Relevant bibliographies by topics / Colon cell lines

Academic literature on the topic 'Colon cell lines'

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Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "Colon cell lines"

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O’Donoghue, Tristan, and Andrej Podlutsky. "DNA Repair in Colon Cancer Cell Lines." FASEB Journal 34, S1 (April 2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.08754.

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Kleivi, Kristine, Manuel R. Teixeira, Mette Eknæs, Chieu B. Diep, Kjetill S. Jakobsen, Richard Hamelin, and Ragnhild A. Lothe. "Genome signatures of colon carcinoma cell lines." Cancer Genetics and Cytogenetics 155, no. 2 (December 2004): 119–31. http://dx.doi.org/10.1016/j.cancergencyto.2004.03.014.

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Yang, S. K., L. Eckmann, and M. F. Kagnoff. "Colon epithelial cell lines express multiple chemokines." Gastroenterology 108, no. 4 (April 1995): A946. http://dx.doi.org/10.1016/0016-5085(95)28090-1.

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VAN KLINKEN, B. JAN-WILLEM, ESMERALDA OUSSOREN, JAN-JOHAN WEENINK, HANS A. BÜLLER, JAN DEKKER, and ALEXANDRA W. C. EINERHAND. "Mucin expression in colon adenocarcinoma cell lines." Biochemical Society Transactions 23, no. 4 (November 1, 1995): 529S. http://dx.doi.org/10.1042/bst023529s.

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Warns, Jessica, Gurdeep Marwarha, Natalie Freking, and Othman Ghribi. "27-hydroxycholesterol decreases cell proliferation in colon cancer cell lines." Biochimie 153 (October 2018): 171–80. http://dx.doi.org/10.1016/j.biochi.2018.07.006.

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Reda, F., J. Borjac, R. Fakhouri, and J. Usta. "Cytotoxic effect ofMoringa oleiferaon colon cancer cell lines." Acta Horticulturae, no. 1158 (April 2017): 269–78. http://dx.doi.org/10.17660/actahortic.2017.1158.30.

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Ophir, I., E. Cohen, and Y. Ben Shaul. "Apical polarity in human colon carcinoma cell lines." Tissue and Cell 27, no. 6 (December 1995): 659–66. http://dx.doi.org/10.1016/s0040-8166(05)80021-7.

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Hasenoehrl, Carina, David Feuersinger, Melanie Kienzl, and Rudolf Schicho. "GPR55-Mediated Effects in Colon Cancer Cell Lines." Medical Cannabis and Cannabinoids 2, no. 1 (February 22, 2019): 22–28. http://dx.doi.org/10.1159/000496356.

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The cannabinoid-responsive G protein-coupled receptor GPR55 and its endogenous ligand L-α-lysophosphatidyl­inositol (LPI) have been reported to play a role in several cancers. A proliferation-enhancing effect of GPR55 has been described for several cancer cell lines and LPI has been found elevated in cancer patients. The aim of this study was to investigate whether GPR55 signaling had an effect on the proliferation of colon cancer cell lines. Using cell viability assays and Western blotting, we show that stable overexpression of the GPR55 receptor led to a growth advantage of SW480 cells per se. Proliferation of native colon cancer cell lines, however, was not affected by pharmacological manipulation of GPR55. Interestingly though, GPR55 signaling was responsive to treatment with both the GPR55 agonist LPI and the antagonist CID16020046 in the overexpressing cancer cell lines. This was evident through significantly increased or decreased levels of phosphorylated ERK1/2, respectively. Taken together, our findings suggest that GPR55 is constitutively activated in overexpressing colon cancer cells affecting ERK1/2 phosphorylation and cell proliferation.
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Imperlini, Esther, Irene Colavita, Marianna Caterino, Peppino Mirabelli, Daniela Pagnozzi, Luigi Del Vecchio, Rosa Di Noto, Margherita Ruoppolo, and Stefania Orrù. "The secretome signature of colon cancer cell lines." Journal of Cellular Biochemistry 114, no. 11 (September 13, 2013): 2577–87. http://dx.doi.org/10.1002/jcb.24600.

