Journal articles: '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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Caulier, A., L. Guyonneau Harmand, and L. Garçon. "Immortalisation érythrocytaire pour production de globules rouges in vitro." Transfusion Clinique et Biologique 24, no. 3 (September 2017): 263–67. http://dx.doi.org/10.1016/j.tracli.2017.06.030.

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12

Argyle, D., V. Ellsmore, E. A. Gault, A. F. Munro, and L. Nasir. "Equine telomeres and telomerase in cellular immortalisation and ageing." Mechanisms of Ageing and Development 124, no. 6 (June 2003): 759–64. http://dx.doi.org/10.1016/s0047-6374(03)00104-0.

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Crameri, Gary, Shawn Todd, Samantha Grimley, Jennifer A. McEachern, Glenn A. Marsh, Craig Smith, Mary Tachedjian, et al. "Establishment, Immortalisation and Characterisation of Pteropid Bat Cell Lines." PLoS ONE 4, no. 12 (December 11, 2009): e8266. http://dx.doi.org/10.1371/journal.pone.0008266.

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14

Vyas, Nihar. "The Birth of a Detective: Edgar Allan Poe's Immortalisation." Motifs : A Peer Reviewed International Journal of English Studies 8, no. 1 (2022): 98–108. http://dx.doi.org/10.5958/2454-1753.2022.00012.5.

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Georgopoulos, Nikolaos T., Lisa A. Kirkwood, Claire L. Varley, Nicola J. MacLaine, Naveed Aziz, and Jennifer Southgate. "Immortalisation of Normal Human Urothelial Cells Compromises Differentiation Capacity." European Urology 60, no. 1 (July 2011): 141–49. http://dx.doi.org/10.1016/j.eururo.2011.02.022.

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Sonigra, Rakesh J., Shivanthi S. Kandiah, and Caroline B. Wigley. "Spontaneous immortalisation of ensheathing cells from adult rat olfactory nerve." Glia 16, no. 3 (March 1996): 247–56. http://dx.doi.org/10.1002/(sici)1098-1136(199603)16:3<247::aid-glia7>3.0.co;2-z.

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Keough, R., B. Powell, and G. Rogers. "Targeted expression of SV40 T antigen in the hair follicle of transgenic mice produces an aberrant hair phenotype." Journal of Cell Science 108, no. 3 (March 1, 1995): 957–66. http://dx.doi.org/10.1242/jcs.108.3.957.

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Directed expression of SV40 large T antigen (TAg) in transgenic mice can induce tissue-specific tumorigenesis and useful cell lines exhibiting differentiated characteristics can be established from resultant tumor cells. In an attempt to produce an immortalised mouse hair follicle cortical cell line for the study of hair keratin gene control, SV40 TAg expression was targeted to the hair follicles of transgenic mice using a sheep hair gene promoter. Expression of SV40 TAg in the follicle cortex disrupted normal fiber ultrastructure, producing a marked phenotypic effect. Affected hairs were wavy or severely kinked (depending on the severity of the phenotype) producing an appearance ranging from a ruffled coat to a stubble covering the back of the mouse. The transgenic hairs appeared to be weakened at the base of the fibers, leading to premature hair-loss and a thinner pelage, or regions of temporary nudity. No follicle tumors or neoplasia were apparent and immortalisation of cortical cells could not be established in culture. In situ hybridisation studies in the hair follicle using histone H3 as a cell proliferation marker suggested that cell proliferation had ceased prior to commencement of K2.10-TAg expression and was not re-established in the differentiating cortical cells. Hence, TAg was unable to induce cell immortalisation at that stage of cortical cell differentiation. However, transgenic mice developed various other abnormalities including vertebral abnormalities and bladder, liver and intestinal tumors, which resulted in reduced life expectancy.

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18

Karwat, Mirosław. "Związki między koncentracją, kumulacją i monopolizacją władzy. Analiza modelowa." Studia Politologiczne 2020, no. 55 (March 19, 2020): 19–40. http://dx.doi.org/10.33896/spolit.2020.55.1.

