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Littérature scientifique sur le sujet « Cell death »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 9 juin 2025

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Articles de revues sur le sujet "Cell death"

1

Fernández-Lázaro, Diego, César Ignacio Fernández-Lázaro, and Martínez Alfredo Córdova. "Cell Death: Mechanisms and Pathways in Cancer Cells." Cancer Medicine Journal 1, no. 1 (August 31, 2018): 12–23. http://dx.doi.org/10.46619/cmj.2018.1-1003.

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Programmed cell death is an essential physiological and biological process for the proper development and functioning of the organism. Apoptosis is the term that describes the most frequent form of programmed cell death and derives from the morphological characteristics of this type of death caused by cellular suicide. Apoptosis is highly regulated to maintain homeostasis in the body, since its imbalances by increasing and decreasing lead to different types of diseases. In this review, we aim to describe the mechanisms of cell death and the pathways through apoptosis is initiated, transmitted, regulated, and executed.

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Lockshin, Richard A., and Zahra Zakeri. "Cell Death (Apoptosis, Programmed Cell Death)." Directions in Science 1 (February 27, 2002): 41–44. http://dx.doi.org/10.1100/tsw.2002.161.

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Yao, Nan, and Jean T. Greenberg. "Arabidopsis ACCELERATED CELL DEATH2 Modulates Programmed Cell Death." Plant Cell 18, no. 2 (December 30, 2005): 397–411. http://dx.doi.org/10.1105/tpc.105.036251.

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Deniz, Özdemir. "KAN0438757: A NOVEL PFKFB3 INHIBITOR THAT INDUCES PROGRAMMED CELL DEATH AND SUPPRESSES CELL MIGRATION IN NON-SMALL CELL LUNG CARCINOMA CELLS." Biotechnologia Acta 16, no. 5 (October 31, 2023): 34–44. http://dx.doi.org/10.15407/biotech16.05.034.

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Aim. PFKFB3 is glycolytic activators that is overexpressed in human lung cancer and plays a crucial role in multiple cellular functions including programmed cell death. Despite the many small molecules described as PFKFB3 inhibitors, some of them have shown disappointing results in vitro and in vivo. On the other hand KAN0438757, selective and potent, small molecule inhibitor has been developed. However, the effects of KAN0438757, in non-small cell lung carcinoma cells remain unknown. Herein, we sought to decipher the effect of KAN0438757 on proliferation, migration, DNA damage, and programmed cell death in non-small cell lung carcinoma cells. Methods. The effects of KAN0438757 on cell viability, proliferation, DNA damage, migration, apoptosis, and autophagy in in non-small cell lung carcinoma cells was tested by WST-1, real-time cell analysis, comet assay, wound-healing migration test, and MMP/JC-1 and AO/ER dual staining assays as well as western blot analysis. Results. Our results revealed that KAN0438757 significantly suppressed the viability and proliferation of A549 and H1299 cells and inhibited migration of A549 cells. More importantly, KAN0438757 caused DNA damage and triggered apoptosis and this was accompanied by the up-regulation of cleaved PARP in A549 cells. Furthermore, treatment with KAN0438757 resulted in increased LC3 II and Beclin1, which indicated that KAN0438757 stimulated autophagy. Conclusions. Overall, targeting PFKFB3 with KAN0438757 may be a promising effective treatment approach, requiring further in vitro and in vivo evaluation of KAN0438757 as a therapy in non-small cell lung carcinoma cells.

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Sarosiek, Kristopher. "Blocking cell death to enhance cell death." Science Translational Medicine 9, no. 408 (September 20, 2017): eaao6129. http://dx.doi.org/10.1126/scitranslmed.aao6129.

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M, Aloysius Dhivya, Kishore A, and Bharathidevi SR. "Down-Regulation of NRF2 Signaling Triggers Cell Death in Y79 Cells upon Copper Chelation." Open Access Journal of Ophthalmology 10, no. 1 (2025): 1–10. https://doi.org/10.23880/oajo-16000329.

