Relevant bibliographies by topics / CELL CYCLE DEREGULATION

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Academic literature on the topic 'CELL CYCLE DEREGULATION'

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Published: 11 September 2023

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Journal articles on the topic "CELL CYCLE DEREGULATION"

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Sánchez-Beato, Margarita, Abel Sánchez-Aguilera, and Miguel A. Piris. "Cell cycle deregulation in B-cell lymphomas." Blood 101, no. 4 (February 15, 2003): 1220–35. http://dx.doi.org/10.1182/blood-2002-07-2009.

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Disruption of the physiologic balance between cell proliferation and death is a universal feature of all cancers. In general terms, human B-cell lymphomas can be subdivided into 2 main groups, low- and high-growth fraction lymphomas, according to the mechanisms through which this imbalance is achieved. Most types of low-growth fraction lymphomas are initiated by molecular events resulting in the inhibition of apoptosis, such as translocations affecting BCL2, in follicular lymphoma, or BCL10 and API2/MLT1, in mucosa-associated lymphoid tissue (MALT) lymphomas. This results in cell accumulation as a consequence of prolonged cell survival. In contrast, high-growth fraction lymphomas are characterized by an enhanced proliferative activity, as a result of the deregulation of oncogenes with cell cycle regulatory functions, such asBCL6, in large B-cell lymphoma, or c-myc, in Burkitt lymphoma. Low- and high-growth fraction lymphomas are both able to accumulate other alterations in cell cycle regulation, most frequently involving tumor suppressor genes such asp16INK4a, p53, andp27KIP1. As a consequence, these tumors behave as highly aggressive lymphomas. The simultaneous inactivation of several of these regulators confers increased aggressivity and proliferative advantage to tumoral cells. In this review we discuss our current knowledge of the alterations in each of these pathways, with special emphasis on the deregulation of cell cycle progression, in an attempt to integrate the available information within a global model that describes the contribution of these molecular changes to the genesis and progression of B-cell lymphomas.
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Savona, Michael, and Moshe Talpaz. "Cell-cycle deregulation in progressive CML." Nature Reviews Cancer 8, no. 7 (July 2008): 563. http://dx.doi.org/10.1038/nrc2368-c2.

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Kowalewski, Ashley A., R. Lor Randall, and Stephen L. Lessnick. "Cell Cycle Deregulation in Ewing's Sarcoma Pathogenesis." Sarcoma 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/598704.

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Ewing's sarcoma is a highly aggressive pediatric tumor of bone that usually contains the characteristic chromosomal translocation t(11;22)(q24;q12). This translocation encodes the oncogenic fusion protein EWS/FLI, which acts as an aberrant transcription factor to deregulate target genes necessary for oncogenesis. One key feature of oncogenic transformation is dysregulation of cell cycle control. It is therefore likely that EWS/FLI and other cooperating mutations in Ewing's sarcoma modulate the cell cycle to facilitate tumorigenesis. This paper will summarize current published data associated with deregulation of the cell cycle in Ewing's sarcoma and highlight important questions that remain to be answered.
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El-Deiry, Wafik S. "Akt takes centre stage in cell-cycle deregulation." Nature Cell Biology 3, no. 3 (March 2001): E71—E73. http://dx.doi.org/10.1038/35060148.

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Nacusi, Lucas P., and Robert J. Sheaff. "Deregulation of Cell Cycle Machinery in Pancreatic Cancer." Pancreatology 7, no. 4 (September 2007): 373–77. http://dx.doi.org/10.1159/000107398.

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Barlin, J., M. Leitao, L. Qin, M. Bisogna, N. Olvera, K. Shih, M. Hensley, G. Schwartz, J. Boyd, and D. Levine. "Uterine leiomyosarcomas are driven by cell cycle deregulation." Gynecologic Oncology 125 (March 2012): S135. http://dx.doi.org/10.1016/j.ygyno.2011.12.329.

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Clurman, Bruce E., James M. Roberts, and 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.

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Jackson, Kimberly M., Marisela DeLeon, C. Reynold Verret, and Wayne B. Harris. "Dibenzoylmethane induces cell cycle deregulation in human prostate cancer cells." Cancer Letters 178, no. 2 (April 2002): 161–65. http://dx.doi.org/10.1016/s0304-3835(01)00844-8.

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Azzam, Edouard I., Hatsumi Nagasawa, Yongjia Yu, Chuan-Yuan Li, and John B. Little. "Cell Cycle Deregulation and Xeroderma Pigmentosum Group C Cell Transformation." Journal of Investigative Dermatology 119, no. 6 (December 2002): 1350–54. http://dx.doi.org/10.1046/j.1523-1747.2002.19628.x.