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Russo, Suzanne, Nan Li, Kevin Lee, Yaguang Xi, Bing Zhu, Bernard Gary, Veronica Ramirez, et al. "Phosphodiesterase 10, a novel target in colon cancer." Journal of Clinical Oncology 32, no. 3_suppl (January 20, 2014): 503. http://dx.doi.org/10.1200/jco.2014.32.3_suppl.503.

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503 Background: Elevation of intracellular cGMP is known to inhibit tumor proliferation and induce apoptosis, although the phosphodiesterase (PDE) isozymes that regulate cGMP levels in tumor cells have not been well studied. We report first evidence that PDE10 is elevated in colon tumors compared with normal colon and suggest that PDE10 inhibitors can be used for the treatment or prevention of colon cancer. Methods: PDE10 protein and mRNA levels were measured in human colon tumor cells (HT29, HCT116, SW480, Caco2), normal colonocytes (NCM460), human clinical samples, and ApcMin/+ mouse model. Two chemically distinct PDE10 selective inhibitors, PQ-10 and Pf-2545920, were tested against the cell lines. The NCI-60 panel of human tumor cell lines was also screened against Pf-2545920 to identify potential differences in sensitivity among histologically diverse tumor types. We also performed siRNA knockdown studies in colonocytes and tumor cell lines. To determine the effect of the PDE10 siRNA knockdown on cyclic nucleotide hydrolysis, whole cell lysates from transfected cells were assayed for PDE activity using cGMP or cAMP as substrates. Results: PDE10 levels were low in normal colonocytes (NCM460) and elevated in tumor cell lines. Similarly, PDE10 was elevated human clinical specimens and the ApcMin+/ mouse model compared with normal mucosa. PDE10 inhibitors and siRNA selectively inhibited colonic tumor growth while stable knockdown inhibited colony formation and increased doubling time. Pf-2545920 also supressed growth of all cell lines within the NCI-60 panel. In comparison with lysates from vector control cells, transfection with PDE10 siRNA reduced cGMP hydrolysis by ~35% in both HCT116 and HT29 cell lines, but did not affect cGMP hydrolysis in colonocytes; siRNA did not significantly affect cAMP degradation in all 3 cell lines. Conclusions: PDE10 plays a role in colon tumorgenesis whereby inhibitors can selectively suppress tumor cell growth. The mechanism by which PDE10 inhibition affects growth appears to involve activation of cGMP/PKG signalling. PDE10 represents a novel anticancer target for the treament and prevention of colon cancer.
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Dissertations / Theses on the topic "Colon cell lines"

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Limer, Jane Louise. "Cell cycle regulation of human colon adenocarcinoma cell lines by transforming growth factor-#beta#1." Thesis, University of Sheffield, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392353.

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Gardner, Austin, Sam Ngata, La'Travia Howard, Caden Cox, and Victoria Palau. "Metabolic Targets of Gnaphalin Mediated Apoptosis in Colon and Pancreatic Cancer Cell Lines." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/63.