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Background: Retinoblastoma is a rare intraocular malignancy that leads to vision loss in children. While copper (Cu) chelation has been reported as a therapy in many cancers, its relevance to retinoblastoma has not yet been explored. Objectives: In this study, we have explored the role of penicillamine (a Cu chelator) as a therapeutic target for retinoblastoma using Y79 cells as a model. Methods: The effect of the Cu chelator on the viability of Y79 was assessed using the MTT assay. Additionally, we performed nuclear fractionation to assess Nuclear factor erythroid 2–related factor 2 (NRF2) activation, evaluated the downstream targets of NRF2 at transcript and protein levels, and measured SOD (superoxide dismutase) activity. Results: Penicillamine (2 mM) induced cell death in Y79 cells, inhibited NRF2 signaling, and reduced SOD activity. Furthermore, the downstream targets of NRF2 namely VEGF as well as PCNA (proliferating cell nuclear antigen) were decreased with penicillamine, which induced cell death in Y79 cells. We observed similar results in HeLa cells (positive control) comparable to Y79 cells. Conclusion: Therefore, we speculate that penicillamine could be a target for retinoblastoma as it induces cell death in Y79 cells by regulating NRF2 nuclear translocation and decreasing its downstream targets.

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Medema, J. P., H. Walczak, M. Hahne, and V. de Laurenzi. "Cell Death." Cell Death & Differentiation 17, no. 4 (March 15, 2010): 730–32. http://dx.doi.org/10.1038/cdd.2010.11.

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Hotchkiss, Richard S., Andreas Strasser, Jonathan E. McDunn, and Paul E. Swanson. "Cell Death." New England Journal of Medicine 361, no. 16 (October 15, 2009): 1570–83. http://dx.doi.org/10.1056/nejmra0901217.

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Vogel, Michael W. "Cell Death." American Journal of Psychiatry 162, no. 8 (August 2005): 1503. http://dx.doi.org/10.1176/appi.ajp.162.8.1503.

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MALORNI, WALTER, and GIANFRANCO DONELLI. "Cell Death." Annals of the New York Academy of Sciences 663, no. 1 Aging and Cel (November 1992): 218–33. http://dx.doi.org/10.1111/j.1749-6632.1992.tb38666.x.

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Thèses sur le sujet "Cell death"

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Pat, Sze Wa. "Cell metabolism in cell death and cell growth." HKBU Institutional Repository, 2007. http://repository.hkbu.edu.hk/etd_ra/775.

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Crisby, Milita. "Cell death in atherosclerosis /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3191-7/.

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Ellison, David William. "Cell proliferation, cell death, and differentiation in gliomas." Thesis, University of Southampton, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295912.

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Uppington, Kay Marie. "Cell death in prion disease." Thesis, University of Bath, 2008. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.488879.

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Prion diseases are a group of fatal neurodegenerative diseases, including CJD and scrapie, which are thought to be caused by a protein termed a prion (PrP). As manganese has previously been suggested to be involved in prion disease we have investigated manganese binding to PrP and its role in the toxicity of the protein. We have shown that manganese bound PrP (MnPrP) has several of the characteristics of the disease form of PrP, including protease resistance and toxicity that is dependent on cellular PrP expression. Further investigation into the mechanism of toxicity revealed that MnPrP is significantly more toxic to neuronal cells than nonmanganese bound PrP and that toxicity requires the presence of known metal binding residues within the protein. We have demonstrated that treatment of neuronal cells with MnPrP causes caspase 3 activation and apoptosis, as demonstrated by DNA laddering, and we hypothesise that caspase 3 is activated by a p38 pathway. Treatment of neurones with MnPrP also caused a significant increase in cellular ROS production, although this did not appear to be a major cause of cell death as antioxidants were unable to save cells from cell death. We also investigated mechanisms by which cells can survive scrapie infection and MnPrP toxicity. We have shown that cells infected with scrapie have increased ERK activation which was important for their survival. Cells that survived MnPrP treatment were also found to have increased ERK activation. This suggests that ERK may have a protective role in prion diseases and may be a potential therapeutic target.

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Beeharry, Neil. "Cell death in insulin-containing cells : induction and prevention." Thesis, University of Brighton, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.401600.