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Shao, 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 (November 16, 2005): 4897. http://dx.doi.org/10.1182/blood.v106.11.4897.4897.

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Abstract Deregulation of the cell cycle machinery, especially G1/S phase deregulation, is known to contribute to the uncontrolled cell proliferation and malignant transformation in haematological malignances. However, little is known about the aberrant bone marrow cell cycle and its molecular mechanisms in myelodysplastic syndromes (MDS). In this study, we conducted the cell cycle analysis of bone marrow mononuclear cells (BMMC) before and after exposure to haematopoietic growth factors (HGFs) cocktail, in combination with the analysis of the expression of Ki-67 antigen in BMMC and CD34+ cells in twenty-seven MDS patients. In addition, we examined the expression profiles of cell cycle regulatory genes. We found that MDS patients had higher percentage of BMMC in G0/G1 phase and lower ratio of cells in S+G2/M, and higher proportion of CD34+ Ki-67+ cells. After exposure to HGFs cocktail in vitro, high proportion of G0/G1 phase cells decreased significantly in MDS. All types of four cyclins (cyclin D2, D3, E, and A1) were at higher level had high amount of mRNA transcripts in MDS, together with higher activation of CDK2, CDK6, and RB genes. Furthermore, we also demonstrated higher activation of p21 and p27 genes. These results demonstrated that G1 arrest occurred in MDS Ki-67+ hematopoietic cells. High activation of cyclins, CDKs, and RB genes are the molecular bases of large proportion of Ki-67+ proliferate BMMC population. High activation of p21 and p27 genes in MDS blocked hematopoietic cells entry into the following cell cycle.
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Dissertations / Theses on the topic "CELL CYCLE DEREGULATION"

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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.

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Skalska, 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.

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Cyclin-dependent kinase inhibitor p16INK4A is an important tumour suppressor and inducer of cellular senescence often inactivated during the development of cancer. I investigated the mechanism by which EBV latency-associated nuclear antigens EBNA3A and EBNA3C repress p16INK4A expression. Using lymphoblastoid cell lines (LCL) expressing a conditional EBNA3C, I demonstrate that EBNA3C inactivation resets the epigenetic status of p16INK4A to permit transcriptional activation: the polycomb-associated repressive H3K27me3 histone modification is substantially reduced, while the activation-related mark H3K4me3 is modestly increased. Activation of EBNA3C reverses the distribution of these epigenetic marks, represses p16INK4A transcription and allows proliferation. LCL lacking EBNA3A express relatively high levels of p16INK4A and have a similar pattern of histone modifications on p16INK4A as produced by the inactivation of EBNA3C. Since binding to the co-repressor of transcription CtBP was linked to the oncogenic activity of EBNA3C and EBNA3A, LCL with viruses encoding EBNA3C- and/or EBNA3A-mutants that no longer bind CtBP were established. These novel LCL revealed that the epigenetic repression of p16INK4A requires the interaction of both EBNA3C and EBNA3A with CtBP. Epigenetic repression of p16INK4A by latent EBV may facilitate p16INK4A DNA methylation during lymphomagenesis. Furthermore, by transforming the peripheral blood lymphocytes (PBL) from an individual homozygous for a deletion in CDKN2A locus with recombinant EBV viruses expressing conditional EBNA3C, we developed a system that allows inactivation of EBNA3C in LCL lacking functional p16INK4A protein (p16-null LCL 3CHT). EBNA3C inactivation has no impact on the proliferation rate of p16-null LCL, proving that the repression of p16INK4A is the main function of EBNA3C in EBV-driven LCL proliferation. The p16INK4A locus is epigenetically modified by EBNA3C despite the absence of functional p16INK4A protein. Since the selection pressure based on faster outgrowth of advantageously modified subset of cells is removed, the gradual and relatively slow kinetics of H3K27me3 restoration at p16INK4A following EBNA3C reactivation in p16-null LCL 3CHT seems to be genuinely related to the mechanism of EBNA3C-mediated p16INK4A regulation. The p16-null LCL 3CHT system further allows distinguishing genes regulated specifically by EBNA3C, rather than as a consequence of activation of p16INK4A/Rb/E2F1 axis. Lastly, new cellular targets of EBNA3C and/or EBNA3A from the group of microRNAs are identified in this work. Most notably, both EBNA3C and EBNA3A are shown to repress the tumour supressor miR-143/145 cluster and their precursor long non-coding RNAs in LCL.
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Pantelidou, 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.

