Littérature scientifique sur le sujet « CELL CYCLE DEREGULATION »
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Articles de revues sur le sujet "CELL CYCLE DEREGULATION"
Sánchez-Beato, Margarita, Abel Sánchez-Aguilera et Miguel A. Piris. « Cell cycle deregulation in B-cell lymphomas ». Blood 101, no 4 (15 février 2003) : 1220–35. http://dx.doi.org/10.1182/blood-2002-07-2009.
Texte intégralSavona, Michael, et Moshe Talpaz. « Cell-cycle deregulation in progressive CML ». Nature Reviews Cancer 8, no 7 (juillet 2008) : 563. http://dx.doi.org/10.1038/nrc2368-c2.
Texte intégralKowalewski, Ashley A., R. Lor Randall et Stephen L. Lessnick. « Cell Cycle Deregulation in Ewing's Sarcoma Pathogenesis ». Sarcoma 2011 (2011) : 1–10. http://dx.doi.org/10.1155/2011/598704.
Texte intégralEl-Deiry, Wafik S. « Akt takes centre stage in cell-cycle deregulation ». Nature Cell Biology 3, no 3 (mars 2001) : E71—E73. http://dx.doi.org/10.1038/35060148.
Texte intégralNacusi, Lucas P., et Robert J. Sheaff. « Deregulation of Cell Cycle Machinery in Pancreatic Cancer ». Pancreatology 7, no 4 (septembre 2007) : 373–77. http://dx.doi.org/10.1159/000107398.
Texte intégralBarlin, J., M. Leitao, L. Qin, M. Bisogna, N. Olvera, K. Shih, M. Hensley, G. Schwartz, J. Boyd et D. Levine. « Uterine leiomyosarcomas are driven by cell cycle deregulation ». Gynecologic Oncology 125 (mars 2012) : S135. http://dx.doi.org/10.1016/j.ygyno.2011.12.329.
Texte intégralClurman, Bruce E., James M. Roberts et Mark Groudine. « Deregulation of cell cycle control in hematologic malignancies ». Current Opinion in Hematology 3, no 4 (1996) : 315–20. http://dx.doi.org/10.1097/00062752-199603040-00011.
Texte intégralJackson, Kimberly M., Marisela DeLeon, C. Reynold Verret et Wayne B. Harris. « Dibenzoylmethane induces cell cycle deregulation in human prostate cancer cells ». Cancer Letters 178, no 2 (avril 2002) : 161–65. http://dx.doi.org/10.1016/s0304-3835(01)00844-8.
Texte intégralAzzam, Edouard I., Hatsumi Nagasawa, Yongjia Yu, Chuan-Yuan Li et John B. Little. « Cell Cycle Deregulation and Xeroderma Pigmentosum Group C Cell Transformation ». Journal of Investigative Dermatology 119, no 6 (décembre 2002) : 1350–54. http://dx.doi.org/10.1046/j.1523-1747.2002.19628.x.
Texte intégralShao, Zonghong, Jun Shi, Hong Liu, Juan Sun, Hairong Jia, Jie Bai, Guangsheng He et al. « Aberrant Cell Cycle and Expression Profiles of Cell Cycle Regulatory Genes in Myelodysplastic Syndrome. » Blood 106, no 11 (16 novembre 2005) : 4897. http://dx.doi.org/10.1182/blood.v106.11.4897.4897.
Texte intégralThèses sur le sujet "CELL CYCLE DEREGULATION"
Higginbottom, Karen. « Cell cycle deregulation and apoptosis in leukaemia ». Thesis, Queen Mary, University of London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407739.
Texte intégralSkalska, Lenka. « Deregulation of the cell cycle by EBV nuclear antigens EBNA3A and EBNA3C ». Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/10161.
Texte intégralPantelidou, Constantia. « E1B19K-deleted oncolytic adenoviruses enhancee the cytotoxicity of DNA-damaging drugs in pancreatic cancer through deregulation of cell-cycle mechanisms ». Thesis, Queen Mary, University of London, 2014. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8819.