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Gorak-Stolinska, Patricia. "Activation induced cell death in human T cell subsets." Thesis, King's College London (University of London), 2002. http://kclpure.kcl.ac.uk/portal/en/theses/activation-induced-cell-death-in-human-t-cell-subsets(eb708e24-eccb-42fc-8930-d62ddf6794c1).html.

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Cheng, Jade. "Regulation of cell division and cell death by GRASP65." Thesis, University of Bristol, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.544414.

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RUNYAN, CHRISTOPHER MICHAEL. "The Role of Cell Death in Germ Cell Migration." University of Cincinnati / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1210732680.

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Courtois-Moreau, Charleen Laetitia. "Programmed Cell Death in Xylem Development." Doctoral thesis, Umeå universitet, Umeå Plant Science Centre, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1831.

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Concerns about climate changes and scarcity of fossil fuels are rising. Hence wood is becoming an attractive source of renewable energy and raw material and these new dimensions have prompted increasing interest in wood formation in trees, in both the scientific community and wider public. In this thesis, the focus is on a key process in wood development: programmed cell death (PCD) in the development of xylem elements. Since secondary cell wall formation is dependent, inter alia, upon the life time of xylem elements, the qualitative features of wood will be affected by PCD in xylem, about which there is little information. This thesis focuses on the anatomical, morphological and transcriptional features of PCD during xylem development in both the stem of hybrid aspen, Populus tremula (L.) x tremuloides (Michx.) and the hypocotyl of the herbaceous model system Arabidopsis thaliana (L. Heynh.). In Populus, the progressive removal of organelles from the cytoplasm before the time of death (vacuolar bursts) and the slowness of the cell death process, illustrated by DNA fragmentation assays (such as TUNEL and Comet assays), have been ascertained in the xylem fibres by microscopic analyses. Furthermore, candidate genes for the regulation of fibre cell death were identified either from a Populus EST library obtained from woody tissues undergoing fibre cell death or from microarray experiments in Populus stem, and further assessed in an in silico comparative transcriptomic analysis of Arabidopsis thaliana. These candidate genes were either putative novel regulators of fibre cell death or members of previously described families of cell death-related genes, such as autophagy-related genes. The induction of the latter and the previous microscopic observations suggest the importance of autophagy in the degradation of the cytoplasmic contents specifically in the xylem fibres. Vacuolar bursts in the vessels were the only previously described triggers of PCD in the xylem, which induce the very rapid degradation of the nuclei and surrounding cytoplasmic contents, therefore unravelling a unique previously unrecorded type of PCD in the xylem fibres, principally involving autophagy. Arabidopsis is an attractive alternative model plant for exploring some aspects of wood formation, such as the characterisation of negative regulators of PCD. Therefore, the anatomy of Arabidopsis hypocotyls was also investigated and the ACAULIS5 (ACL5) gene, encoding an enzyme involved in polyamine biosynthesis, was identified as a key regulator of xylem specification, specifically in the vessel elements, though its negative effect on the cell death process. Taken together, PCD in xylem development seems to be a highly specific process, involving unique cell death morphology and molecular machinery. In addition, the technical challenges posed by the complexity of the woody tissues examined highlighted the need for specific methods for assessing PCD and related phenomena in wood.<br>Oron för klimatförändringar och brist på fossila bränslen har ökat påtagligt under de senaste åren. De enorma möjligheter som skogsråvaran erbjuder som alternativ källa för förnyelsebar energi och råmaterial har väckt ett stort intresse också för den biologiska processen bakom vedbildning i träd. Denna avhandling fokuserar på en viktig process i vedbildning: programmerad celldöd (PCD) i xylemet. Xylemcellernas livstid påverkar bildningen av sekundära cellväggar, vilket i sin tur påverkar vedens kvalitativa egenskaperna, så som veddensitet. Trots dess betydelse för viktiga egenskaper hos vedråvaran existerar fortfarande väldigt lite information om xylem PCD på cellulär eller molekylär nivå. I den här avhandlingen belyses de anatomiska, morfologiska och genetiska aspekterna av PCD i xylemutveckling i både stam av hybridasp, Populus tremula (L.) x tremuloides (Michx.) och hypokotyl av det örtartade modellsystemet Arabidopsis thaliana (L. Heynh.). Xylemet i både Populus och Arabidopsis består av två olika celltyper; de vattentransporterade kärlen och de stödjande fibrerna. Det är känt att celldöd i kärlen pågår mycket snabbt efter att den centrala vakuolen brister och de hydrolytiska enzymer släpps in i cytoplasman. I den här avhandlingen ligger fokus på fibrerna i Populus xylemet. Med hjälp av mikroskopianalyser av cellmorfologin (elektronmikroskopi) och DNA-fragmentering i cellkärnan (TUNEL- och Comet-analyser) kunde vi konstatera att till skillnad från kärlen så uppvisar fibrerna en långsam och progressiv nedbrytning av organellerna och cellkärnans DNA före vakuolbristning. Dessutom har kandidatgener för reglering av fibercelldöd identifierats antingen från ett Populus EST bibliotek från vedartade vävnader som genomgår fibercelldöd eller från mikroarray experiment i Populus stam. Dessa kandidatgener är antingen potentiella nya regulatorer av fibercelldöd eller medlemmar av tidigare beskrivna familjer av celldödsrelaterade gener. Bland de sistnämnda finns autofagi-relaterade gener, vilket stöder funktionen av autofagi i samband med autolys av cellinnehållet i xylemfibrerna. Dessa studier pekar därför på en typ av PCD som har inte tidigare beskrivits för xylemet. Arabidopsis är ett alternativt växtmodellsystem för studier av vissa aspekter av vedbildningen, såsom karakteriseringen av negativa regulatorer av PCD. Därför har också hypokotylanatomin analyserats, och ACAULIS5 (ACL5) genen, som kodar för ett enzym i biosyntesen av polyaminer, har visats vara en viktig regulator av xylemspecifikation genom dess negativa effekt på kärlens celldöd. Sammantaget visar denna avhandling att PCD i xylemutvecklingen verkar involvera unika morfologiska och molekylära mekanismer. Vi visar dessutom att komplexiteten hos de vedartade vävnaderna leder till ett behov av bättre anpassade verktyg för att djupare kunna bedöma PCD och liknande fenomen i veden.<br>Även med namnet Moreau-Courtois, Charleen L. samt Moreau, Charleen.