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Pancreatic cancer is an aggressive disease with poor prognosis and a high fatality rate. Gemcitabine, the standard first-line chemotherapy for advanced disease, has negligible effects, necessitating the development of new therapies. We previously demonstrated that deletion of the anti-apoptotic gene E1B19K (AdΔ19K) in a replication-selective adenoviral mutant, caused synergistically-enhanced cell-killing when combined with low-dose DNA-damaging drugs in pancreatic cancer xenograft models. To delineate the cellular pathways targeted by the combination treatment we employed AdΔ19K and gemcitabine or irinotecan, with the goal of identifying cellular factors that are essential for the synergistic cell-killing. We hypothesised that AdΔ19K and DNA-damaging drugs act synergistically to deregulate cell-cycle mechanisms. Pancreatic cancer cell death induced by AdΔ19K and DNA-damaging drugs is apoptotic and time-dependent. AdΔ19K could not block DNA-damage responses (DDR) elicited by the drugs, despite virus-mediated degradation of the DDR factor Mre11. Mre11 siRNA-mediated knockdown augmented the synergistic cell death. Mitotic-index analysis in synchronised cells and immunofluorescence microscopy suggested that AdΔ19K promotes mitotic entry of gemcitabine-treated DNA-damaged cells. Moreover, AdΔ19K inhibited drug-induced accumulation of Claspin, a DDR protein whose degradation is required for checkpoint recovery. Treatment with AdΔ19K and gemcitabine accelerated Claspin degradation, and siRNA-mediated Claspin knockdown enhanced the synergistic cell death. Time-lapse microscopy in histoneH2B mCherry-expressing cells showed that AdΔ19K enhanced gemcitabine-induced mitotic catastrophe, characterised by prolonged mitosis, chromosome missegregation errors, cytokinesis failure and formation of multinucleated cells. Moreover, live-cell imaging revealed that the majority of cells treated with AdΔ19K and gemcitabine die before mitotic entry. 5 These findings suggest that E1B19K-deleted adenoviruses cannot prevent cell-cycle checkpoint responses elicited by DNA-damaging drugs, but enhance drug-induced cell death by downregulating DDR factors, such as Mre11 and Claspin. Additionally, the virus enhances mitotic catastrophe of DNA-damaged cells escaping cell-cycle checkpoints, eventually leading to increased apoptosis. Through these studies cellular pathways and factors involved in the synergistic cell killing were identified, that could be explored in the future to develop improved targeted therapies for pancreatic cancer.
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Daniel, 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.

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Badran, 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.

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La pollution de l'air et les particules fines (PM₂.₅) ont été classées cancérigènes (groupe 1) par le Centre International de la Recherche sur le Cancer en 2013. Cette fraction particulaire représente un mélange complexe dont la composition, très variable, influe sur la toxicité. Cependant, peu d'études ont déterminé l'implication respective des différentes fractions chimiques constitutives des PM dans leurs effets toxiques. Dans ce travail de thèse, des particules fines (PM₂.₅₋₀.₃) et quasi-ultrafines (PM₀.₃) ont été échantillonnées au niveau d'un site urbain à Beyrouth (Liban). Après avoir réalisé la caractérisation physico-chimique de ces deux types de particules, leurs effets toxiques (cytotoxicité globale, activation métabolique, génotoxicité, inflammation, stress oxydant, autophagie et apoptose) ont été étudiés sur une lignée de cellules épithéliales bronchiques humaines (BEAS-2B). L'analyse des fractions organiques a révélé des différences entre les teneurs en hydrocarbures aromatiques polycycliques (HAP), de même qu'en congénères oxygénés (O-HAP) et nitrés (N-HAP), respectivement 43, 17 et 4 fois plus élevées dans les PM₀.₃ que dans les PM₂.₅₋₀.₃. L'étude toxicologique a porté sur les particules fines considérées dans leur entièreté (PM₂.₅₋₀.₃), la fraction organique extractible (EOM₂.₅₋₀.₃) et la fraction non-extractible par le dichlorométhane (NEM₂.₅₋₀.₃). De plus, les effets spécifiques de la fraction organique extraite des particules quasi-ultrafines (EOM₀.₃) ont été comparés à ceux de la fraction organique extraite des particules fines (EOM₂.₅₋₀.₃). Nos résultats montrent que chacune des fractions considérées a été capable d'activer au moins un des mécanismes étudiés. Les PM₂.₅₋₀.₃ ont induit des effets toxiques généralement plus marqués que les EOM₂.₅₋₀.₃ et NEM₂.₅₋₀.₃. La fraction organique des particules quasi-ultrafines (EOM₀.₃), plus riche en composés organiques et notamment en HAP et autres congénères, est apparue responsable d'effets délétères globalement plus importants que celle extraite des particules fines (EOM₂.₅₋₀.₃). Les résultats de ce travail ont apporté des éléments nouveaux sur la toxicité relative des différentes fractions extractibles et non extractibles des particules fines et soulignent le rôle crucial joué par les particules ultrafines, encore trop peu étudiées
Air 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
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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.