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The concentration of powerin onestate(or: party, church,social movement) decision-making centre makes it possible to cumulate power. One kind of institution join the several types and areas of power (e.g. subordination of the legislative and judicial authorities to the will and disposition oftheexecutive, conversion of parliament and orchards, public prosecutor’s office into tools of government, governing party). The permanent effect of such changes may bethe monopolisation of the authorities – theexclusive practical ability to govern for a given political force and the process of immortalisation,reproductionofsuch a monopoly

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Evrard, C., M. Le Bert, I. Borde, P. Rouget, E. Galiana, and R. Bemard. "Transfert de gènes dans les cellules nerveuses: immortalisation cellulaire et marquage génétique." médecine/sciences 7, no. 4 (1991): IX. http://dx.doi.org/10.4267/10608/4373.

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20

Inokuchi, S., H. Handa, T. Imai, H. Makuuchi, M. Kidokoro, H. Tohya, S. Aizawa, et al. "Immortalisation of human oesophageal epithelial cells by a recombinant SV40 adenovirus vector." British Journal of Cancer 71, no. 4 (April 1995): 819–25. http://dx.doi.org/10.1038/bjc.1995.158.

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21

Rood, Calafat, Kr. Von dem Borne, Gerritsen, and Van Der Schoot. "Immortalisation of human bone marrow endothelial cells: characterisation of new cell lines." European Journal of Clinical Investigation 30, no. 7 (July 2000): 618–29. http://dx.doi.org/10.1046/j.1365-2362.2000.00672.x.

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22

Gray-Schopfer, V. C., S. C. Cheong, H. Chong, J. Chow, T. Moss, Z. A. Abdel-Malek, R. Marais, D. Wynford-Thomas, and D. C. Bennett. "Cellular senescence in naevi and immortalisation in melanoma: a role for p16?" British Journal of Cancer 95, no. 4 (August 2006): 496–505. http://dx.doi.org/10.1038/sj.bjc.6603283.

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23

Thiers, B. H. "Cellular senescence in naevi and immortalisation in melanoma: a role for p16?" Yearbook of Dermatology and Dermatologic Surgery 2007 (January 2007): 340–41. http://dx.doi.org/10.1016/s0093-3619(08)70622-1.

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Kolch, Walter, Ashwin Kotwaliwale, Keith Vass, and Petra Janosch. "The role of Raf kinases in malignant transformation." Expert Reviews in Molecular Medicine 4, no. 8 (April 25, 2002): 1–18. http://dx.doi.org/10.1017/s1462399402004386.

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The Raf kinases are proto-oncogenes that work at the entry point of the mitogen-activated protein kinase/extracellular-signal-regulated kinase (MAPK/ERK) pathway, a signalling module that connects cell-surface receptors and Ras proteins to nuclear transcription factors. The pathway impinges on all the functional hallmarks of cancer cells: immortalisation, growth-factor-independent proliferation, insensitivity to growth-inhibitory signals, ability to invade and metastasise, ability to attract blood vessels, and evasion of apoptosis. Indeed, the pathway is hyperactivated in 30% of all human tumours including prevalent cancers of the colon and lung. The molecular mechanisms underlying the role of Raf kinase in tumourigenesis and the opportunities for therapeutic intervention are reviewed in this article.

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Ngo, Greg, Sam Hyatt, Julia Grimstead, Rhiannon Jones, Eric Hendrickson, Chris Pepper, and Duncan Baird. "PARP inhibition prevents escape from a telomere-driven crisis and inhibits cell immortalisation." Oncotarget 9, no. 101 (December 25, 2018): 37549–63. http://dx.doi.org/10.18632/oncotarget.26499.

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26

Rassoul-Zadegan, M., V. Paquis, F. Vidal, R. Loubière, and F. Cuzin. "Immortalisation de cellules germinales mâles de souris transgéniques par l'antigène T du virus polyome." médecine/sciences 7, no. 4 (1991): R12. http://dx.doi.org/10.4267/10608/4374.