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Colorectal and pancreatic cancer are leading causes of cancer related mortality, suggesting the need for further development of treatment approaches. Gnaphalin, a flavone derived from Gnaphalium gracile H. B. K. which is found in the Andean regions of South America, has shown anti-proliferative properties in solid tumors. Further investigation has shown this compound interferes with signaling conducive to proliferation and cell adhesion, inducing the cell to undergo apoptosis. The primary objective of the study was to look at key regulatory proteins in the cell survival and proliferative pathways to determine Gnaphalin’s mechanism of action. Cytotoxic activity was measured using MTT analysis on the colon cancer cell lines Caco2 and HCT-116, and on the pancreatic cancer cell lines MIA PaCa and Panc28. Apoptosis was determined by the presence of fragmented DNA via TUNEL and cleaved effector caspase 3. Finally, immunoblots were used to determine the mechanism of action using key proteins involved in both the intrinsic and extrinsic apoptotic pathways. Gnaphalin showed the highest activities in colon cancer HCT-116 and pancreatic cancer Panc 28 cells with a half maximal effective concentrations of 25.82±1.0887 and 30.07 ± 1.553 µM respectively. Gnaphalin impediment of cell viability involves the inhibition of phospho-ERK proliferation of the MAPK pathway along with phospho-FAK and c-Met, which are adhesion molecules. Gnaphalin has shown cytotoxic activity towards several colon cancer and pancreatic cancer cell lines by targeting cell proliferation and adhesion, and ultimately causing apoptosis.
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Rekas, Agata. "Application of Magnetic Resonance Spectroscopy in Tumor Pathology." University of Sydney, Institute for Magnetic Resonance Research, 1999. http://hdl.handle.net/2123/406.

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Palmer, D. Gail. "Modulation of p53 expression and function in colorectal adenoma cell lines by naturally occuring factors." Thesis, University of Bristol, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265455.

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Ross, Paul Jonathan. "Design and evaluation of antisense oligonucleotides targeted against kirsten RAS in colon adenocarcinoma cell lines." Thesis, Institute of Cancer Research (University Of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368694.

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Yan, Mei-kum, and 甄美琴. "Evaluation of a human colon adeno-carcinoma (Caco-2) cell line for isolation of respiratory viruses in nasopharyngeal aspirates frompatients with respiratory disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48334406.

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Background: Isolation of respiratory viruses routinely requires a panel of cell lines. Management of these cell lines is usually considered complex, cumbersome, long turnaround time and high cost. In order to improve the detection rate and cost, there is a need to evaluate any other cell line that could be as sensitive as the routine cell line for the detection of respiratory viruses. The human colon adeno-carcinoma (Caco-2) cell line has been shown to support the growth of enteroviruses, enteric viruses, and influenza A virus, and ability to grow coronavirus NL63 and SARS from culture isolates. In the present study, the isolation rate of respiratory viruses in Caco-2 from clinical specimens was studied and compared with the conventional panel of cell lines for the diagnosis of respiratory virus disease. Material and methods: The study was performed in two stages. In the first stage, one hundred and eighty-nine nasopharyngeal aspirates confirmed positive by direct immunofluorescence were used to inoculate onto Caco-2, and HEp-2, A549, MDCK, LLC-MK2 cell lines at the same time. In the second stage, fifty-six nasopharyngeal aspirates were randomly selected and cultured on Caco-2, HEp-2, A549, MDCK and LLC-MK2. Infected cells were examined daily for cytopathic effect for up to 10 days. Virus was further identified by performing direct immunofluorescence test for detection of eight common respiratory viruses (respiratory syncytial virus, influenza A and B viruses, parainfluenza type 1, 2, 3, 4 viruses and adenovirus). Results: Caco-2 (84%) was found to be the most efficient cell line to propagate the respiratory viruses from nasopharyngeal aspirate when compared with any positive by these conventional panel cells (78%) or individual cell line MDCK (38%), HEp-2 (21%), LLC-MK2 (27%) and A549 (37%). The latter differences were statistically significant (p = <0.000001). Furthermore, Caco-2 recovered 86% (36/42) viruses of conventional panel cells negative samples, while conventional panel cells recovered 80% (24/30) viruses of Caco-2 cells negative samples. Conclusion: Caco-2 is sensitive to a wide range of virus and can greatly simplify routine cell culture service for isolation of respiratory viruses.
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Beaumont, Peter Orton. "Role of glutathione S-transferases in the resistance of human colon cancer cell lines to doxorubicin." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq28796.pdf.

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Borkowski, Tomasz. "Evaluation of plant extracts for anticancer potential in in vitro assays using colon cancer cell-lines." Thesis, University of Ulster, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.554236.

