Relevant bibliographies by topics / Immortalisation

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Immortalisation'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 May 2024

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Journal articles on the topic "Immortalisation"

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Drayton, S. "Immortalisation and transformation revisited." Current Opinion in Genetics & Development 12, no. 1 (February 1, 2002): 98–104. http://dx.doi.org/10.1016/s0959-437x(01)00271-4.

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Petzoldt, J. L., I. M. Leigh, P. G. Duffy, C. Sexton, and J. R. W. Masters. "Immortalisation of human urothelial cells." Urological Research 23, no. 6 (November 1995): 377–80. http://dx.doi.org/10.1007/bf00698738.

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Kalsi, J. K., and D. A. Isenberg. "Immortalisation of Human Antibody Producing Cells." Autoimmunity 13, no. 3 (January 1992): 249–58. http://dx.doi.org/10.3109/08916939209004831.

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Hilton, Craig. "The Immortalisation of Billy Apple®: An Art-Science Collaboration." Leonardo 47, no. 2 (April 2014): 109–13. http://dx.doi.org/10.1162/leon_a_00709.

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In The Immortalisation of Billy Apple®, Billy Apple® is simultaneously a subject of art and of scientific endeavor. This project has resulted in the first biological tissue made available for artists and the first biological tissue for science research made available by an artist as art. It has long been understood that Homo sapiens are a selective force of nature. Here the tissue and genetic information survive artistic and scientific natural selection. The Immortalisation of Billy Apple® provides an ongoing opportunity for cultural engagement with biological technology. This paper poses the question: Can genuine science and art output emerge from collaboration? As the author explores this question, other questions emerge around the scope of art in the realm of science and the roles of collaborators.
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Carnero, Amancio, and Matilde E. LLeonart. "Epigenetic mechanisms in senescence, immortalisation and cancer." Biological Reviews 86, no. 2 (September 16, 2010): 443–55. http://dx.doi.org/10.1111/j.1469-185x.2010.00154.x.

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Pestana, Ana, João Vinagre, Manuel Sobrinho-Simões, and Paula Soares. "TERT biology and function in cancer: beyond immortalisation." Journal of Molecular Endocrinology 58, no. 2 (February 2017): R129—R146. http://dx.doi.org/10.1530/jme-16-0195.

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Evasion of replicative senescence and proliferation without restriction, sometimes designated as immortalisation, is one of the hallmarks of cancer that may be attained through reactivation of telomerase in somatic cells. In contrast to most normal cells in which there is lack of telomerase activity, upregulation ofTERTtranscription/activity is detected in 80–90% of malignant tumours. In several types of cancer, there is a relationship between the presence ofTERTpromoter mutations,TERTmRNA expression and clinicopathological features, but the biological bridge between the occurrence ofTERTpromoter mutations and the aggressive/invasive features displayed by the tumours remains unidentified. We and others have associated the presence ofTERTpromoter mutations with metastisation/survival in several types of cancer. In follicular cell-derived thyroid cancer, such mutations are associated with worse prognostic features (age of patients, tumour size and tumour stage) as well as with distant metastases, worse response to treatment and poorer survival. In this review, we analyse the data reported in several studies that implyTERTtranscription reactivation/activity with cell proliferation, tumour invasion and metastisation. A particular attention is given to the putative connections betweenTERTtranscriptional reactivation and signalling pathways frequently altered in cancer, such as c-MYC, NF-κB and B-Catenin.
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Ritso, M., L. Jørgensen, S. Laval, V. Straub, K. Bushby, and H. Lochmüller. "P35 Immortalisation and characterisation of muscle stem cells." Neuromuscular Disorders 20 (March 2010): S14. http://dx.doi.org/10.1016/s0960-8966(10)70050-x.

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Allain, JE, A. Weber, and P. LeBoulch. "Immortalisation réversible : vers une nouvelle stratégie de thérapie cellulaire." médecine/sciences 16, no. 11 (2000): 1266. http://dx.doi.org/10.4267/10608/1569.

