Littérature scientifique sur le sujet « Cancer cell physiology »
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Articles de revues sur le sujet "Cancer cell physiology"
Gao, Sumei, Xiaoyan Li, Xia Ding, Wenwen Qi et Qifeng Yang. « Cepharanthine Induces Autophagy, Apoptosis and Cell Cycle Arrest in Breast Cancer Cells ». Cellular Physiology and Biochemistry 41, no 4 (2017) : 1633–48. http://dx.doi.org/10.1159/000471234.
Texte intégralWang, Zhongli, et Chao Liu. « Lgr5-Positive Cells are Cancer-Stem-Cell-Like Cells in Gastric Cancer ». Cellular Physiology and Biochemistry 36, no 6 (2015) : 2447–55. http://dx.doi.org/10.1159/000430205.
Texte intégralYin, Yu-Chun, Chao-Cheng Lin, Tzu-Ting Chen, Jen-Yeu Chen, Hui-Ju Tsai, Chia-Yu Wang et Shiow-Yi Chen. « Clozapine Induces Autophagic Cell Death in Non-Small Cell Lung Cancer Cells ». Cellular Physiology and Biochemistry 35, no 3 (2015) : 945–56. http://dx.doi.org/10.1159/000369751.
Texte intégralLuo, Hua-Rong, Ying Liu, Xiao-Dong Wan, Jun-Liang Li, Min Wu, Qi-Min Zhang, Deng-Long Wu, Xin Zhao et Tian-Ru Wang. « Sumoylation Negatively Regulates CSR1-Dependent Prostate Cancer Cell Death ». Cellular Physiology and Biochemistry 46, no 5 (2018) : 1861–67. http://dx.doi.org/10.1159/000489370.
Texte intégralCheng, Kunrong, Roxana Samimi, Guofeng Xie, Jasleen Shant, Cinthia Drachenberg, Mark Wade, Richard J. Davis, George Nomikos et Jean-Pierre Raufman. « Acetylcholine release by human colon cancer cells mediates autocrine stimulation of cell proliferation ». American Journal of Physiology-Gastrointestinal and Liver Physiology 295, no 3 (septembre 2008) : G591—G597. http://dx.doi.org/10.1152/ajpgi.00055.2008.
Texte intégralBose, Shree, Vijyendra Ramesh et Jason W. Locasale. « Acetate Metabolism in Physiology, Cancer, and Beyond ». Trends in Cell Biology 29, no 9 (septembre 2019) : 695–703. http://dx.doi.org/10.1016/j.tcb.2019.05.005.
Texte intégralLiu, Shunli, Mingrui Chen, Pengcheng Li, Yujia Wu, Chunjuan Chang, Yabin Qiu, Ling Cao, Zhen Liu et Chiyu Jia. « Ginsenoside Rh2 Inhibits Cancer Stem-Like Cells in Skin Squamous Cell Carcinoma ». Cellular Physiology and Biochemistry 36, no 2 (2015) : 499–508. http://dx.doi.org/10.1159/000430115.
Texte intégralBai, Xiaoxue, Lin Meng, Huijie Sun, Zhuo Li, Xiufang Zhang et Shucheng Hua. « MicroRNA-196b Inhibits Cell Growth and Metastasis of Lung Cancer Cells by Targeting Runx2 ». Cellular Physiology and Biochemistry 43, no 2 (2017) : 757–67. http://dx.doi.org/10.1159/000481559.
Texte intégralGao, Zhuo, Ruiqi Liu, Na Ye, Chao Liu, Xiuli Li, Xiaodong Guo, Zhuoran Zhang, Xiaoxi Li, Yuanfei Yao et Xiaofeng Jiang. « FOXO1 Inhibits Tumor Cell Migration via Regulating Cell Surface Morphology in Non-Small Cell Lung Cancer Cells ». Cellular Physiology and Biochemistry 48, no 1 (2018) : 138–48. http://dx.doi.org/10.1159/000491670.
Texte intégralArcangeli, Annarosa, et Jason X. J. Yuan. « American Journal of Physiology-Cell Physiology theme : ion channels and transporters in cancer ». American Journal of Physiology-Cell Physiology 301, no 2 (août 2011) : C253—C254. http://dx.doi.org/10.1152/ajpcell.00159.2011.