Texte intégralDaniel, Peter. « Deregulation von Zellzyklus und Apoptose als molekulare Grundlage der Therapieresistenz von Tumoren ». Doctoral thesis, [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=968783066.
Texte intégralBadran, Ghidaa. « Pollution atmosphérique particulaire : caractérisation physico-chimique et comparaison des effets toxiques des fractions extractible et non-extractible des PM₂.₅ In-vitro evaluation of organic extractable matter from ambient PM₂.₅ using human bronchial epithelial BEAS-2B cells : Cytotoxicity, oxidative stress, pro-inflammatory response, genotoxicity, and cell cycle deregulation. Toxicity of fine and quasi-ultrafine particles : focus on the effects of organic extractable and non-extractable matter fractions. Toxicological appraisal of the chemical fractions of ambient fine (PM₂.₅-₀.₃) and quasi-ultrafine (PM₀.₃) particles in human bronchial epithelial BEAS-2B cells ». Thesis, Littoral, 2019. http://www.theses.fr/2019DUNK0547.
Texte intégralAir pollution and particulate matter (PM₂.₅) were classified as carcinigens (group 1) by the International Agency for Research on Cancer in 2013. This particulate fraction represents a complex mixture with a highly variable composition influencing the toxicity. However, few studies have determined the respective involvement of the different chemical fractions of PM in their toxic effects. In this work, fine particles (PM₂.₅₋₀.₃) and quasi-ultrafine particles (PM₀.₃) were sampled in an urban site located in Beirut (Lebanon). After performing the physicochemical characterization of these two types of particles, their toxic effects (global cytotoxicity, metabolic activation, genotoxicity, inflammation, oxidative stress, autophagy and apoptosis) were investigated on a human bronchial epithelial cell line (BEAS-2B). The analysis of the organic content revealed differences between the concentrations of polycyclic aromatic hydrocarbons (PAHs), as welle as oxygenated (O-PAH) and nitrated (N-PAH) congeners, respectively 43, 17 and 4 times higher in PM₀.₃ than in PM₂.₅₋₀.₃.The toxicological study was based on the comparison of the toxicity of the fine particles considered in their entirety (PM₂.₅₋₀.₃), the extracted organic fraction (OEM₂.₅₋₀.₃) and the fraction not extracted by the dichloromethane (NEM₂.₅₋₀.₃). In addition, the specific effects of the organic fraction extrated from the quasi-ultrafine particles (OEM₀.₃) were compared with those of the organic fraction extracted from the fine particles (OEM₂.₅₋₀.₃). Our results showed that all the studied fractions were able to induce at least one of the studied mechanisms. PM₂.₅₋₀.₃ was able to induce toxic effects greater than those induced by OEM₂.₅₋₀.₃ and NEM₂.₅₋₀.₃. The organic fraction extracted from the quasi-ultrafine particles (OEM₀.₃), richer in organic compounds and in particular in PAHs and other congeners, appeared to be responsible for deleterious effects globally greater than that extracted from the fine particles (OEM₂.₅₋₀.₃). The results of this work have brought new elements on the relative toxicity of the different fractions of the fine particles and underline the crucial role played by ultrafine particles, still too little studied
Neuwirth, Anke. « Regulation des Zellzyklus durch das Maus- und Ratten-Zytomegalievirus ». Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2005. http://dx.doi.org/10.18452/15363.