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Allain, Jean-Étienne, Dominique Mahieu-Caputo, Nathalie Loux, Ibrahim Dagher, Virginie Di Rico, Marion Andréoletti, Dominique Franco, Frédérique Capron, and Anne Weber. "Allotransplantation in utero et immortalisation d’hépatocytes fœtaux de primates." Journal de la Société de Biologie 195, no. 1 (2001): 57–63. http://dx.doi.org/10.1051/jbio/2001195010057.

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Sapich, Sandra, Marius Hittinger, Remi Hendrix-Jastrzebski, Urska Repnik, Gareth Griffiths, Tobias May, Dagmar Wirth, Robert Bals, Nicole Schneider-Daum, and Claus-Michael Lehr. "Murine Alveolar Epithelial Cells and Their Lentivirus-mediated Immortalisation." Alternatives to Laboratory Animals 46, no. 2 (May 2018): 73–89. http://dx.doi.org/10.1177/026119291804600207.

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In this study, we describe the isolation and immortalisation of primary murine alveolar epithelial cells (mAEpC), as well as their epithelial differentiation and barrier properties when grown on Transwell® inserts. Like human alveolar epithelial cells (hAEpC), mAEpC transdifferentiate in vitro from an alveolar type II (ATII) phenotype to an ATI-like phenotype and exhibit features of the air–blood barrier, such as the establishment of a thin monolayer with functional tight junctions (TJs). This is demonstrated by the expression of TJ proteins (ZO-1 and occludin) and the development of high transepithelial electrical resistance (TEER), peaking at 1800ω•cm2. Transport across the air–blood barrier, for general toxicity assessments or preclinical drug development, is typically studied in mice. The aim of this work was the generation of novel immortalised murine lung cell lines, to help meet Three Rs requirements in experimental testing and research. To achieve this goal, we lentivirally transduced mAEpC of two different mouse strains with a library of 33 proliferation-promoting genes. With this immortalisation approach, we obtained two murine alveolar epithelial lentivirus-immortalised (mAELVi) cell lines. Both showed similar TJ protein localisation, but exhibited less prominent barrier properties (TEERmax ~250Ω•cm2) when compared to their primary counterparts. While mAEpC demonstrated their suitability for use in the assessment of paracellular transport rates, mAELVi cells could potentially replace mice for the prediction of acute inhalation toxicity during early ADMET studies.
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Dissertations / Theses on the topic "Immortalisation"

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Seow, Choon Sheong. "Analysis of gene expression in tumour immortalisation." Thesis, University of Aberdeen, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251848.

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Cellular senescence is an irreversible growth-arrested state seen in primary human cells after a finite number of cell divisions both in culture and in vivo. The escape from senescence to immortalisation is often thought to be a prerequisite for carcinogenesis. Many changes in senescent cells are consistent with changes in tissue and organ function with age. I used serial analysis of gene expression (SAGE) to analyse global gene expression profiles in senescent and early passage human foetal fibroblasts (hff). A total of over 20,000 SAGE tags were sequenced and characterised, corresponding to 2,675 unique transcripts. Relative to the early passage hff, transcripts which were found to be markedly increased in senescent hff included those encoding p21WAF1, Cyclin D1, ferritin heavy chain, transforming growth factor-beta induced gene (BIGH3), skin collagenase and amyloid. Amongst them, genes such as skin collagenase and amyloid are known to be up-regulated in human ageing. Together with these known genes, a number of "unknown" genes were up-regulated. Seven differentially expressed genes, up-regulated in senescence (BIGH3, prion, dickkopf (Xenopus laevis) homolog 1 (dkk1), Cbp/p300-interacting transactivator, with Glu/Asp-rich carboxy-terminal domain, 2 (CITED2), Rap1a and Cysteine knot superfamily 1, bone morphogenetic protein antagonist 1 and retinoic acid receptor, alpha (RARA)) were selected for validation with reverse transcriptase-polymerase chain reaction (RT-PCR). The roles of these genes are discussed in relation to cancer and neurodegenerative diseases. My study demonstrates that replicative senescence is a complex phenomenon involving genes from the wingless-type (Wnt), mitogen-activated protein (Map) kinase kinases extracellular signal-regulated (Erk) kinase, transforming growth factor beta signalling and epigenetic pathways. The challenges remaining now are to identify senescence-related tumour suppressor gene(s) and to elucidate further the biochemical pathways of senescence.
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Wen, Victoria Wei-Yu Women's &amp Children's Health Faculty of Medicine UNSW. "Molecular alterations during immortalisation of human endothelial cells." Awarded by:University of New South Wales. Women's & Children's Health, 2009. http://handle.unsw.edu.au/1959.4/44743.