Texte intégralThèses sur le sujet "Cancer cell physiology"
Choi, Mi-Yon. « P53 mediated cell motility in H1299 lung cancer cells ». VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/109.
Texte intégralLevitt, Randy J. « Aspects of insulin-like growth factor physiology in cancer ». Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111826.
Texte intégralAlthough the roles of the IGFs, IGF-IR and IGFBPs in cancer have been studied extensively, this thesis describes several new links between IGF physiology and neoplasia. In the first section, we demonstrate that IGF-I can attenuate growth inhibition and apoptosis induced by a class of drugs called COX-2 inhibitors in BxPC-3 pancreatic cancer cells. This effect could be attributed to opposite influences of IGF-IR signalling and COX-2 inhibitors on activation of Akt, with IGF-IR signalling increasing activity and COX-2 inhibitors decreasing activity. In the second section, we demonstrate that in 184htert cells, an immortal but untransformed breast epithelial cell line, COX-2 inhibitors can induce IGFBP-3 expression. We go on to show that IGFBP-3 can inhibit growth of this cell line in an IGF-dependent manner, and speculate that this action of COX-2 inhibitors may be relevant to data linking use of this class of drugs to decreased breast cancer risk. In the third section, we demonstrate that the expression of IGFBP-2 in U251 glioma cells is inhibited by the induction of the tumor suppressor PTEN. Furthermore, IGFBP-2 does not effect the growth of this cell line, indicating that published associations between tumor IGFBP-2 expression and grade of glioma may be a result of IGFBP-2 acting as a marker for loss of function of PTEN. In the fourth and final section, we demonstrate that in MDA-MB-231 breast cancer cells, over-expression of IGFBP-2 can enhance growth, indicating that the effect of IGFBP-2 on growth of neoplastic cells is tissue specific. Furthermore, antisense strategies targeting IGFBP-2 mRNA (antisense oligonucleotides and siRNA) can inhibit growth of IGFBP-2-expressing breast cancer cells both in vitro and in vivo.
Taken together, these results extend the existing body of evidence demonstrating that IGF physiology contributes to neoplastic growth, and suggest that strategies to inhibit IGF-IR signalling and/or IGFBP-2 expression may have therapeutic value for some types of cancers.
Tang, Haoran. « Scar/WAVE complex suppresses cell invasion and cancer cell transformation ». Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/3633/.
Texte intégralBehmoaram, Emy. « Biological studies of fascin function in cancer cell invasion and cancer progression ». Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111596.
Texte intégralGuerrini, Giuditta, et Fabio Carraro. « Hedgehog signalling pathway and Carbonic Anhydrases in Breast cancer cell physiology ». Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1071510.
Texte intégralScott, Hannah Elizabeth. « PKC-δ, its C2 domain and breast cancer cell lines ». Thesis, University of Nottingham, 2012. http://eprints.nottingham.ac.uk/12668/.
Texte intégralKumar, Jothi Dinesh. « Novel stromal cell signalling systems in oesophageal cancer ». Thesis, University of Liverpool, 2013. http://livrepository.liverpool.ac.uk/15257/.
Texte intégralSwanson, Tara. « Physiological correlates of cancer-related fatigue in advanced non-small cell lung cancer patients ». Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=98503.
Texte intégralMethods. Participants were evaluated by a physical therapist within the McGill Cancer Nutrition and Rehabilitation Program. Performance-based measures of physical function [upper limb strength and endurance (Jamar dynamometry), lower limb strength (30sec chair rise), cardiorespiratory function (2 minute walk - 2MW)] and a symptom questionnaire (Edmonton Symptom Assessment Scale) were conducted at one point in time. The primary endpoint of global fatigue rating was assessed using the Brief Fatigue Inventory (BFI).
Results. Fifty-eight patients (30M:28F, mean age 68 +/- 12) participated in the study. Forty-three percent were actively receiving treatment at the time of assessment. On the BFI, 67% had moderate or severe fatigue and 84% indicated fatigue had interfered with their functioning during the past 24 hours. Global fatigue scores were unrelated to hand grip strength or endurance measurements, hematological parameters or sleep quality but were significantly correlated with chair rise performance, overall rating of breathlessness, patient rating of pain and patient rated weakness. Multivariate regression analysis suggested the best model for global fatigue scores incorporates patients' ratings of weakness, breathlessness and chair rise performance.