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Colorectal cancer is one of the most prevailing cancers worldwide with particularly high incidence and mortality rates in the Western countries. Compelling evidence indicates that diet is considered as an important etiological factor of colorectal cancer risk. Consumption of vegetables has been shown in numerous epidemiological, case-control and prospective studies to be inversely associated with the pathogenesis of several cancers including cancers of colon and rectum. Leguminous and cruciferous vegetables abundant in every day diet are a rich source of many bioactive compounds. Some of those phytochemicals such as glucosinolates and their derivatives, flavonoids - especially isoflavones and saponins have been demonstrated to be potent chemoprotective agents with an ability to inhibit carcinogenesis. Recently, sprouting seed of many plants has been popularized as a healthy and nutritious food plentiful in proteins, minerals, vitamins and a range of phytochemicals. The germination process results in significant increases in concentrations of particular compounds as compared to the mature plants and may contribute to enhanced anticancer activity of sprouts. The focus of this study was primarily to evaluate the anti-cancer effects of the extracts prepared from leguminous (alfalfa, red clover) and cruciferous (Raab broccoli, Daikon radish) sprouts on key stages of colon carcinogenesis, namely initiation, promotion and invasion using in vitro model systems. The shoots were investigated as a commercial product - BroccoShoots sprouts mixture which were processed following extraction methods to obtain crude juice, methanol and in vitro digested extracts to assess how changes in the chemical characteristics could affect the biological activity of the samples. BroccoShoots extract at the highest concentrations (100, 150, 200 ug/ml) inhibited growth of CaCo-2 cells. At non-toxic range of concentrations (0 - 50 ug/ml) BroccoShoots extracts reduced H202 induced DNA damage in CaCo-2 cells and significantly inhibited migration and invasion of the HT115 cell-line. These effects appeared to be stronger for the crude juice extracts than for the other two types of extracts. There were no evident changes in the epithelial integrity of CaCo-2 cells (measured as trans-epithelial electrical resistance) and in cell cycle progression (24 hours) after exposure to the extracts. Then individual plants were prepared as crude juice extracts to examine the extent to which particular species contributed to the overall activity of the mixture. It was found that anti-genotoxic, anti-proliferative, anti-migrative and anti-invasive effects observed for Daikon radish extracts were the highest among all individual sprouts. Further, Daikon radish extracts at non-toxic concentrations (35, 50 ug/ml) were shown to induce G2/M phase cell cycle arrest in CaCo-2 cells and significantly reduce cell proliferation (over 144 hours) due to cytostatic effects. Thus, it was postulated that anti- cancer effects exerted by BroccoShoots mixture were mainly mediated by activity of Daikon radish extracts. These results demonstrate that sprouts and notably Daikon radish sprouts were effective in inhibiting several stages of colon carcinogenesis in vitro. Also, hypothesis was proposed that lymphocytes could be used as a surrogate biomarker of colonic tissue in assessment of DNA hypermethylation status of genes involved in colon carcinogenesis and that supplementation with folate rich watercress could affect promoter methylation of these genes. However, no detectable levels in promoter methylation ofp16INK4a, MGMT, CDX-2 and C-Myc genes were found in lymphocytes from healthy volunteers. Moreover, there was no evidence that watercress consumption could change methylation status of investigated genes. This indicates that lymphocytes may not be a suitable marker for measurement of DNA hypermethylation in the selected genes.
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Kilner, Jo. "Systems biology study of distinct actions by short-chain fatty acids in colon cancer cell-lines." Thesis, University of Sheffield, 2013. http://etheses.whiterose.ac.uk/4332/.