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Replicative exhaustion of endothelial cells (ECs) contributes to the pathogenesis of age-related vascular disorders, including atherosclerosis and impaired wound healing. Conversely, abnormal proliferation of ECs underlies the development of EC-derived malignancies, such as haemangioblastoma and angiosarcoma. The central objective of this thesis was to delineate mechanisms that regulate the replicative lifespan of human ECs and molecular alterations that occur during immortalisation of ECs. The gradual shortening of telomeres (chromosome-end structures) is one mechanism that restricts the replicative lifespan of human ECs. Telomere shortening initiates an irreversible growth arrest or senescence through activation of a TP53-mediated DNA damage response. Expression of the cyclin-dependent kinase inhibitor, p16INK4a, is also increased and reinforces senescence via the retinoblastoma pathway. Overexpression of telomerase reverse transcriptase (hTERT) reconstitutes telomerase activity and extends the lifespan of human ECs, but is not sufficient for immortalisation. The current study demonstrated that p16INK4a repression by promoter methylation was a frequent event during immortalisation of hTERT-transduced bone marrow ECs (BMECs), occurring in 5 of 12 clones. Repression of p16INK4a concurred with the development of recurring chromosomal aberrations, which appeared to be a consequence of telomere dysfunction and chromosome fusions. Loss of p16INK4a and the development of a complex karyotype were associated with a more transformed phenotype in hTERT-immortalised BMECs. The investigations described in this thesis were the first to associate loss of p16INK4a expression with the accumulation of chromosome aberrations. Repression of p16INK4a in only a subset of immortal BMECs provided impetus for investigating whether there was a functionally analogous defect in the hTERT-immortalised BMECs that retained p16INK4a expression. In normal human cells, oncogenic Ras upregulates p16INK4a and induces senescence independently of telomere shortening. This thesis demonstrates that the immortal BMECs that retained p16INK4a expression had a defective response to oncogenic Ras, which may have contributed to the immortalisation of these cells. Whole genome and proteome analyses identified additional alterations in gene copy number and protein expression specific to p16INK4a-positive or -negative immortal BMECs. Overall, these investigations provide new insight to the potential consequences of p16INK4a repression during carcinogenesis and describe novel molecular alterations that occur during immortalisation of human ECs.
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Grix, Nicola. "Conditional immortalisation of mouse auditory sensory epithelial cells." Thesis, University of Bristol, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414134.

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Linne, Hannah Louise. "Investigating telomerase regulation in human breast cancer cells : a search for telomerase repressor sequences localised to chromosome 3P." Thesis, Brunel University, 2015. http://bura.brunel.ac.uk/handle/2438/11620.