Conclusions. Fatigue is prevalent and impacts on the function of advanced NSCLC patients. Several key factors contribute to this fatigue, with muscular and cardiorespiratory restrictions playing an important role. Such findings may have clinical implications in the recommendations of rest and exercise to best manage fatigue.
Christofakis, Emil Paul. « Effects of CXCL8 Overexpression on Tumor Cell Proliferation and Migration in an HNSCC Cell Model ». VCU Scholars Compass, 2007. http://scholarscompass.vcu.edu/etd/1475.
Texte intégralThomas, Mark Peter. « Differential tolerance of a cancer and a non-cancer cell line to amino acid deprivation : mechanistic insight and clinical potential ». Thesis, Stellenbosch : Stellenbosch University, 2012. http://hdl.handle.net/10019.1/19912.
Texte intégralENGLISH ABSTRACT: Introduction – Due to spatial separation from the native vascular bed, solid tumours develop regions with limited access to nutrients essential for growth and survival. The promotion of a process known as macroautophagy may facilitate in the maintenance of intracellular amino acid levels, through breakdown of cytoplasmic proteins, so that they remain available for macromolecular biosynthesis and ATP production. Several studies point to the potential ability of some cancers to temporarily increase autophagy and thereby prolong cell survival during metabolic stress. The validity of these claims is assessed when a commonly used breast cancer cell line and an epithelial breast cell line are starved of amino acids in this study. Furthermore, we go on to hypothesize that acute amino acid deprivation during treatment will result in an elevated sensitivity of MDAMB231 cells to doxorubicin toxicity but limit its cytotoxic side-effects in MCF12A cells. Methods and study design- Human breast cancer cells (MDAMB231) and breast epithelial cells (MCF12A) cultured in complete growth medium were compared to those incubated in medium containing no amino acids. Steady state autophagy levels were monitored using classical protein markers of autophagy (LC3-II and beclin-1) and the acidic compartmentalization in cells (Lysotracker™ red dye) in conjunction with autophagy inhibition (bafilomycin A1 and ATG5 siRNA). Cell viability was monitored using several techniques, including caspase 3/7 activity. ATP levels were assessed using a bioluminescent assay, while mass spectrometry based proteomics was used to quantify cellular amino acid levels. Similar techniques were used to monitor autophagy during doxorubicin treatment, while cellular doxorubicin localization was monitored using immunofluorescence microscopy. Finally, a completely novel GFP-LC3 mouse tumour model was designed to assess autophagy and caspase activity within tumours in vivo, during protein limitation and doxorubicin treatment. Results - Amino acid deprivation resulted in a transient increase in autophagy at approximately 6 hours of amino acid starvation in MDAMB231 cells. The amino acid content was preserved within these cells in an autophagy-dependent manner, a phenomenon that correlated with the maintenance of ATP levels. Inhibition of autophagy during these conditions resulted in decreased amino acid and ATP levels and increased signs of cell death. MCF12A cells displayed a greater tolerance to amino acid starvation during 24 hours of amino acid starvation. Evidence indicated that autophagy was important for the maintenance of amino acid and ATP levels in these cells and helped prevent starvation-induced cell death. Furthermore, data showed that concomitant amino acid withdrawal resulted in decreased cellular acidity in MDAMB231 cells, and increased acidity in MCF12A cells, during doxorubicin treatment. These changes correlated with evidence of increased cell death in MDAMB231 cells, but a relative protection in MCF12A cells. A novel model was used to apply these techniques in vivo, and although mice fed on a low protein diet during high dose doxorubicin treatment had increased mean survival and smaller tumour sizes, evidence suggested that autophagy is protecting a population of cells within these tumours. Conclusions - This novel approach to tumour sensitization could have several implications in the context of cancer therapy, and given the delicate relationship that autophagy has with the cancer microenvironment, efforts to determine the mechanisms involved in autophagy and sensitization could lead to new and innovative treatment opportunities for cancer management.