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27

Mahomva, Richard. "Umdala wethu legacy: The contested memories and the fatherhead role of Joshua Nkomo in Zimbabwe." DANDE Journal of Social Sciences and Communication 2, no. 2 (2018): 41–56. http://dx.doi.org/10.15641/dande.v2i2.47.

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his paper revisits the under-currencies of the normative and empirical motivations of the official iconic ornamentation of Joshua Nkomo’s legacy during the Mugabe era. The urgency of this analysis is justified by how the ruling and Zimbabwe’s former Head of State, Robert Gabriel Mugabe, strategically exploited the memorialization of Joshua Nkomo for political expedience. This was orchestrated through the state’s Umdala wethu ‘cultural nationalism’ since 1999 as well as the infrastructural immortalisation of Umdala wethu in 2013. The state’s monopoly over Nkomo’s legacy competed with the anti-establishment and ethnicity inclined appropriation of Joshua Nkomo’s legacy in the Matebeleland regions. One refers to this alternative and public consented appropriation of Joshua Nkomo’s legacy as the traditional affirmative reposition of Father-Zimbabwe’s political fatherhood in Zimbabwe’s body politic. Further, the paper posits that the clashing entitlements to Nkomo’s legacy represents polarity of national memory in Zimbabwe.

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Nelson, K. "Immortalisation of a mucopolysaccharidosis type IIIC fibroblast cell line via expression of SV40 T antigen." Cell Biology International 27, no. 7 (July 2003): 567–70. http://dx.doi.org/10.1016/s1065-6995(03)00097-0.

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Davies, B. "Immortalisation of human ovarian surface epithelium with telomerase and temperature-senstitive SV40 large T antigen." Experimental Cell Research 288, no. 2 (August 15, 2003): 390–402. http://dx.doi.org/10.1016/s0014-4827(03)00218-0.

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Pecher, G., A. Schwenk, M. Ziegner, E. Kilger, and W. Hammerschmidt. "Generation and immortalisation of a tumor specific cytotoxic T cell line from a healthy donor." European Journal of Cancer 33 (June 1997): S27. http://dx.doi.org/10.1016/s0959-8049(97)89408-7.

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Cornet, Anne M., Emmanuel Hanon, Eric R. Reiter, Marc Bruyninx, Viet Ha Nguyen, Beno�t R. Hennuy, Georges P. Hennen, and Jean L. Closset. "Prostatic androgen repressed message-1 (PARM-1) may play a role in prostatic cell immortalisation." Prostate 56, no. 3 (May 20, 2003): 220–30. http://dx.doi.org/10.1002/pros.10254.

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32

Powter, Branka, Sarah A. Jeffreys, Heena Sareen, Adam Cooper, Daniel Brungs, Joseph Po, Tara Roberts, et al. "Human TERT promoter mutations as a prognostic biomarker in glioma." Journal of Cancer Research and Clinical Oncology 147, no. 4 (February 6, 2021): 1007–17. http://dx.doi.org/10.1007/s00432-021-03536-3.

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AbstractThe TERT promoter (pTERT) mutations, C228T and C250T, play a significant role in malignant transformation by telomerase activation, oncogenesis and immortalisation of cells. C228T and C250T are emerging as important biomarkers in many cancers including glioblastoma multiforme (GBM), where the prevalence of these mutations is as high as 80%. Additionally, the rs2853669 single nucleotide polymorphism (SNP) may cooperate with these pTERT mutations in modulating progression and overall survival in GBM. Using liquid biopsies, pTERT mutations, C228T and C250T, and other clinically relevant biomarkers can be easily detected with high precision and sensitivity, facilitating longitudinal analysis throughout therapy and aid in cancer patient management.In this review, we explore the potential for pTERT mutation analysis, via liquid biopsy, for its potential use in personalised cancer therapy. We evaluate the relationship between pTERT mutations and other biomarkers as well as their potential clinical utility in early detection, prognostication, monitoring of cancer progress, with the main focus being on brain cancer.