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Cellular immortality is one of the ten hallmarks of human cancer and has been shown to be an essential prerequisite for malignant progression (Hanahan and Weinberg., 2011, Newbold et al., 1982, Newbold and Overell., 1983). In contrast, normal human somatic cells proliferate for a limited number of population doublings before entering permanent growth arrest known as replicative senescence. This is thought to be due to the progressive shortening of telomeric sequences with each round of cell division. Over 90% of human tumours, but not the majority of human somatic cells, have been found to express telomerase activity (Kim et al., 1994). The rate-limiting component of the human telomerase enzyme is the telomerase reverse transcriptase subunit, which is encoded by the hTERT gene. Transfection of hTERT cDNA into normal human fibroblasts and epithelial cells may sometimes be sufficient to confer cellular immortality (Newbold., 2005, Stampfer and Yaswen., 2002). Therefore, de-repression of hTERT and telomerase re-activation are thought to be critical events in human carcinogenesis and is the predominant mechanism by which cancer cells maintain their proliferative capacity. Previously, our group has shown that introduction of a normal, intact copy of human chromosome 3 into the 21NT primary breast cancer cell line by microcell-mediated monochromosome transfer (MMCT), is associated with strong telomerase repression and induction of cell growth arrest within the majority of hybrid clones (Cuthbert et al., 1999). Structural mapping of chromosome 3 within telomerase-positive revertent clones revealed two regions of deletion: 3p21.3-p22 and 3p12-p21.1, thought to harbour the putative telomerase repressor sequence(s). Subsequent studies showed that the chromosome 3p-encoded telomerase repressor sequence(s) mediates its function by means of transcriptional silencing of hTERT, in part, through chromatin remodelling of two sites within intron 2 of the hTERT gene (Ducrest et al., 2001, Szutorisz et al., 2003). Attempts to achieve positional cloning of hTERT repressor sequences on chromosome 3p identified two interesting candidates; the histone methyltransferase SETD2 and an adjacent long non-coding RNA (lncRNA) sequence known as FLJ/KIF9-AS1 (Dr. T. Roberts, unpublished data). Through MMCT-mediated introduction of intact chromosomes 3 and 17 into the 21NT cell line, I have demonstrated that at least two as yet unidentified telomerase repressor sequences (one located on each of these two normal chromosomes) may function to repress telomerase activity within the same breast cancer cell line, which suggests that multiple, independent telomerase regulatory pathways may be inactivated within the same cancer type. Furthermore, by examining the consequences of forced SETD2 and FLJ expression within the 21NT cell line, together with siRNA-mediated knockdown of SETD2 within a single telomerase-repressed 21NT-chromosome 3 hybrid, I have provided evidence to show that neither of these two candidate genes may function as a regulator of hTERT transcription. Through interrogation of relevant literature, a set of four candidate 3 telomerase regulatory genes (BAP1, RASSF1A, PBRM1 and PARP-3) were selected for further investigation based on their location within the 3p21.1-p21.3 region together with their documented role in the epigenetic regulation of target gene expression. Using mammalian expression vectors containing candidate gene cDNA sequences, my colleague Dr. T. Roberts and I demonstrated that forced overexpression of BAP1 and PARP-3 within the 21NT cell line is associated with consistent, but not always sustained, repression of hTERT transcriptional activity and telomerase activity. It is therefore possible that at least two sequences may exist on chromosome 3p that function collectively to regulate hTERT expression within breast cancer cells. Finally, using an in vitro model of human mammary epithelial cell (HMEC) immortalization, involving the targeted abrogation of two pathologically relevant genes, p16 and p53 to generate a series of variant clones at different stages of immortal transformation (developed by my colleague Dr. H. Yasaei), I have shown that single copy deletions on chromosome 3p are a frequent, clonal event, specifically associated with hTERT de-repression and immortal transformation. Subsequent high-density single nucleotide polymorphism (SNP) array analysis of immortal variants carried out by Dr. H. Yasaei, identified a minimal common region of deletion localized to 3p14.2-p22. Together, these findings provide additional evidence to show that chromosome 3p may harbour critical hTERT repressor sequences, that are lost as an early event during breast carcinogenesis.
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Kan, Chin-Yi. "Human Papillomavirus in human breast cancer and cellular immortalisation." Sydney : University of New South Wales. Biotechnology and Biomolecular Sciences, 2007. http://www.library.unsw.edu.au/~thesis/adt-NUN/public/adt-NUN20071004.080541/.