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Klassen, Shaun Scott. "Nitric oxide-induced cardiomyocyte cell death." Thesis, University of British Columbia, 2006. http://hdl.handle.net/2429/31539.

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Nitric oxide (NO), a regulator of diverse cardiovascular functions, modifies cardiac cell viability through mechanisms that remain uncertain. Several pathways were studied to understand these effects. The possibility that the protein p53 is involved in the cardiomyocyte response to the NO donor s-nitrosoglutathione (GSNO) or the peroxynitrite donor 3- morpholinosydnonimine (SIN-1) was explored. These donors induced a concentration-dependent increase of cell death in cultured embryonic chick cardiomyocytes. Expression of p53 protein was increased in response to GSNO, specifically in the nucleus. GSNO also caused DNA damage, but pifithrin, an inhibitor of p53 transactivation activity, did not alter the extent of this damage or cell death. Therefore, the role of increased nuclear p53 in response to NO and NO-induced DNA damage may not be specifically operative in NO-induced cell death. The action of GSNO also appears independent of mitochondrial pathways in cell death, as there was no association of p53 with the mitochondria. Neither GSNO- or SIN-1-induced cell death was altered by cyclosporin A, suggesting that permeability transition pore opening is not operative in these modes of induction of death. In contrast to SIN-1, GSNO did not reduce mitochondrial transmembrane potential, implying separate mechanisms of cell death. Immunocytochemistry demonstrated increased amounts of nitrotyrosine in response to GSNO or SIN-1, confirmed by Western blot following SIN-1. FeTPPS, an isomerase that converts peroxynitrite into the less toxic nitrate, produced a significant reduction of SIN-1-induced cell death and cellular protein nitration. FeTPPS did not reduce cell death from GSNO alone, but did from the combination of GSNO and hydrogen peroxide, a condition which promotes the generation of peroxynitrite. In summary, NO-induced cardiomyocyte cell death is due in part to the disruption of normal cellular functions by nitration of key proteins. Peroxynitrite decomposition reduces protein nitration and cell death, while p53 appears functions independent of the mitochondria or gene transactivation and may act in other pathways, such as cell repair.<br>Medicine, Faculty of<br>Medicine, Department of<br>Experimental Medicine, Division of<br>Graduate

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Livres sur le sujet "Cell death"

1

Melino, Gerry. Cell death. Chichester, UK: Wiley-Blackwell, 2010.