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Eccleston, P. A., R. Mirsky, and K. R. Jessen. "Spontaneous immortalisation of Schwann cells in culture: short-term cultured Schwann cells secrete growth inhibitory activity." Development 112, no. 1 (May 1, 1991): 33–42. http://dx.doi.org/10.1242/dev.112.1.33.

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In the developing peripheral nerve, Schwann cells proliferate rapidly and then become quiescent, an essential step in control of Schwann cell differentiation. Cell proliferation is controlled by growth factors that can exert positive or inhibitory influences on DNA synthesis. It has been well established that neonatal Schwann cells divide very slowly in culture when separated from neurons but here we show that when culture was continued for several months some cells began to proliferate rapidly and non-clonal lines of immortalised Schwann cells were established which could be passaged for over two years. These cells had a similar molecular phenotype to short-term cultured Schwann cells, except that they expressed intracellular and cell surface fibronectin. The difference in proliferation rates between short- and long-term cultured Schwann cells appeared to be due in part to the secretion by short-term cultured Schwann cells of growth inhibitory activity since DNA synthesis of long-term, immortalised Schwann cells was inhibited by conditioned medium from short-term cultures. This conditioned medium also inhibited DNA synthesis in short-term Schwann cells stimulated to divide by glial growth factor or elevation of intracellular cAMP. The growth inhibitory activity was not detected in the medium of long-term immortalised Schwann cells, epineurial fibroblasts, a Schwannoma (33B), astrocytes or a fibroblast-like cell-line (3T3) and it did not inhibit serum-induced DNA synthesis in epineurial fibroblasts, 33B cells or 3T3 cells. The activity was apparently distinct from transforming growth factor-beta, activin, IL6, epidermal growth factor, atrial natriuretic peptide and gamma-interferon and was heat and acid stable, resistant to collagenase and destroyed by trypsin treatment. We raise the possibility that loss of an inhibitory autocrine loop may contribute to the rapid proliferation of long-term cultured Schwann cells and that an autocrine growth inhibitor may have a role in the cessation of Schwann cell division that precedes differentiation in peripheral nerve development.

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Dale, Tina P., Alice de Castro, Nicola J. Kuiper, E. Kenneth Parkinson, and Nicholas R. Forsyth. "Immortalisation with hTERT Impacts on Sulphated Glycosaminoglycan Secretion and Immunophenotype in a Variable and Cell Specific Manner." PLOS ONE 10, no. 7 (July 21, 2015): e0133745. http://dx.doi.org/10.1371/journal.pone.0133745.

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35

Parkinson, E. K., R. F. Newbold, and W. N. Keith. "The genetic basis of human keratinocyte immortalisation in squatnous cell carcinoma development: The role of telomerase reactivation." European Journal of Cancer 33, no. 5 (April 1997): 727–34. http://dx.doi.org/10.1016/s0959-8049(97)00063-4.

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36

Martin, Simon. "From Cycling Priests to the ‘Sportsman's Pope’. Italy, Sport and the Catholic Church." European Review 19, no. 4 (August 30, 2011): 545–61. http://dx.doi.org/10.1017/s1062798711000184.

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This article surveys the Catholic Church's exploitation of sport in Liberal (1861–1922), Fascist (1922–1943), and post-war Italy. It examines how and why the Church overcame its initial reticence to embrace sport and turn it into a fundamental pillar of an alternative culture that challenged the monopoly of national sporting federations. Following the rise of Fascism, sport became one of the principal means by which the Church resisted a complete takeover by the regime. Analysis of the devout Catholic cyclist Gino Bartali reveals how the Church maintained its identity and tradition of sporting independence despite the inevitable suppression of Catholic sporting organisations. Culminating in an examination of the ‘immortalisation’ of Bartali after his win in the 1948 Tour De France – a victory popularly credited with saving Italy from civil war – the article illuminates the processes by which sport became a central feature of Catholicism in national life. It highlights the Church's contribution to the development of Italian sport, assesses the wider impact of sport's role in forming alternative cultures, and argues that sport perfectly positioned the Church to respond to the demands of Reconstruction Italy and provided opportunities to secure a post-war Christian Democratic society.