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Colorectal cancer (CRC) is the third largest cause of cancer deaths worldwide. Short-chain fatty acids (SCFA) are reported to be chemoprotective against CRC and are beneficial to colon epithelia by virtue of being their preferred energy source. Despite being essential to human metabolism and health, SCFAs are only accessible to humans as nutritional by-products of the anaerobic fermentation of dietary fibre by gut bacteria. Identifying novel chemotherapeutic roles for SCFAs is attractive due to their high tolerance by colonocytes, however the underlying metabolic actions are not fully understood. This project took a Systems Biology approach by employing high-throughput, quantitative proteomic and cellomic experimentation to investigate whether the three principle SCFAs in colon epithelia, butyrate, propionate and valerate, display unique roles with potentially chemoprotective actions. A hypothesised anti-mitotic pathway was formulated in which odd-chain SCFAs at above physiological concentrations induce downstream epigenetic acetylation of transcriptional regulators to differentially regulate β-tubulin isotypes. This creates an aberrant tubulin code leading to the disruption of microtubule (MT) dynamics, failure of critical MT cellular functions and eventual cell death. The pathway was simulated by computational dynamical modelling to predict the behaviour of SCFAs in relation to MT dynamics under both treatment and physiological conditions. This verified the plausibility of the hypothesis and provided valuable insights into the underlying mechanisms. Bioinformatic searches, combined with proteomic evidence, indicated that propionate and valerate, the odd-chain SCFAs, differentially regulated pro-tumourigenic β-tubulin isotypes. The alteration of the β-tubulin expression pattern countered potential metabolic adaptions in colon cancer cells, suggesting a chemopreventive action. Anti-microtubule drugs (AMD) are among the most successful chemotherapies to date, however their toxicity and drug resistance increase with successive rounds of treatment. This project has demonstrated that odd-chain SCFAs may act as novel chemotherapeutics by reducing the negative effects of AMDs while enhancing their efficacy.
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Rainer, Roman Josef. "Identification of differential regulation in central carbon metabolism between related cell lines." Doctoral thesis, Humboldt-Universität zu Berlin, 2020. http://dx.doi.org/10.18452/22117.

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Darmkrebszellen und T-Zellen regulieren ihren zentralen Kohlenstoffmetabolismus um ihren anabolen Bedarf zu erfüllen. Tumorzellen mit einer KRAS- oder BRAF-Mutation zeigen ein schnelles Wachstum, welches eine Umprogrammierung des Metabolismus vor aussetzt. Der mitochondriale T-Zellen-Aktivierungsinhibitor (TCAIM) ist bekannt dafür die mitochondriale Zellstruktur zu beeinflussen. Der Einfluss auf den Metabolismus nicht klar. In dieser Arbeit präsentiere ich erstmalig ein mathematische Model des zentralen Kohlen stoffmetabolismus in Darmkrebszellen und T-Zellen. Mithilfe dieses Modells analysiere ich, wie sich die Regulation in ähnlichen Zelllinien unterscheidet. In Bezug auf die Darm krebszellen vergleiche ich BRAF-(CaCO2-BRAFV600E), KRAS-(CaCO2-KRASG12V) mu tierte Zelllinien mit einer Basiszelllinie (CaCO2-control) und zeige, dass der Kohlenstoff metabolismus in BRAF-mutierten Zellen im Vergleich zu den beiden übrigen Zelllinien herabreguliert ist. Das Modell bestätigt außerdem, dass der Monocarboxylattransporter (MCT) in den Darmkrebszellen eine wichtige Rolle, insbesondere in den KRAS mu tierten Zellen, spielt. In T-Zellen zeigt der Vergleich von Wildtypzellen (CD8 T-Zellen) mit TCAIM homozygoten Zellen (TCAIM homozygote CD8 T-Zellen), dass der Kohlen stoffmetabolismus in zweiteren überwiegend herabreguliert und weniger aktiv ist. Diesen Effekt konnte ich durch die Analyse von RNASeq-Daten der jeweiligen Zelltypen bestä- tigen. Des Weiteren stelle ich fest, dass sich der Tricarbonsäurezyklus umkehrt, wenn durch die Glykolyse nicht ausreichend Laktat exportiert und die Biomasseproduktion unterstützt werden kann. Meine Arbeit stellt damit insgesamt einen neuartigen Ansatz zur Integration von Meta bolomik und RNAseq Daten dar, um die Regulation des zentralen Kohlenstoffmetabo lismus zu verstehen.
Colon cancer cells and T cells regulate central carbon metabolism to meet their anabolic needs. In KRAS and BRAF tumors, metabolic reprogramming is a premise to support rapid proliferation. In T cells, the mitochondrial T cell activation inhibitor (TCAIM) is known to affect mitochondrial morphology but its effect on cellular metabolism is not well understood. Via mathematical modelling, I investigate the differential regulation of closely related cell lines. I present the first mathematical model for colon cancer and T cell metabolism, unraveling differential regulation between related cell lines. The model shows that CaCO2-BRAFV600Ecells are mostly downregulated compared to CaCO2-KRASG12Vand CaCO2-control. Additionally, it demonstrates the critical role of monocarboxylate transporter (MCT), especially for CaCO2-KRASG12V. Concerning T cells, I compare wild-type T cells to homozygous TCAIM T cells. This unveils that TCAIM homozygous cells have a mostly downregulated TCA cycle, validated by RNASeq data, and are less metabolically active than wild-type T cells. Furthermore, if the glycolytic flux is not sufficient to support lactate export and biomass production, the model reveals that the TCA cycle is reversed as it requires less regulation. Taken together, this work presents a novel approach to integrate data referring to metabolic and genetic regulation of metabolism. On this basis, we can now better discriminate the metabolic capacity of CaCO2-control, CaCO2-BRAFV600E, CaCO2-KRASG12V, wildtype CD8 T cells, and homozygous TCAIM CD8 T cells.
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Books on the topic "Colon cell lines"