Texte intégralHuman Cytomegalovirus (HCMV) is an ubiquitous, species-specific beta-herpesvirus that, like other herpesviruses, can establish lifelong latency following primary infection. HCMV infection becomes virulent only in immunocompromised patients such as premature infants, transplant recipients and AIDS patients where the virus causes severe disease like hepatitis, pneumonitis and retinitis. Congenital infection produces birth defects, most commonly hearing loss. To develop rational-based strategies for prevention and treatment of HCMV infection, it is crucial to understand the interactions between the virus and its host cell that support the establishment and progression of the virus replicative cycle. In general, herpesviruses are known to replicate most efficiently in the absence of cellular DNA synthesis. What is more, they have evolved mechanisms to avoid the cell´s DNA replication phase by blocking cell cycle progression outside S phase. HCMV has been shown to specifically inhibit the onset of cellular DNA synthesis resulting in cells arrested with a G1 DNA content. Towards a better understanding of CMV-mediated cell cycle alterations in vivo, we tested murine and rat CMV (MCMV/RCMV), being common animal models for CMV infection, for their influence on the host cell cycle. It was found that both MCMV and RCMV exhibit a strong anti-proliferative capacity on immortalised and primary embryonic fibroblasts after lytic infection. This results from specific cell cycle blocks in G1 and G2 as demonstrated by flow cytometry analysis. The G1 arrest is at least in part caused by a specific inhibition of cellular DNA synthesis and involves both the formation and activation of the cells’ DNA replication machinery. Interestingly, and in contrast to HCMV, the replicative cycle of rodent CMVs started from G2 as efficiently as from G1. Whilst the cell cycle arrest is accompanied by a broad induction of cyclin-cdk2 and cyclin-cdk1 activity, cyclin D1-cdk4/6 activity is selectively suppressed in MCMV and RCMV infected cells. Thus, given that both rodent and human CMVs are anti-proliferative and arrest cell cycle progression we found a surprising divergence of some of the underlying mechanisms. Therefore, any question put forward to a rodent CMV model involving cell cycle regulation has to be well defined in order to extrapolate meaningful information for the human system.
De, Marco Carmela. « Molecular Mechanisms of cell cycle deregulation in thiroid cancer ». Tesi di dottorato, 2008. http://www.fedoa.unina.it/2601/1/De_marco_Oncologia_Endocrinologia_Molecolare.pdf.
Texte intégralBlack, Riva. « Oral papillary squamous cell carcinoma : its relation to human papillomavirus infection and associated cell cycle deregulation ». 2005. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=370189&T=F.
Texte intégralKai-HsiHsu et 許凱熙. « The Effect of CD44 Cleavage in Cell Cycle Deregulation and Enhanced Mitosis in Gastrointestinal Stromal Tumors ». Thesis, 2010. http://ndltd.ncl.edu.tw/handle/45544824025216211586.
Texte intégral國立成功大學
臨床醫學研究所
99
Gastrointestinal stromal tumors (GISTs) originate from the interstitial cell of Cajal (ICC) in the muscular layer of the gut. The pathogenesis of GIST is gain-of-function mutations in KIT gene in ICC with consequent uncontrolled cell proliferation and anti-apoptosis. Being associated with variable cellular functions, CD44 belongs to the type I transmembrane glycoprotein that is encoded by a 20-exon CD44 gene. We previously found that loss of CD44 expression is related to poor prognosis in GIST. However, the significance of CD44 expression has been controversial. It is thus likely that the mechanism underlying the change in CD44 expression may be more important than the expression of CD44 itself in human cancer. The proteolytic cleavage of membrane proteins, including CD44, has been considered an important mechanism for the regulation of cellular functions. Our study showed that CD44 cleavage is specifically overexpressed in the majority of GIST tumor samples. In the clinicopathologic factors associated with CD44 cleavage, increased mitosis was the most significant one. The aim of this study is to evaluate the possible mechanism underlying the association between increased CD44 cleavage and increased mitosis in GIST. We also aim to investigate the significance and effects of osteopontin (OPN), a multifunctional secreted glycophosphoprotein functionally related to CD44, in relation to tumor proliferation as well as apoptosis. In GIST tumor samples and their normal counterpart tissues, we analyzed the expression of specific cell cycle proteins in relation to CD44 cleavage activity. We also evaluated the expression and the significance of osteopontin (OPN), a molecule closely related to CD44. Cyclin D1 and its important regulator, β-catenin, showed similar tumor-specificity and overexpression as did CD44 cleavage activity in GIST. Cyclin D1 and β-catenin, in addition to their significant correlation, were also associated with CD44 cleavage, indicating a potential role of these two molecules in the mitotic effect of CD44 cleavage in GIST. OPN, being associated with CD44 and CD44 cleavage, was also found to be an independent prognostic factor clinically, and its interaction with CD44 most significantly correlated with increased mitosis. Further in vitro studies revealed the significant proliferation-promoting and anti-apoptotic effects of OPN and its interaction with CD44 with respect to CD44 cleavage in GIST. In conclusion, we identified the significant mitotic effect of CD44 cleavage in relation to OPN/CD44 interaction and dysregulated cell cycle in GIST. Increased OPN expression was an independent poor prognostic factor and its interaction with CD44 significantly correlated with increased mitosis as well as in vitro proliferation-promoting and anti-apoptotic effects through upregulation of cyclin D1 and Mcl-1 expression, respectively, in GIST.