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Buc, MH, JM Launay, P. Marie, and O. Kellerman. "IMMORTALISATION A PARTIR DU TERATOCARCINOME DE LIGNEES CELLULAIRES CORRESPONDANT A DES STADES PRECOCES DE L'EMBRYOGENESE DE LA SOURIS." Reproduction Nutrition Développement 29, Suppl. 1 (1989): 17. http://dx.doi.org/10.1051/rnd:19890724.

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Benedetti, Sara, Hidetoshi Hoshiya, Narumi Uno, Giulia Ferrari, Yasuhiro Kazuki, Sara Maffioletti, Tamara Casteels, et al. "Reversible immortalisation, human artificial chromosomes, and induced pluripotency: new gene and cell therapy technologies for Duchenne muscular dystrophy." Lancet 387 (February 2016): S98. http://dx.doi.org/10.1016/s0140-6736(16)00485-2.

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Tirnitz-Parker, Janina E. E., Joanne N. Tonkin, Belinda Knight, John K. Olynyk, and George C. T. Yeoh. "Isolation, culture and immortalisation of hepatic oval cells from adult mice fed a choline-deficient, ethionine-supplemented diet." International Journal of Biochemistry & Cell Biology 39, no. 12 (2007): 2226–39. http://dx.doi.org/10.1016/j.biocel.2007.06.008.

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Cockerill, Fiona, Patricia Purkis, and Anthony G. Quinn. "Transformation and immortalisation of skin keratinocytes is associated with changes in genomic DNA methylation of HIC1 but not P16." Journal of Dermatological Science 16 (March 1998): S23. http://dx.doi.org/10.1016/s0923-1811(98)83135-6.

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Kaura, V., M. Shaw, P. Allen, and P. Hopkins. "Towards the immortalisation of primary human myoblasts derived from patients susceptible to malignant hyperthermia and their non-susceptible relatives." British Journal of Anaesthesia 120, no. 5 (May 2018): e23. http://dx.doi.org/10.1016/j.bja.2017.11.054.

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Norton, J. D. "ID helix-loop-helix proteins in cell growth, differentiation and tumorigenesis." Journal of Cell Science 113, no. 22 (November 15, 2000): 3897–905. http://dx.doi.org/10.1242/jcs.113.22.3897.

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The ubiquitously expressed family of ID helix-loop-helix (HLH) proteins function as dominant negative regulators of basic HLH (bHLH) transcriptional regulators that drive cell lineage commitment and differentiation in metazoa. Recent data from cell line and in vivo studies have implicated the functions of ID proteins in other cellular processes besides negative regulation of cell differentiation. ID proteins play key roles in the regulation of lineage commitment, cell fate decisions and in the timing of differentiation during neurogenesis, lymphopoiesis and neovascularisation (angiogenesis). They are essential for embryogenesis and for cell cycle progression, and they function as positive regulators of cell proliferation. ID proteins also possess pro-apoptotic properties in a variety of cell types and function as cooperating or dominant oncoproteins in immortalisation of rodent and human cells and in tumour induction in Id-transgenic mice. In several human tumour types, the expression of ID proteins is deregulated, and loss- and gain-of-function studies implicate ID functions in the regulation of tumour growth, vascularisation, invasiveness and metastasis. More recent biochemical studies have also revealed an emerging ‘molecular promiscuity’ of mammalian ID proteins: they directly interact with and modulate the activities of several other families of transcriptional regulator, besides bHLH proteins.

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Bernal, Aina, Elisenda Zafon, Daniel Domínguez, Enric Bertran, and Laura Tusell. "Generation of Immortalised But Unstable Cells after hTERT Introduction in Telomere-Compromised and p53-Deficient vHMECs." International Journal of Molecular Sciences 19, no. 7 (July 17, 2018): 2078. http://dx.doi.org/10.3390/ijms19072078.