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McDonald, Jacqueline. "Conditional immortalisation of myeloid-precursors to model innate immunity." Thesis, Cardiff University, 2013. http://orca.cf.ac.uk/45729/.

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The prevalence of fungal infections is on the rise due to the increase of immune suppressed individuals. Neutrophils are key immune cells in the fight against fungal infections. The study of neutrophil biology is hampered by the short lived nature of the cells and the fact that they cannot be easily genetically modified. In this thesis, I generate and characterise myeloid precursor cell lines that can be genetically manipulated and differentiated into functional neutrophils. These in vitro generated neutrophils were adoptively transferred into live animals and tracked during inflammatory responses. Clec7a, a cell surface β-glucan receptor found on myeloid cells, and its role in immune response to fungal infections has been well characterised in macrophages and dendritic cells but less so on neutrophils. In this thesis, a model for elucidating the role of Clec7a on neutrophils was developed using primary cells and was able to show that Clec7a deficiency on neutrophils impairs recognition of zymosan and C. albicans but that this impairment was largely overcome by serum opsonisation of the particles. The in vitro generated neutrophils were comparably tested and, although the cells have their limitations, they largely supported the conclusions found using primary cells.
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Flanagan, James Michael. "The immortalisation of B-lymphocytes with Epstein-Barr virus /." St. Lucia, Qld, 2001. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16501.pdf.

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Kohli, Jaskaren Singh. "Senescence and immortalisation in melanoma progression and multiple primary melanoma." Thesis, St George's, University of London, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.706529.

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Multiple primary melanoma is defined as the gain of at least one additional independent melanoma and occurs in approximately 5% of melanoma patients. Germline mutations can be identified in genes in these patients, which are known to, or are predicted to result in an extension of melanocyte lifespan e.g. pl6, CDK4, and components of the telomere shelterin cap. We therefore hypothesised that 'normal' melanocytes from pl6 and CDK4 wild-type multiple primary melanoma patients have a statistically longer lifespan compared to those from single primary melanoma patients. Melanocytes from multiple primary melanoma patients did display a significantly extended culture lifespan, independently of donor age. Multiple primary melanoma is therefore commonly associated with a delay in normal melanocyte senescence. There is currently a shortage of diagnostic markers for melanoma and novel ones are needed for more accurate diagnosis and prognosis. TERT (the enzymatic component of telomerase) expression is the commonest route to telomere maintenance, required for melanoma immortality. TERT expression was tested via immunohistochemistry in a series of melanoma precursor and melanoma lesions, to analyse at which point in progression its expression is activated. The protein was found to be localised in either the nucleolus, the nucleoplasm (designated non-nucleolarTERT), or both. Only non-nucleolarTERT expression significantly increased with melanoma progression, suggesting this location is associated with immortality. As senescence likely needs to be bypassed for advanced melanoma development, microarrays were previously carried out comparing growing and senescent wild-type and pl6-null melanocyte lines to evaluate significantly up- or downregulated genes which could be used as future markers. In the present study, potential novel markers were authenticated using PCR and immunoblotting and validated genes were analysed via immunohistochemistry in a series of melanoma precursor and melanoma lesions. ETS1 was tested owing to recent findings that it can bind to and activate the mutant TERT promoter found commonly in melanomas. ETS1 was expressed at all stages from benign nevi onwards, perhaps owing to its link with the MAPK pathway.
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Zwermann, Birgit. "Die Rolle der Telomerase in der Immortalisation und malignen Transformation von Nebennierenrindenzellen." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-145498.

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Whitaker, Noel James. "Involvement of p53 and RB-1 in the immortalisation of human cells." Thesis, The University of Sydney, 1995. https://hdl.handle.net/2123/27505.