AFRIKAANSE OPSOMMING: Inleiding – As gevolg van hul skeiding van die oorpronklike vaskulêre netwerk, ontwikkel soliede gewasse areas met beperkte toegang tot noodsaaklike voedingstowwe. Die bevordering van 'n proses wat as makro-autofagie bekend staan, kan die handhawing van intrasellulêre aminosuur vlakke fasiliteer. Voorafgenoemde proses word waarskynlik deur die afbreek van sitoplasmiese proteïene teweegebring om sodoende vir makro-molekulêre biosintese en ATP produksie beskikbaar te kan wees. Verskeie studies dui daarop dat sommige kankersoorte die vermoë het om autofagie tydelik te verhoog, en daarby sel oorlewing gedurende metaboliese stress te verleng. Die geldigheid van hierdie eise word evalueer wanneer 'n algemeen beskikbare borskanker sellyn, en 'n borsepiteelsellyn in hierdie studie van aminosure verhonger word. Verder, veronderstel ons dat akute aminosuur ontneming gedurende behandeling 'n verhoogde sensitiwiteit van MDAMB231 selle tot doxorubicin toksisiteit tot gevolg sal hê, maar terselfdetyd die middel se sitotoksiese newe-effekte in MCF12A selle sal beperk. Metodes en studie ontwerp – Menslike borskanker- (MDAMB231) en bors epiteel selle (MCF12A) wat in volledige groeimedium gekweek is, is vergelyk met selle wat in aminosuur vrye medium gekweek is. Basislyn autofagie-vlakke is gemonitor deur die gebruik van klassieke autofagie proteïen merkers (LC3-II en beclin-1) en die asidiese kompartementalisering in selle (Lysotracker™ rooi kleurstof) saam met autofagie inhibisie (bafilomycin A1 and ATG5 siRNA). Sellewensvatbaarheid is deur die gebruik van verskeie tegnieke, insluitend caspase 3/7 aktiwiteit, gemonitor. ATP-vlakke is deur die gebruik van 'n bioluminiserende tegniek gemeet, terwyl massa-spektrometrie-gebaseerde “proteomics” gebruik is om sel aminosuur vlakke te kwantifiseer. Soortgelyke tegnieke is gebruik om autofagie gedurende doxorubicin behandeling waar te neem, terwyl sellulêre doxorubicin lokalisasie deur die gebruik van immunofluoresensie mikroskopie gemonitor is. Ten slotte, is 'n unieke GFP-LC3 muismodel in hierdie studie ontwikkel. Hierdie model is gebruik om autofagie en caspase aktiwiteit in gewasse in vivo te bestudeer tydens proteïen beperking en doxorubicin behandeling. Resultate – Aminosuur ontneming het tot 'n tydelike verhoging in autofagie na ongeveer 6 ure van aminosuur verhongering in MDAMB231 selle gelei. Die aminosuur inhoud van hierdie selle het op 'n autofagie-afhanklike manier behoue gebly. Hierdie verskynsel het met die handhawing van ATP-vlakke gekorreleer. Autofagie inhibisie gedurende hierdie kondisies het 'n verlaging in aminosuur en ATP-vlakke teweeggebring, sowel as vermeerderde tekens van seldood tot gevolg gehad. MCF12A selle het 'n groter toleransie tot aminosuur verhongering tydens die 24 uur aminosuur verhongeringsperiode getoon. Getuienis het aangedui dat autofagie belangrik vir die handhawing van aminosuur en ATP-vlakke in hierdie selle was, en gehelp het om verhongerings-geïnduseerde seldood te voorkom. Verder het data gewys dat aminosuur ontrekking tot verminderde sellulêre asiditeit in MDAMB231 selle, en verhoogde asiditeit in MCF12A selle gedurende doxorubicin behandeling gelei het. Hierdie veranderinge stem ooreen met getuienis van toenemende seldood in MDAMB231 selle, maar 'n relatiewe beskerming in MCF12A selle. 'n Unieke model was gebruik om hierdie tegnieke in vivo toe te pas. Alhoewel verhoogde oorlewing en kleiner gewasse in muise op 'n lae proteïen dieet gedurende hoë dosis doxorubicin behandeling opgemerk is, het bewyse voorgestel dat autofagie 'n populasie selle binne die gewasse beskerm. Gevolgtrekkings – Hierdie unieke benadering tot tumor sensitisering kan verskeie implikasies in die konteks van kanker behandeling hê. Gegewe die delikate verhouding van autofagie met die kanker mikro-omgewing, kan pogings om die meganismes betrokke in autofagie en sensitisering te bepaal, tot nuwe en innoverende behandelings vir kanker lei.