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Peter, Thomas. Metastatic potential of human colorectal cancer cell lines. Austin: R.G. Landes Co., 1993.

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Beaumont, Peter Orton. Role of glutathione S-transferases in the resistance of human colon cancer cell lines to doxorubicin. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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United States. National Aeronautics and Space Administration., ed. Morphological differentiation of colon carcinoma cell lines in rotating wall vessels. [Washington, DC: National Aeronautics and Space Administration, 1994.

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Grant, Warren, and Martin Scott-Brown. Prevention of cancer. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0350.

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In the UK, the four commonest cancers—lung cancer, breast cancer, colon cancer, and prostate cancer—result in around 62 000 deaths every year. Although deaths from cancer have fallen in the UK over the last 20 years, the UK still suffers from higher cancer death rates than many other countries in Western Europe. In 1999, the UK government produced a White Paper called Saving Lives: Our Healthier Nation that outlined a national target to reduce the death rate from cancer by at least 20% in people under 75 by 2010. The subsequent NHS Cancer Plan of 2000 designed a framework by which to achieve this target through effective prevention, screening, and treatment programmes as well as restructuring and developing new diagnostic and treatment facilities. But do we know enough about the biology of the development of cancer for government health policies alone to force dramatic changes in survival? The science behind the causes of cancer tells us that its origin lies in acquired or inherited genetic abnormalities. Inherited gene mutation syndromes and exposure to environmental mutagens cause cancer, largely through abnormalities in DNA repair mechanisms, leading to uncontrolled cell proliferation. Although screening those thought to be at highest risk, and regulating exposure to environmental carcinogens such as tobacco or ionizing radiation, have reduced, and will continue to reduce, cancer deaths, there are many other environmental factors that have been shown to increase the population risk of cancer. These will be outlined in this chapter. However, the available evidence is largely from retrospective and cross-sectional population-based studies and therefore limits the ability to apply this knowledge to the risk of the individual patient who may been seen in clinic. Although we may be able to put him or her into a high-, intermediate-, or low-risk category, the question ‘will I get cancer, doc?’ is one that we cannot answer with certainty. The NHS Cancer Plan of 2000, designed to reduce cancer deaths in this country and to bring UK treatment results in line with those other countries in Europe, focuses on preventing malignancy as part of its comprehensive cancer management strategy. It highlights that the rich are less likely to develop cancer, and will survive longer if they are diagnosed than those who live in poverty. This may reflect available treatment options, but is more likely to be related to the lifestyle of those with regular work, as they may be more health aware. The Cancer Plan, however, suggests that relieving poverty may be more labour intensive and less rewarding than encouraging positive risk-reducing behaviour in all members of the population. Eating well can reduce the risk of developing many cancers, particularly of the stomach and bowel. The Cancer Plan outlines the ‘Five-a-Day’ programme which was rolled out in 2002 and encouraged people to eat at least five portions of fruit and vegetables per day. Obese people are also at higher risk of cancers, in particular endometrial cancer. A good diet and regular exercise not only reduce obesity but are also independent risk-reducing factors. Alcohol misuse is thought to be a major risk factor in around 3% of all cancers, with the highest risk for cancers of the mouth and throat. As part of the Cancer Plan, the Department of Health promotes physical activity and general health programmes, as well as alcohol and smoking programmes, particularly in deprived areas. Focusing on these healthy lifestyle points can potentially reduce an individual lifetime risk of all cancers. However, our knowledge of the biology of four cancers in particular has led to the development of specific life-saving interventions. Outlined in this chapter are details regarding ongoing prevention strategies for carcinomas of the lung, the breast, the bowel, and the cervix.
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Book chapters on the topic "Colon cell lines"