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Wu, Hao, ed. Cell Death. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-9302-0.

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Gerry, Melino, and Vaux David, eds. Cell death. Chichester, West Sussex: John Wiley & Sons, 2010.

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Jahani-Asl, Arezu, ed. Neuronal Cell Death. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2409-8.

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Shen, Han-Ming, and Peter Vandenabeele, eds. Necrotic Cell Death. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8220-8.

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Puthalakath, Hamsa, and Christine J. Hawkins, eds. Programmed Cell Death. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3581-9.

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Lossi, Laura, and Adalberto Merighi, eds. Neuronal Cell Death. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2152-2.

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Shi, Yun-Bo, Yufang Shi, Yonghua Xu, and David W. Scott, eds. Programmed Cell Death. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-0072-2.

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Paul, Mattson Mark, Estus Steven, and Rangnekar Vivek, eds. Programmed cell death. Amsterdam: Elsevier, 2001.

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Yun-Bo, Shi, and International Symposium on Programmed Cell Death (1996 : Shanghai, China), eds. Programmed cell death. New York: Plenum Press, 1997.

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Chapitres de livres sur le sujet "Cell death"

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Lockshin, Richard A. "Cell Death." In Studies of Aging, 58–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59916-3_5.

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Burke, Thomas J., and Robert W. Schrier. "Cell Death." In Molecular Biology of Membrane Transport Disorders, 485–505. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1143-0_24.

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Knudsen, T. B. "Cell Death." In Drug Toxicity in Embryonic Development I, 211–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60445-4_8.

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Vaux, David L. "Historical Perspective: The Seven Ages of Cell Death Research." In Cell Death, 1–14. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9302-0_1.

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Chan, Francis Ka-Ming. "Programmed Necrosis/Necroptosis: An Inflammatory Form of Cell Death." In Cell Death, 211–28. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9302-0_10.

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Gavathiotis, Evripidis. "Structural Perspectives on BCL-2 Family of Proteins." In Cell Death, 229–51. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9302-0_11.

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Li, Jixi, and Hao Wu. "Structural Basis of Death Receptor Signaling." In Cell Death, 253–66. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9302-0_12.

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Jiang, Xuejun. "The Intrinsic Apoptotic Pathway." In Cell Death, 15–40. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9302-0_2.

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Lucas, Carrie L., and Michael J. Lenardo. "Molecular Basis of Cell Death Programs in Mature T Cell Homeostasis." In Cell Death, 41–59. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9302-0_3.

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Liu, Qian, Xiaoke Chi, Brian Leber, and David W. Andrews. "Bcl-2 Family and Their Therapeutic Potential." In Cell Death, 61–96. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9302-0_4.

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Actes de conférences sur le sujet "Cell death"

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Bilgic, Elif. "Endocannabinoid induced apoptotic cell death on endometriotic cells." In 15th International Congress of Histochemistry and Cytochemistry. Istanbul: LookUs Scientific, 2017. http://dx.doi.org/10.5505/2017ichc.op-12.

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Wright, Neil T. "Parameter Correlation in Models of Hyperthermic Cell Death." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53933.

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A number of mathematical models have been developed to predict the survival of cells after heating. Some of these models have been based on first principle arguments, while others have been empirically motivated. Some models have been inspired by analogs of damage to cells by ionizing radiation. Evidence exists for multiple targets leading to cell death, although precise definition of the pathways for the various temperature ranges and environmental conditions remains in question. For reviews of the cellular targets of heating, see [1], [2], or [3].