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Normal diploid mammalian cells undergo a finite number of population doublings in culture before they undergo senescence [Hayflick & Moorhead, 1961]. In contrast, tumours often contain "immortalised" cells that exhibit an apparently unlimited in vitro and in vivo proliferative potential. Fusion of normal and immortalised cells usually results in hybrids with limited proliferative potential [Bunn & Tarrant, 1980; Muggleton-Harris & DeSimone, 1980] indicating that immortalisation is probably due to loss of normal gene function. Similarly, fusion of different immortalised human cell lines with each other often results in mortal hybrids, indicating that the cell lines have become immortalised via different genetic events. Such studies have identified at least four complementation groups for immortalisation, referred to as groups A, B, C and D (Pereira—Smith & Smith, 1988).
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Book chapters on the topic "Immortalisation"

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Rajah, A. R. Sriskanda. "Politics of Immortalisation." In Tamil Nationalism in Sri Lanka, 74–99. London: Routledge, 2022. http://dx.doi.org/10.4324/9781003301677-4.

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Stacey, Glyn, and Caroline MacDonald. "Immortalisation of Primary Cells." In Cell Culture Methods for In Vitro Toxicology, 27–42. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-017-0996-5_3.

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West, Michelle J., and Paul J. Farrell. "Roles of RUNX in B Cell Immortalisation." In Advances in Experimental Medicine and Biology, 283–98. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3233-2_18.

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Chiwaura, Henry. "The Immortalisation of Joshua Mqabuko Nyongolo Nkomo." In Joshua Mqabuko Nkomo of Zimbabwe, 389–403. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-60555-5_17.

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Griffin, Beverly E. "Epstein-Barr Virus and Immortalisation of Epithelial Cells." In Cell Transformation, 157–65. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-5009-5_9.

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Williams, A. C., A. Manning, S. J. Harper, and C. Paraskeva. "Multiple Steps in the in vitro Immortalisation and Neoplastic Conversion of Human Colonic Epithelial Cells." In Neoplastic Transformation in Human Cell Culture, 281–90. Totowa, NJ: Humana Press, 1991. http://dx.doi.org/10.1007/978-1-4612-0411-4_28.

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Altiok, A., M. T. Bejarano, and E. Klein. "Effect of TGF-beta on the Proliferation of B Cell Lines and on the Immortalisation of B Cells by EBV." In Current Topics in Microbiology and Immunology, 375–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75889-8_46.

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Giles, David. "The immortalisation of celebrities." In Postmortal Society, 97–113. Routledge, 2017. http://dx.doi.org/10.4324/9781315601700-6.

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Visigalli, Paolo. "Technologies of self-immortalisation in ancient Greece and early India." In Universe and Inner Self in Early Indian and Early Greek Thought. Edinburgh University Press, 2016. http://dx.doi.org/10.3366/edinburgh/9781474410991.003.0008.

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This chapter adapts Foucault's concept of technologies of the self to the production, by means of certain composite psychophysical practices, of a post-mortem immortal self. Such technologies of self-immortalisation are examined in the Plato's Timaeus (self-immortalisation through the practice of philosophy) and in the ritual construction of an immortal self (atman) in the construction of the Vedic fire altar (agnicayana). There are both similarities and differences between the Greek and Indian practices.
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Tamai, Tadakazu, Nobuyuki Sato, Shoji Kimura, Sanetaka Shirahata, and Hiroki Murakami. "IMMORTALISATION OF FLATFISH (PARALICHTHYS OLIVACEUS) LEUKOCYTES BY ONCOGENE TRANSFECTION." In Animal Cell Technology, 29–31. Elsevier, 1992. http://dx.doi.org/10.1016/b978-0-7506-0421-5.50016-7.

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Conference papers on the topic "Immortalisation"

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Katsumiti, Alberto, Pakatip Ruenraroengsak, Miren P. Cajaraville, Andrew J. Thorley, and Teresa D. Tetley. "Immortalisation of human alveolar epithelial cells to investigate the mechanistic effects of inhaled airborne materials in vitro." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa3910.

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