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Das humane Zytomegalievirus, ist ein ubiquitäres Pathogen, welches akute und persistierende Infektionen verursacht. Bei immunsupprimierten Patienten kann das Virus zu schweren Erkrankungen, wie Hepatitis, Pneumonie und bei kongenitaler Infektion außerdem zu Schädigungen des ZNS führen. HCMV blockiert die Zellproliferation durch einen Arrest am G1/S-Übergang des Zellzyklus, andererseits wird aber gleichzeitig die Expression S-Phase spezifischer Gene aktiviert. Teilweise lässt sich dies durch eine Virus vermittelte spezifische Inhibition der zellulären DNA-Repliaktion sowie durch eine massive Deregulation Zyklin-assozzierter Kinasen erklären. Zellkulturexperimente deuten darauf hin, dass die Zellzyklusalterationen wichtige Voraussetzungen für eine erfolgreiche Virusreplikation darstellen. Es ist hingegen nicht bekannt, welche Relevanz sie für die Virusvermehrung in vivo und das pathologische Erscheinungsbild im erkrankten Organismus besitzen. Diese Frage kann nur in einem Tiermodell sinnvoll angegangen werden. Aufgrund der Wirtsspezifität der Zytomegalieviren, ist man dabei auf die Verwendung der jeweiligen artspezifischen CMV angewiesen. Murines CMV (MCMV) und Ratten-CMV (RCMV) sind dabei die bislang bestuntersuchtesten Systeme. Das Anliegen dieser Arbeit war es zu prüfen, inwieweit die für HCMV beschriebenen Zellzyklusregulationen in MCMV und RCMV auf Zellkulturbasis konserviert sind. Es konnte gezeigt werden, dass sowohl RCMV als auch MCMV einen antiproliferativen Effekt auf infizierte Zellen besitzen und ebenso wie HCMV zu einem Zellzyklusarrest führen. Nager-Zytomegalieviren können Zellen auch in der G2-Phase arretieren und in dieser Zellzyklusphase auch effizient replizieren können. Die Infektion mit Nager-CMV führt außerdem auf breiter Basis zur Veränderung Zyklin-assoziierter Kinaseaktivitäten. Allen Zytomegalieviren ist die Hemmung der zellulären DNA-Synthese am G1/S-Übergang durch die Inhibition des replication licensing, dem Beginn der DNA-Synthese gemein. Durch diese vergleichende Studie wird einerseits deutlich, dass wesentliche funktionelle Schritte der Zellzyklusregulation zwischen den Zytomegalieviren konserviert sind, aber andererseits die zu Grunde liegenden molekularen Mechanismen zum Teil deutlich variieren.
Human 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.
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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.

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Black, 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.

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Kai-HsiHsu and 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.

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博士
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.
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Books on the topic "CELL CYCLE DEREGULATION"

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Enders, Greg H. Cell cycle deregulation in cancer. New York: Springer, 2010.

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Enders, Greg H., ed. Cell Cycle Deregulation in Cancer. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1770-6.

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Enders, Greg H. Cell Cycle Deregulation in Cancer. Springer, 2012.

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Enders, Greg H. Cell Cycle Deregulation in Cancer. Springer London, Limited, 2010.

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Black, Riva. Oral papillary squamous cell carcinoma: Its relation to human papillomavirus infection and associated cell cycle deregulation. 2005.

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Book chapters on the topic "CELL CYCLE DEREGULATION"

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Sotillo, Elena, and Xavier Graña. "Escape from Cellular Quiescence." In 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.

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Lao-Sirieix, Pierre, and Rebecca C. Fitzgerald. "Cell Cycle Deregulation in Pre-neoplasia: Case Study of Barrett’s Oesophagus." In 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.

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Johnson, Neil, and Geoffrey I. Shapiro. "Targeting Cyclin-Dependent Kinases for Cancer Therapy." In 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.

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Ji, Jun-Yuan, and Nicholas J. Dyson. "Interplay Between Cyclin-Dependent Kinases and E2F-Dependent Transcription." In 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.