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Telomeres, the natural ends of chromosomes, hide the linear telomeric DNA from constitutive exposure to the DNA damage response with a lariat structure or t-loop. Progressive telomere shortening associated with DNA replication in the absence of a compensatory mechanism culminates in t-loop collapse and unmasked telomeres. Dysfunctional telomeres can suppress cancer development by engaging replicative senescence or apoptosis, but they can also promote tumour initiation when cell cycle checkpoints are disabled. In this setting, telomere dysfunction promotes increasing chromosome instability (CIN) through breakage-fusion-bridge cycles. Excessive instability may hamper cell proliferation but might allow for the appearance of some rare advantageous mutations that could be selected and ultimately favour neoplastic progression. With the aim of generating pre-malignant immortalised cells, we ectopically expressed telomerase in telomere-compromised variant human mammary epithelial cells (vHMECs), proficient and deficient for p53, and analysed structural and numerical chromosomal aberrations as well as abnormal nuclear morphologies. Importantly, this study provides evidence that while immortalisation of vHMECs at early stages results in an almost stable karyotype, a transient telomere-dependent CIN period—aggravated by p53 deficiency—and followed by hTERT overexpression serves as a mechanism for the generation of immortal unstable cells which, due to their evolving karyotype, could attain additional promoting properties permissive to malignancy.

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Hölzl-Armstrong, Kucab, Korenjak, Luijten, Phillips, Zavadil, and Arlt. "Characterising Mutational Spectra of Carcinogens in the Tumour Suppressor Gene TP53 Using Human TP53 Knock-in (Hupki) Mouse Embryo Fibroblasts." Methods and Protocols 2, no. 4 (November 13, 2019): 85. http://dx.doi.org/10.3390/mps2040085.

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DNA in dividing cells is prone to mutagenesis, with mutations making key contributions to human disease including cancer. The tumour suppressor gene TP53 is the most frequently mutated gene in human tumours. Here, we present a robust protocol for studying TP53 mutagenesis utilising human TP53 knock-in (Hupki) mouse embryonic fibroblasts (HUFs). In the HUF immortalisation assay (HIMA), primary HUFs are treated with known or suspected carcinogens at 3% oxygen and then transferred to 20% atmospheric oxygen to induce senescence. Cells containing mutations (e.g., in TP53) that allow bypassing of senescence eventually emerge as immortalised clonal cell lines after 2–3 months of serial passaging. As not all immortalised HUF cells contain TP53 mutations, we developed a Nutlin-3a counter-screen to select for TP53-mutated clones prior to sequencing. TP53 mutation spectra generated can be compared with those of human tumours recorded in the International Agency for Research on Cancer TP53 mutation database. Environmental mutagens that have demonstrated and validated the utility of the HIMA include ultraviolet radiation, aristolochic acid, and benzo[a]pyrene. The TP53 mutation patterns induced by these mutagens in the HIMA corresponded to those found in human tumours from patients exposed to these mutagens. The approach presented helps to deepen our understanding of human cancer aetiology.

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Tomasova, Kristyna, Michal Kroupa, Asta Forsti, Pavel Vodicka, and Ludmila Vodickova. "Telomere maintenance in interplay with DNA repair in pathogenesis and treatment of colorectal cancer." Mutagenesis 35, no. 3 (February 21, 2020): 261–71. http://dx.doi.org/10.1093/mutage/geaa005.

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Abstract Colorectal cancer (CRC) continues to be one of the leading malignancies and causes of tumour-related deaths worldwide. Both impaired DNA repair mechanisms and disrupted telomere length homeostasis represent key culprits in CRC initiation, progression and prognosis. Mechanistically, altered DNA repair results in the accumulation of mutations in the genome and, ultimately, in genomic instability. DNA repair also determines the response to chemotherapeutics in CRC treatment, suggesting its utilisation in the prediction of therapy response and individual approach to patients. Telomere attrition resulting in replicative senescence, simultaneously by-passing cell cycle checkpoints, is a hallmark of malignant transformation of the cell. Telomerase is almost ubiquitous in advanced solid cancers, including CRC, and its expression is fundamental to cell immortalisation. Therefore, there is a persistent effort to develop therapeutics, which are telomerase-specific and gentle to non-malignant tissues. However, in practice, we are still at the level of clinical trials. The current state of knowledge and the route, which the research takes, gives us a positive perspective that the problem of molecular models of telomerase activation and telomere length stabilisation will finally be solved. We summarise the current literature herein, by pointing out the crosstalk between proteins involved in DNA repair and telomere length homeostasis in relation to CRC.