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Jain, Shruti, Pradeep K. Naik, and Sunil V. Bhooshan. "BiCMOS Implementation of Cell Signaling for Cell Survival/Death." In 2010 International Conference on Signal Acquisition and Processing (ICSAP). IEEE, 2010. http://dx.doi.org/10.1109/icsap.2010.36.

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Gu, Ying, Shanxiang Jiang, Elahe Mahdavian, and Shile Huang. "Abstract 4566: Fusarochromanone inhibits cell proliferation and induces cell death in COS7 cells." 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.am2014-4566.

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Pearce, John A. "Considerations in Modeling Cell Death Processes." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80191.

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Traditional single-reaction Arrhenius models have been successfully used for many years in burn studies[1–3] and have been adapted and used to predict quantitative histologic results in laser, RF and microwave heating at high temperatures.[4–6] The single reaction kinetics model also forms the basis for the time scaling ratio as is currently used in calculating the cumulative equivalent minutes (CEM) assessment of tumor hyperthermia treatments.[7] Recently, it has been clearly demonstrated that these models are not acceptably accurate predictors of the early stages of cell death processes in hyperthermic heating — moderate temperature rises (< ∼15 C) for times from several minutes to hours.[8, 9] A typical ensemble of cell survival curves has an initial slowly-developing shoulder region, a constant-rate region and, often, a “foot’, as it were, which has a much slower death rate. Simple first-order Arrhenius predictions are constant-rate models, only, and substantially over-estimate population cell death in the early stages of heating.

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"Regulated cell death in Hetherocephalus glaber." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-365.

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Kessel, David, and John J. Reiners, Jr. "Cell death pathways associated with PDT." In Biomedical Optics 2006, edited by David Kessel. SPIE, 2006. http://dx.doi.org/10.1117/12.639925.

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Zitvogel, Laurence, and Guido Kroemer. "Abstract SY03-01: The desirable death of the cancer cell: Immunogenic cell death for optimal chemotherapy." 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-sy03-01.

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9

Hadji, Abbas, Annika Hau, and Marcus E. Peter. "Abstract 4847: CD95/Fas protects cancer cells from cell death." 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.am2012-4847.

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10

Jo, Jae-Cheol, Sook-Kyoung Heo, Eui-Kyu Noh, Jeong Yi Kim, Jun Young Sung, Ho-Min Yu, Yoo Kyung Jeong, Lan Jeong Ju, and Yunsuk Choi. "Abstract 1250: Radotinib induces cell death of multiple myeloma cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1250.

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Rapports d'organisations sur le sujet "Cell death"

1

Baker, Nicholas E. Cell Proliferation, Cell Death, and Size Regulation. Fort Belvoir, VA: Defense Technical Information Center, October 1998. http://dx.doi.org/10.21236/adb248354.

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2

Distelhorst, Clark W. Programmed Cell Death in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 1995. http://dx.doi.org/10.21236/ada300581.

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3

Distelhorst, Clark W. Programmed Cell Death in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 1997. http://dx.doi.org/10.21236/ada340671.

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4

Chung, Leland W. K. Accelerated Tumor Cell Death by Anglogenic Modifiers. Fort Belvoir, VA: Defense Technical Information Center, August 2005. http://dx.doi.org/10.21236/ada441865.

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5

Drews, Gary, N. Programmed Cell Death During Female Gametophyte Development. Office of Scientific and Technical Information (OSTI), September 2004. http://dx.doi.org/10.2172/1014978.

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6

Chung, Leland W., Chia-Ling Hsieh, Michael Bradley, and Mitchell H. Sokoloff. Accelerated Tumor Cell Death by Angiogenic Modifiers. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada403672.

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7

Tyler, Kenneth L. Mechanisms of Virus-Induced Neural Cell Death. Fort Belvoir, VA: Defense Technical Information Center, March 2005. http://dx.doi.org/10.21236/ada435392.

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8

Chung, Leland W. Accelerated Tumor Cell Death by Angiogenic Modifiers. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada418654.

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9

Kornbluth, Sally. Metabolic Regulation of Ovarian Cancer Cell Death. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada570124.

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10

Tyler, Kenneth L. Mechanisms of Virus-Induced Neural Cell Death. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada419455.

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