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McClendon, A. Kathleen, Jeffry L. Dean, and Erik S. Knudsen. "Regulation of Pre-RC Assembly: A Complex Symphony Orchestrated by CDKs." In 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.

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Huang, Haomin, and Timothy J. Yen. "Mitotic Checkpoint and Chromosome Instability in Cancer." In 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.

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Chow, Jeremy P. H., and Randy Y. C. Poon. "Mitotic Catastrophe." In 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.

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Hontz, Robert D., and Maureen E. Murphy. "p53, ARF, and the Control of Autophagy." In 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.

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Viale, Andrea, and Pier Giuseppe Pelicci. "Regulation of Self-Renewing Divisions in Normal and Leukaemia Stem Cells." In 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.

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Denchi, Eros Lazzerini. "Maintenance of Telomeres in Cancer." In 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.

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Conference papers on the topic "CELL CYCLE DEREGULATION"

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Ouhtit, Allal, Ishita Gupta, Zakariya Y. Abd Elmageed, and Therese M. Becker. "Abstract A20: Deregulation of cell cycle and apoptotic mechanisms in UVB-irradiated p16-mutant inducible melanoma cell lines." In 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.

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Castellsague, Ester, Jian Carrot-Zhang, Isabelle Gamache, Barbara Rivera, Mohamed Moustafa, David Barford, Jacek Majewski, Jose Teodoro, and William David Foulkes. "Abstract PR13: Germ-line mutations in CDC20 result in familial cancers via deregulation of the cell cycle." In 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.

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Adams, 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." In 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.

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Bai, Jian, Qiyan Wang, Kenan Gong, Hong Cai, Yang Ke, and Changqing Zeng. "Abstract C03: A comprehensive study of genomic alterations reveals deregulation of the cell cycle in most esophageal squamous cell carcinomas." In 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.

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Qiao, Dianhua, Kristy Meyer, and Andreas Friedl. "Abstract 1307: c-Myc is a key mediator of glypican-1 (GPC1)-dependent deregulation of the cell cycle." In 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.

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KIM, 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." 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.am2015-3032.

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Subbiah, Ishwaria M., Gauri Varadhachary, Apostolia M. Tsimberidou, Jennifer J. Wheler, Vivek Subbiah, Filip Janku, Sinchita Roy Chowdhuri, Ralph Zinner, and 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." 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.am2015-604.

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Reports on the topic "CELL CYCLE DEREGULATION"

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Shani, Moshe, and C. P. Emerson. Genetic Manipulation of the Adipose Tissue via Transgenesis. United States Department of Agriculture, April 1995. http://dx.doi.org/10.32747/1995.7604929.bard.

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The long term goal of this study was to reduce caloric and fat content of beef and other red meats by means of genetic modification of the animal such that fat would not be accumulated. This was attempted by introducing into the germ line myogenic regulatory genes that would convert fat tissue to skeletal muscle. We first determined the consequences of ectopic expression of the myogenic regulatory gene MyoD1. It was found that deregulation of MyoD1 did not result in ectopic skeletal muscle formation but rather led to embryonic lethalities, probably due to its role in the control of the cell cycle. This indicated that MyoD1 should be placed under stringent control to allow survival. Embryonic lethalities were also observed when the regulatory elements of the adipose-specific gene adipsin directed the expression of MyoD1 or myogenin cDNAs, suggesting that these sequences are probably not strong enough to confer tissue specificity. To determine the specificity of the control elements of another fat specific gene (adipocyte protein 2-aP2), we fused them to the bacterial b-galactosidase reporter gene and established stable transgenic strains. The expression of the reporter gene in none of the strains was adipose specific. Each strain displayed a unique pattern of expression in various cell lineages. Most exciting results were obtained in a transgenic strain in which cells migrating from the ventro-lateral edge of the dermomyotome of developing somites to populate the limb buds with myoblasts were specifically stained for lacZ. Since the control sequences of the adipsin or aP2 genes did not confer fat specificity in transgenic mice we have taken both molecular and genetic approaches as an initial effort to identify genes important in the conversion of a multipotential cell such as C3H10T1/2 cell to adipoblast. Several novel adipocyte cell lines have been established that differ in the expression of transcription factors of the C/EBP family known to be markers for adipocyte differentiation. These studies revealed that one of the genetic programming changes which occur during 10T1/2 conversion from multipotential cell to a committed adipoblast is the ability to linduce C/EBPa gene expression. It is expected that further analysis of this gene would identify elements which regulate this lineage-specific expression. Such elements might be good candidates in future attempts to convert adipoblasts to skeletal muscle cells in vivo.
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