract 652:GPX3promoter hypermethylation predicts platinum sensitivity in colorectal cancer cells.“ 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.am2013-652.

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7

Chang, Shih-Shin, Hirohito Yamaguchi und Mien-Chie Hung. „Abstract B03: Cisplatin-resistant cells possess collateral sensitivity to folate antimetabolites“. In Abstracts: AACR Precision Medicine Series: Drug Sensitivity and Resistance: Improving Cancer Therapy; June 18-21, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.pms14-b03.

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8

Lopez-Diaz, Fernando, Mei-Chong Wendy Lee, Muhammad Tariq, Shahid Khan, Yelena Dayn, Charlie Vaske, Nader Pourmand und Beverly M. Emerson. „Abstract A09: Single-cell RNA sequencing reveals phenotypic plasticity of drug tolerant, clonal populations of cancer cells“. In Abstracts: AACR Precision Medicine Series: Drug Sensitivity and Resistance: Improving Cancer Therapy; June 18-21, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.pms14-a09.

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9

Eunkyoung, Choi, Jung Hana, Ahn Hojung, Hong Seung-Woo, Moon Jai-Hee, Shin Jae-Sik, Kim Kyu-Pyo et al. „Abstract A46: INCB018424 induces apoptotic cell death through the suppression of pJAK1 in human colon cancer cells“. In Abstracts: AACR Precision Medicine Series: Drug Sensitivity and Resistance: Improving Cancer Therapy; June 18-21, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.pms14-a46.

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10

Lupo, Barbara, Jorge Vialard, Andrea Bertotti, Letizia Lanzetti und Livio Trusolino. „Abstract A48: Tankyrase inhibitors impair directional cell migration of cancer cells by affecting microtubule dynamics and polarity signals“. In Abstracts: AACR Precision Medicine Series: Drug Sensitivity and Resistance: Improving Cancer Therapy; June 18-21, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.pms14-a48.

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Berichte der Organisationen zum Thema "Sensitivity of the cancer cells"

1

McConkey, David J. Cell Cycle Dependence of TRAIL Sensitivity in Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, November 2006. http://dx.doi.org/10.21236/ada466697.

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2

McConkey, David J. Cell Cycle Dependence of TRIAL Sensitivity in Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, November 2007. http://dx.doi.org/10.21236/ada481365.

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3

Londono-Joshi, Angelina I. Sensitivity of Breast Cancer Stem Cells to TRA-8 Anti-DR5 Monoclonal Antibody. Fort Belvoir, VA: Defense Technical Information Center, Februar 2013. http://dx.doi.org/10.21236/ada577680.

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4

Joshi, Angelina L. Sensitivity of Breast Cancer Stem Cells to TRA-8 Anti-DR5 Monoclonal Antibody. Fort Belvoir, VA: Defense Technical Information Center, Februar 2012. http://dx.doi.org/10.21236/ada560119.

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5

Langland, Gregory T. Establishment of an 'In Vitro Cell-Based System' to Assay Radiation Sensitivity in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, Mai 2007. http://dx.doi.org/10.21236/ada472420.

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6

Markovic, Dubravka, und Edward P. Cohen. Treatment of Breast Cancer with Immunogenic Cells Transfected with DNA from Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, Juli 2001. http://dx.doi.org/10.21236/ada396744.

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7

J, Bull Richard, und Larry E. Anderson. Sensitivity to Radiation-Induced Cancer in Hemochromatosis. Office of Scientific and Technical Information (OSTI), Juni 2000. http://dx.doi.org/10.2172/833475.

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8

Lau, Lester. Growth Suppressors of Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada382887.

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9

Doxsey, Stephen. Midbody Accumulation in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, August 2009. http://dx.doi.org/10.21236/ada516482.

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10

Lagasse, Eric. Ovarian Cancer, Stem Cells, and Bioreactors. Fort Belvoir, VA: Defense Technical Information Center, Oktober 2009. http://dx.doi.org/10.21236/ada517343.

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