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Prideaux, Steven M., Emma Conway O'Brien, and Timothy J. Chevassut. "The Genetic Architecture of Multiple Myeloma." Advances in Hematology 2014 (2014): 1–16. http://dx.doi.org/10.1155/2014/864058.

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Multiple myeloma is a malignant proliferation of monoclonal plasma cells leading to clinical features that include hypercalcaemia, renal dysfunction, anaemia, and bone disease (frequently referred to by the acronym CRAB) which represent evidence of end organ failure. Recent evidence has revealed myeloma to be a highly heterogeneous disease composed of multiple molecularly-defined subtypes each with varying clinicopathological features and disease outcomes. The major division within myeloma is between hyperdiploid and nonhyperdiploid subtypes. In this division, hyperdiploid myeloma is characterised by trisomies of certain odd numbered chromosomes, namely, 3, 5, 7, 9, 11, 15, 19, and 21 whereas nonhyperdiploid myeloma is characterised by translocations of the immunoglobulin heavy chain alleles at chromosome 14q32 with various partner chromosomes, the most important of which being 4, 6, 11, 16, and 20. Hyperdiploid and nonhyperdiploid changes appear to represent early or even initiating mutagenic events that are subsequently followed by secondary aberrations including copy number abnormalities, additional translocations, mutations, and epigenetic modifications which lead to plasma cell immortalisation and disease progression. The following review provides a comprehensive coverage of the genetic and epigenetic events contributing to the initiation and progression of multiple myeloma and where possible these abnormalities have been linked to disease prognosis.

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Kerr, Jonathan R. "Epstein-Barr virus (EBV) reactivation and therapeutic inhibitors." Journal of Clinical Pathology 72, no. 10 (July 17, 2019): 651–58. http://dx.doi.org/10.1136/jclinpath-2019-205822.

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Epstein-Barr virus (EBV) is a ubiquitous human virus which infects almost all humans during their lifetime and following the acute phase, persists for the remainder of the life of the individual. EBV infects B lymphocytes leading to their immortalisation, with persistence of the EBV genome as an episome. In the latent phase, EBV is prevented from reactivating through efficient cytotoxic cellular immunity. EBV reactivates (lytic phase) under conditions of psychological stress with consequent weakening of cellular immunity, and EBV reactivation has been shown to occur in a subset of individuals with each of a variety of cancers, autoimmune diseases, the autoimmune-like disease, chronic fatigue syndrome/myalgic encephalitis and under other circumstances such as being an inpatient in an intensive care unit. Chronic EBV reactivation is an important mechanism in the pathogenesis of many such diseases, yet is rarely tested for in immunocompetent individuals. This review summarises the pathogenesis of EBV infection, EBV reactivation and its role in disease, and methods which may be used to detect it. Known inhibitors of EBV reactivation and replication are discussed, including drugs licensed for treatment of other herpesviruses, licensed or experimental drugs for various other indications, compounds at an early stage of drug development and nutritional constituents such as vitamins and dietary supplements.

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Toussaint, Olivier, Patrick Dumont, Jose Remacle, Jean-Francois Dierick, Thierry Pascal, Christophe Frippiat, Joao Pedro Magalhaes, Stephanie Zdanov, and Florence Chainiaux. "Stress-Induced Premature Senescence or Stress-Induced Senescence-Like Phenotype: OneIn VivoReality, Two Possible Definitions?" Scientific World JOURNAL 2 (2002): 230–47. http://dx.doi.org/10.1100/tsw.2002.100.