Livres sur le sujet "Cancer cell physiology"
W, Masters John R., et Palsson Bernhard, dir. Cancer cell lines. Dordrecht : Kluwer Academic Publishers, 1999.
Trouver le texte intégralHarvey, Amanda. Cancer cell signalling. Chichester, West Sussex : John Wiley & Sons, Inc., 2013.
Trouver le texte intégral-Y, Wang J., et Casero Robert Anthony, dir. Polyamine cell signaling : Physiology, pharmacology, and cancer research. Totowa, N.J : Humana Press, 2006.
Trouver le texte intégralAvner, Friedman, et Aguda B, dir. Cell cycle, proliferation, and cancer. Berlin : Springer, 2006.
Trouver le texte intégralMalcolm, Steinberg, dir. The Cell surface in development and cancer. New York : Plenum Press, 1986.
Trouver le texte intégralMirzayans, Razmik. Cellular senescence : Implications for cancer therapy. New York : Nova Biomedical Books, 2009.
Trouver le texte intégralS, Stein Gary, et Pardee Arthur B. 1921-, dir. Cell cycle and growth control : Biomolecular regulation and cancer. 2e éd. Hoboken, NJ : Wiley-Liss, 2004.
Trouver le texte intégral1939-, Wilson Samuel H., et Hoagland Mahlon B, dir. Cancer biology and biosynthesis. Boca Raton, Fla : CRC Press, 1991.
Trouver le texte intégralCalcium, cell cycles, and cancer. Boca Raton, Fla : CRC Press, 1990.
Trouver le texte intégralservice), ScienceDirect (Online, dir. Programmed cell death : General principles for studying cell death. San Diego, Calif : Academic Press, 2008.
Trouver le texte intégralChapitres de livres sur le sujet "Cancer cell physiology"
Wang, Ji Ming, Weipin Shen, Oleg Chertov, Jo Van Damme et Joost J. Oppenheim. « Chemokine Modulation of Tumor Cell Physiology ». Dans Chemokines and Cancer, 129–41. Totowa, NJ : Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-701-7_8.
Texte intégralKampa, M., A. P. Nifli, G. Notas et E. Castanas. « Polyphenols and cancer cell growth ». Dans Reviews of Physiology, Biochemistry and Pharmacology, 79–113. Berlin, Heidelberg : Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/112_2006_0702.
Texte intégralBissell, Mina J. « The Central Role of Basement Membrane in Functional Differentiation, Apoptosis, and Cancer ». Dans Cell Death in Reproductive Physiology, 125–40. New York, NY : Springer New York, 1997. http://dx.doi.org/10.1007/978-1-4612-1944-6_12.
Texte intégralGaudino, G., L. Gandino, M. Cilli, A. Mondino et P. M. Comoglio. « The Bombesin Receptor Complex and Cell Growth : Physiology and Pathology ». Dans New Concepts in Cancer, 196–207. London : Macmillan Education UK, 1990. http://dx.doi.org/10.1007/978-1-349-10671-4_14.
Texte intégralMolino, Natalie, K. Ververis et Tom C. Karagiannis. « Principles of the Warburg Effect and Cancer Cell Metabolism ». Dans Molecular mechanisms and physiology of disease, 355–69. New York, NY : Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0706-9_12.
Texte intégralSidler, F., T. Wermelinger, L. Rist, A. Hensel et A. Viviani. « Influence of Mistletoe Extracts and Its Components on in Vitro Physiology of Cancer Cells ». Dans Animal Cell Technology Meets Genomics, 183–85. Dordrecht : Springer Netherlands, 2005. http://dx.doi.org/10.1007/1-4020-3103-3_36.