Livres sur le sujet "CELL CYCLE DEREGULATION"
Enders, Greg H. Cell cycle deregulation in cancer. New York : Springer, 2010.
Trouver le texte intégralEnders, Greg H., dir. Cell Cycle Deregulation in Cancer. New York, NY : Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1770-6.
Texte intégralEnders, Greg H. Cell Cycle Deregulation in Cancer. Springer, 2012.
Trouver le texte intégralEnders, Greg H. Cell Cycle Deregulation in Cancer. Springer London, Limited, 2010.
Trouver le texte intégralBlack, Riva. Oral papillary squamous cell carcinoma : Its relation to human papillomavirus infection and associated cell cycle deregulation. 2005.
Trouver le texte intégralChapitres de livres sur le sujet "CELL CYCLE DEREGULATION"
Sotillo, Elena, et Xavier Graña. « Escape from Cellular Quiescence ». Dans Cell Cycle Deregulation in Cancer, 3–22. New York, NY : Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1770-6_1.
Texte intégralLao-Sirieix, Pierre, et Rebecca C. Fitzgerald. « Cell Cycle Deregulation in Pre-neoplasia : Case Study of Barrett’s Oesophagus ». Dans Cell Cycle Deregulation in Cancer, 157–66. New York, NY : Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1770-6_10.
Texte intégralJohnson, Neil, et Geoffrey I. Shapiro. « Targeting Cyclin-Dependent Kinases for Cancer Therapy ». Dans Cell Cycle Deregulation in Cancer, 167–85. New York, NY : Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1770-6_11.
Texte intégralJi, Jun-Yuan, et Nicholas J. Dyson. « Interplay Between Cyclin-Dependent Kinases and E2F-Dependent Transcription ». Dans Cell Cycle Deregulation in Cancer, 23–41. New York, NY : Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1770-6_2.
Texte intégralMcClendon, A. Kathleen, Jeffry L. Dean et Erik S. Knudsen. « Regulation of Pre-RC Assembly : A Complex Symphony Orchestrated by CDKs ». Dans Cell Cycle Deregulation in Cancer, 43–55. New York, NY : Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1770-6_3.
Texte intégralHuang, Haomin, et Timothy J. Yen. « Mitotic Checkpoint and Chromosome Instability in Cancer ». Dans Cell Cycle Deregulation in Cancer, 59–77. New York, NY : Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1770-6_4.
Texte intégralChow, Jeremy P. H., et Randy Y. C. Poon. « Mitotic Catastrophe ». Dans Cell Cycle Deregulation in Cancer, 79–96. New York, NY : Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1770-6_5.
Texte intégralHontz, Robert D., et Maureen E. Murphy. « p53, ARF, and the Control of Autophagy ». Dans Cell Cycle Deregulation in Cancer, 97–105. New York, NY : Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1770-6_6.