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No consensus exists so far on the definition of cellular senescence. The narrowest definition of senescence is irreversible growth arrest triggered by telomere shortening counting cell generations (definition 1). Other authors gave an enlarged functional definition encompassing any kind of irreversible arrest of proliferative cell types induced by damaging agents or cell cycle deregulations after overexpression of proto-oncogenes (definition 2). As stress increases, the proportion of cells in “stress-induced premature senescence-like phenotype” according to definition 1 or “stress-induced premature senescence,” according to definition 2, should increase when a culture reaches growth arrest, and the proportion of cells that reached telomere-dependent replicative senescence due to the end-replication problem should decrease. Stress-induced premature senescence-like phenotype and telomere-dependent replicatively senescent cells share basic similarities such as irreversible growth arrest and resistance to apoptosis, which may appear through different pathways. Irreversible growth arrest after exposure to oxidative stress and generation of DNA damage could be as efficient in avoiding immortalisation as “telomere-dependent” replicative senescence. Probabilities are higher that the senescent cells (according to definition 2) appearingin vivoare in stress-induced premature senescence rather than in telomere-dependent replicative senescence. Examples are given suggesting these cells affectin vivotissue (patho)physiology and aging.

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Chastre, E., S. Emami, and C. Gespach. "Immortalisation et transformation tumorale de l'épithélium gastro-intestinal chez l'homme et le rat : applications en cancérologie et dans la mucoviscidose." médecine/sciences 7, no. 4 (1991): R17. http://dx.doi.org/10.4267/10608/4377.

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Anderson, Kristina, Corinne Rusterholz, Robert Mansson, Christina Jensen, Karl Bacos, Yutaka Sasaki, Mikael Sigvardsson, and Sten Eirik W. Jacobsen. "Enforced Expression of Pax-5 Results in Developmental Arrest, Immortalisation and Aberrant Expression of B Lineage Genes in Committed Myeloid Progenitors." Blood 104, no. 11 (November 16, 2004): 2784. http://dx.doi.org/10.1182/blood.v104.11.2784.2784.

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Abstract The paired domain transcription factor Pax-5, has been demonstrated to play a crucial role in development and final commitment of the B cell lineage. In fact, otherwise committed B cell progenitors acquire multipotentiality (myelo-lymphoid) potential upon targeted deletion of Pax-5 expression (Nutt et al. Nature.1999; 401:556–562). Thus, in addition, to promoting B cell development through acting as an activator of transcription of B cell specific genes such as CD19, Pax-5 is also thought to act as a suppressor of transcription of genes involved in determination of other blood cell lineages. However, it remains unclear how Pax-5 might repress myeloid development. Thus, we investigated the effect of Pax-5 expression on lympho-myeloid differentiation by overexpressing human (h)Pax-5 (through retroviral transduction) in adult murine bone marrow Linlo/−Sca-1+c-kit+ (LSK) cells. When compared to cells transduced with a control vector, LSK cells ectopically expressing hPax-5 very efficiently developed into hPax-5+B220+CD19+ pro-B cells in response to flt3 ligand and interleukin-7 in vitro. In contrast, when hPax-5+ LSK cells were cultured under myeloid conditions, we consistently observed development of a highly proliferative and immortalised bi-phenotypic (B-myeloid) hPax-5+B220+Gr-1+Mac-1+ population that predominantly consisted of immature myeloblasts but also maturated granulocytes and monocytes. Global gene expression analysis by micro-array, and confirmation by RT-PCR, demonstrated that hPax-5+B220+Gr-1+Mac-1+ cells also possessed a bi-phenotypic gene expression pattern, characteristic for B-cell as well as myeloid lineages including the Pax-5 target B cell genes mb-1 and BLNK as well as GM-CSFRα and low levels of C/EBPα. Similar findings were observed when targeting committed myeloid progenitors. These findings suggest that in addition to promoting B cell development, Pax-5 is capable of inhibiting/blocking myeloid differentiation and inducing immortalization as well as expression of B cell specific genes in otherwise myeloid committed progenitors. These findings motivate a careful investigation of the potential involvement of Pax-5 also in myeloid leukemias.

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Journal articles on the topic 'Immortalisation'

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