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Whitehead, Robert H. "Establishment of Cell Lines from Colon Carcinoma." In Culture of Human Tumor Cells, 67–80. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2005. http://dx.doi.org/10.1002/0471722782.ch3.

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Glaysher, Sharon, and Ian A. Cree. "Isolation and Culture of Colon Cancer Cells and Cell Lines." In Methods in Molecular Biology, 135–40. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-080-5_12.

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Yamazaki, Yasuyo, Shawn Ritchie, and Yanqiu Jiang. "Phenomenome profilerTM analysis of human colon cancer cell lines." In Animal Cell Technology: Basic & Applied Aspects, 201–9. Dordrecht: Springer Netherlands, 2006. http://dx.doi.org/10.1007/1-4020-4457-7_28.

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Camici, M., M. Turriani, G. Turchi, M. G. Tozzi, J. Cos, C. Alemany, V. Noe, and C. J. Ciudad. "Cytotoxicity of Deoxycoformycin on Human Colon Carcinoma Cell Lines." In Purine and Pyrimidine Metabolism in Man VIII, 275–78. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-2584-4_58.

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Bergman, André M., Veronique W. T. Ruiz van Haperen, Gijsbert Veerman, Catharina M. Kuiper, and Godefridus J. Peters. "Synergistic Interaction between Cisplatin and Gemcitabine in Ovarian and Colon Cancer Cell Lines." In Purine and Pyrimidine Metabolism in Man VIII, 139–43. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-2584-4_32.

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Park, Sungyoun, Haemi Lee, Kun-Koo Park, Ha Won Kim, and Taesun Park. "Protein Kinase C and cAMP Mediated Regulation of Taurine Transport in Human Colon Carcinoma Cell Lines (HT-29 & Caco-2)." In Advances in Experimental Medicine and Biology, 167–74. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0077-3_21.

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Shack, Sonsoles. "Gene Expression Profiling of Tissues and Cell Lines: A Dual-Color Microarray Method." In Methods in Molecular Biology, 125–43. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-61737-954-3_9.

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Moriyama, Minoru. "Physiological and Biochemical Mechanisms of Insect Color Change Towards Understanding Molecular Links." In Pigments, Pigment Cells and Pigment Patterns, 451–72. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-1490-3_15.