Texte intégralTenniswood, Martin, Sean Guenette, Colm Morrissey, Jacintha O’Sullivan, Zhengqi Wang, Ping Zhan, Srikala Sridhar, Johnathon Lakins et Hailun Tang. « Apoptosis and Tumor Invasion in Hormone-Dependent Cancers ». Dans Cell Death in Reproductive Physiology, 208–29. New York, NY : Springer New York, 1997. http://dx.doi.org/10.1007/978-1-4612-1944-6_17.
Texte intégralNguyen, David H. « Cellular Plasticity, Cancer Stem Cells, and Cells-of-Origin ». Dans Systems Biology of Tumor Physiology, 21–31. Cham : Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-25601-6_2.
Texte intégralAviles, Diego, David Warshal, Lauren Krill et Olga Ostrovsky. « Extracellular Vesicles and Ovarian Cancer ». Dans Physiology. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.101412.
Texte intégralJain, Sapna, et Manjari Singh. « Engineering of Extracellular Vesicles as Nano Therapy for Breast Cancer ». Dans Physiology. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.101149.
Texte intégralActes de conférences sur le sujet "Cancer cell physiology"
Takayama, Shuichi, Dongeun Huh, Jonathan Song, Wansik Cha et Yunseok Heo. « Micro- and Nanofluidics for Cell Biology, Cell Therapy, and Cell-Based Drug Testing ». Dans ASME 2009 7th International Conference on Nanochannels, Microchannels, and Minichannels. ASMEDC, 2009. http://dx.doi.org/10.1115/icnmm2009-82151.
Texte intégralMarshall, Lauren, Andra Frost, Tim Fee et Joel Berry. « Assembly and Characterization of 3D, Vascularized Breast Cancer Tissue Mimics ». Dans ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14199.
Texte intégralNagel, Jacquelyn K. S. « Design of a Biologically-Inspired Chemical Sensor ». Dans ASME 2013 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/detc2013-12378.
Texte intégralRecio Boiles, Alejandro, Matthias Ilmer, Jody Vykoukal et Eckhard Alt. « Abstract 2934 : TRAIL-resistance in pancreatic cancer stem cells can be regulated through JNK pathway inhibition without impacting resident stem cell physiology ». 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.am2015-2934.
Texte intégralTakayama, Shuichi, Yi-Chung Tung et Bor-Han Chueh. « Biological Micro/Nanofluidics ». Dans ASME 2008 First International Conference on Micro/Nanoscale Heat Transfer. ASMEDC, 2008. http://dx.doi.org/10.1115/mnht2008-52087.
Texte intégralFilippi, J. F., D. Arnoux, N. Tubiana, B. Boutière, F. Le Caär, J. Sampol, Lab Hématol, Pr J. Sampol et Pr Y. Carcassonne. « PLASMINOGEN ACTIVATOR ACTIVITY OF NORMAL AND MALIGNANT MONONUCLEAR HUMAN CELLS ». Dans XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643167.
Texte intégralMilivojević, Nevena, David Caballero, Mariana Carvalho, Marko Živanović, Nenad Filipovic, Rui Reis et Joaquim Oliveira. « ENGINEERING A MICROFLUDIC PLATFORM AS A PRE-CLINICAL MODEL FOR BIOMEDICAL APPLICATIONS ». Dans 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac,, 2021. http://dx.doi.org/10.46793/iccbi21.259m.
Texte intégralSharma, Puja, Kevin Sheets et Amrinder S. Nain. « The Influence of Polymeric Fiber Stiffness and Alignment on Cytoplasmic Bleb Dynamics and Migration of Glioblastoma Multiforme Cells ». Dans ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80923.
Texte intégralRichmond, Bonnie L., Kyle Damen, Ryan Moore, Alex White et Julia H. Carter. « Abstract 3115 : Physiologic comparisons of five bladder cancer cell lines ». Dans Proceedings : AACR Annual Meeting 2018 ; April 14-18, 2018 ; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3115.
Texte intégralPryse, Kenneth M., Teresa M. Abney, Guy M. Genin et Elliot L. Elson. « Probing Cytoskeletal Mechanics Using Biochemical Inhibitors ». Dans ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19451.
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