Texte intégralViale, Andrea, et Pier Giuseppe Pelicci. « Regulation of Self-Renewing Divisions in Normal and Leukaemia Stem Cells ». Dans Cell Cycle Deregulation in Cancer, 109–25. New York, NY : Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1770-6_7.
Texte intégralDenchi, Eros Lazzerini. « Maintenance of Telomeres in Cancer ». Dans Cell Cycle Deregulation in Cancer, 127–38. New York, NY : Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1770-6_8.
Texte intégralActes de conférences sur le sujet "CELL CYCLE DEREGULATION"
Ouhtit, Allal, Ishita Gupta, Zakariya Y. Abd Elmageed et Therese M. Becker. « Abstract A20 : Deregulation of cell cycle and apoptotic mechanisms in UVB-irradiated p16-mutant inducible melanoma cell lines ». Dans Abstracts : AACR Special Conference on Advances in Melanoma : From Biology to Therapy ; September 20-23, 2014 ; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.mel2014-a20.
Texte intégralCastellsague, Ester, Jian Carrot-Zhang, Isabelle Gamache, Barbara Rivera, Mohamed Moustafa, David Barford, Jacek Majewski, Jose Teodoro et William David Foulkes. « Abstract PR13 : Germ-line mutations in CDC20 result in familial cancers via deregulation of the cell cycle ». Dans Abstracts : AACR Precision Medicine Series : Cancer Cell Cycle - Tumor Progression and Therapeutic Response ; February 28 - March 2, 2016 ; Orlando, FL. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.cellcycle16-pr13.
Texte intégralAdams, Christina, Lynn Wang, Tim S. Wang, Nichol Miller, Elizabeth McMillan, Monica Ramstetter, John Chionis et al. « Abstract 2960 : A novel mouse model of pancreatic cancer reveals new insights into cell cycle deregulation ». Dans Proceedings : AACR Annual Meeting 2021 ; April 10-15, 2021 and May 17-21, 2021 ; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2960.
Texte intégralBai, Jian, Qiyan Wang, Kenan Gong, Hong Cai, Yang Ke et Changqing Zeng. « Abstract C03 : A comprehensive study of genomic alterations reveals deregulation of the cell cycle in most esophageal squamous cell carcinomas ». Dans Abstracts : Third AACR International Conference on Frontiers in Basic Cancer Research - September 18-22, 2013 ; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.fbcr13-c03.
Texte intégralQiao, Dianhua, Kristy Meyer et Andreas Friedl. « Abstract 1307 : c-Myc is a key mediator of glypican-1 (GPC1)-dependent deregulation of the cell cycle ». Dans Proceedings : AACR Annual Meeting 2014 ; April 5-9, 2014 ; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1307.
Texte intégralKIM, Jin-Ah, Ying Tan, Xian Wang, Xixi Cao, Jamunarani Veeraraghavan, Yulong Liang, Dean P. Edwards et al. « Abstract 3032 : Genomic deregulation and therapeutic role of the cell-cycle kinase TLK2 in more aggressive breast cancers ». Dans 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.am2015-3032.
Texte intégralSubbiah, Ishwaria M., Gauri Varadhachary, Apostolia M. Tsimberidou, Jennifer J. Wheler, Vivek Subbiah, Filip Janku, Sinchita Roy Chowdhuri, Ralph Zinner et David S. Hong. « Abstract 604 : Impaired cell cycle arrest with concurrent epigenetic deregulation identified through next generation sequencing in patients with advanced carcinoma of unknown primary : Implications for personalized medicine ». Dans 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.am2015-604.
Texte intégralRapports d'organisations sur le sujet "CELL CYCLE DEREGULATION"
Shani, Moshe, et C. P. Emerson. Genetic Manipulation of the Adipose Tissue via Transgenesis. United States Department of Agriculture, avril 1995. http://dx.doi.org/10.32747/1995.7604929.bard.
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