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Nachbaur, D., H. Denz, H. Zwierzina, F. Schmalzl, and H. Huber. "Stimulation of Colony Formation of Various Human Carcinoma Cell Lines by rhGM-CSF and rhIL-3." In Cytokines in Hemopoiesis, Oncology, and AIDS, 181–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75510-1_25.

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Feitz, W. F. J., A. J. M. C. Beniers, H. L. M. Beck, B. Th Hendriks, W. P. Peelen, and F. M. J. Debruyne. "In Vitro Colony Growth Dynamics of the MATLyLu Tumor and Six New Dunning Rat Prostatic Tumor Cell Lines." In Investigative Urology 2, 87–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72735-1_14.

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Conference papers on the topic "Colon cell lines"

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Wang, Ying, Jiajia Chen, Bairong Shen, Åsa Wallin, and Xiao-feng Sun. "Gene Expression Profile of Colon Cancer Cell Lines Treated with SN38." In 2010 4th International Conference on Bioinformatics and Biomedical Engineering (iCBBE). IEEE, 2010. http://dx.doi.org/10.1109/icbbe.2010.5517918.

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Cetin, Emel, Baki Karaboce, Olca Kilinc, and Oya Orun. "Biological Effects of HIFU on HT-29 Colon Cancer Cell Lines." In 2018 IEEE International Symposium on Medical Measurements and Applications (MeMeA). IEEE, 2018. http://dx.doi.org/10.1109/memea.2018.8438679.

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Sayed, Afreen Asif Ali, Dharmalingam Subramaniam, Shahid Umar, Sufi M. Thomas, and Shrikant Anant. "Abstract 3486: RBM3 causes differential expression lncRNA in colon cancer cell lines." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3486.

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Fadhli, M. R. Mohd Naim, I. Noorfathiah, M. A. Nurul Farah Hana, M. S. Muhammad Ashraf, E. Zolkapli, H. H. Mizaton, and W. I. Wan Iryani. "Gelam (Melaleuca sp.) honey demonstrates antiproliferative effect on colon cancer cell lines (HCT116)." In 2012 IEEE Symposium on Business, Engineering and Industrial Applications (ISBEIA). IEEE, 2012. http://dx.doi.org/10.1109/isbeia.2012.6422904.

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Magoni, C., M. Forcella, Giustra CM, D. Panzeri, F. Saliu, P. Fusi, and M. Labra. "Camelina sativa glucosinolate fraction: NMR characterization and effect on human colon cell lines." In 67th International Congress and Annual Meeting of the Society for Medicinal Plant and Natural Product Research (GA) in cooperation with the French Society of Pharmacognosy AFERP. © Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-3400010.

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Davidson, David, Yunzhe Wang, Raquel Aloyz, and Lawrence Panasci. "Abstract 4692: ABT-888 synergizes treatment of colon cancer cell lines with irinotecan." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4692.

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Sanchez, Jenny E. Paredes, Ping Ji, Maria Munoz-Sagastibelza, Laura Martello-Rooney, and Jennie Williams. "Abstract 2692: Inflammatory patterns exhibited by African American colon tumor-derived cell lines." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2692.

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Guerrero-Valero, Marta, Consuelo Marin-Vicente, Roman A. Zubarev, and Neus Visa. "Abstract 3210: Proteomic study of 5-fluorouracil resistance in colon cancer cell lines." 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.am2013-3210.

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Lee, Choong-kun, Myung Eun Lee, Soojung Hong, Han Sang Kim, Hye Ryun Kim, Yoo Kun Shin, Tae Soo Kim, Joong Bae Ahn, Hyun Cheol Chung, and Sun Young Rha. "Abstract C157: Identification of activated receptor tyrosine kinases in colon cancer cell lines." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-c157.

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Vasilevskaya, Irina A., Muthu Selvakumaran, David Roberts, and Peter J. O'Dwyer. "Abstract 87: Differential effects of JNK1 and JNK2 on cell death in hypoxic colon cancer cell lines." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-87.

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