Established cell line of urinary bladder carcinoma (T24) containing tumour‐specific antigen

Bubenı́k, Jan; Barešová, Magdalena; Viklický, V.; Jakoubková, J; Sainerová, H; Donner, J

doi:10.1002/ijc.2910110327

Cited by 467 publications

(203 citation statements)

References 9 publications

(5 reference statements)

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“…Specifically, the cells exhibit the pleiomorphism characteristic of tumor cells as described previously by Bubeník et al (1973) and by Gilloteaux et al (1998aGilloteaux et al ( , 1998bGilloteaux et al ( , 2001aGilloteaux et al ( , 2001b. Even though the cells are subconfluent, they show overlap that is indicative of the absence of cell contact inhibition.…”

Section: Sham-or Control-treated Cells Sham-treated T24mentioning

confidence: 60%

“…The T24 human urinary bladder carcinoma cell line originated from an 81-year-old patient by Bubeník et al (1973) and was characterized by Marshall et al (1977), Kato et al (1978), Capon et al (1983), andO'Toole et al (1983). Ultrastructural studies reveal a number of features shared by a wide variety of tumors, including high nuclear-to-protoplasmic ratio, a loose chromatin texture, and poor differentiation (Kato et al, 1978;Srigley et al, 1988).…”

Section: Cell Linementioning

confidence: 99%

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Morphology and DNA degeneration during autoschizic cell death in bladder carcinoma T24 cells induced by ascorbate and menadione treatment

Gilloteaux¹,

Jamison²,

Arnold³

et al. 2005

Anat. Rec.

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Feulgen and actin-phalloidin staining as well as gel electrophoresis have been employed in conjunction with cell ultrastructure to describe the effects of 1-, 2-, and 4-hr ascorbate (VC), menadione (VK 3 ), and ascorbate:menadione (VC:VK 3 ) treatments on the T24 human bladder carcinoma cell line. T24 cells exposed to VC alone display blebs and other superficial membrane defects related to membrane alterations and to superficial cytoskeleton changes. VK 3 treatment damages the cell nucleus and organelles, leads to the redistribution of the organelles in the perikaryon as a consequence of cytoskeletal damage, and results in cytoplasmic self-excisions. After VC:VK 3 treatment, the cells show exaggerated alterations characteristic of each vitamin treatment alone, including damaged mitochondria, self-excision of organelle-free pieces of cytoplasm, and extrusion of the perikaryon containing a nucleus surrounded by the damaged organelles. The nuclear envelope appears intact and contains chromatin that decondenses and dissipates. During the cellular demise that concludes with apparent karyolysis, the cells significantly decrease their size and alter their shape. However, the cisterns of rough endoplasmic reticulum are undamaged, but may become dilated. Since the cellular phenomena leading to cell death differ morphologically from apoptosis and necrosis, but entail selfcutting without nuclear bodies, this new form of cell death was called autoschizis. In addition, gel electrophoresis and Feulgen staining demonstrate that autoschizis is accompanied by random DNA degeneration.

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Section: Sham-or Control-treated Cells Sham-treated T24mentioning

confidence: 60%

Section: Cell Linementioning

confidence: 99%

Morphology and DNA degeneration during autoschizic cell death in bladder carcinoma T24 cells induced by ascorbate and menadione treatment

Gilloteaux¹,

Jamison²,

Arnold³

et al. 2005

Anat. Rec.

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“…EJ was established from invasive, poorly differentiated urothelial carcinoma of the bladder (Evans et al, 1977;Hastings and Franks, 1983). T24 was derived from a primary lesion of grade 3 carcinoma of the bladder (Bubenik et al, 1973).…”

Section: Human Cell Linesmentioning

confidence: 99%

Impaired ΔNp63 expression associates with reduced β-catenin and aggressive phenotypes of urothelial neoplasms

et al. 2003

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p63, a homologue of the p53 gene, is considered to be essential for the normal development of stratified epithelia including urothelium. To examine possible roles of p63 in urothelial tumorigenesis, p63 expression was systematically examined in normal urothelium, low-grade papillary noninvasive (LPN) urothelial tumours, and high-grade or invasive carcinomas, using either an isoformnonspecific or a DN-isoform-specific antibody. Expression profiles of p63 were also analysed in cultured cells. Immunoreactivity with the two antibodies was virtually identical in tissue samples examined. Basal and intermediate cell layers of normal urothelium showed intense nuclear p63 immunostaining. This normal staining pattern was preserved in a majority of LPN tumours, whereas it was frequently impaired in high-grade or muscle-invasive carcinomas. At the mRNA level, DNp63 expression predominated over TAp63, and amounts of DNp63 mRNA correlated with p63 immunoreactivity, confirming that DNp63 accounts for p63 expressed in urothelial tissues. In cultured cells, DNp63 was also expressed in low-grade tumour cells as well as normal urothelial cells, but undetectable in high-grade aggressive carcinoma cells. Interestingly, impaired DNp63 expression significantly associated with reduced b-catenin expression that was possibly related to progression of urothelial neoplasms. Thus, impaired DNp63 expression characterises aggressive phenotypes of urothelial neoplasms.

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“…The human bladder carcinoma cell line T24 (European Collection of Cell Cultures; Bubenik et al, 1973;Dirks et al, 1999), the immortalized human microvascular endothelial cell line HMEC-1 (Ades et al, 1992), human squamous carcinoma cell line of the head and neck FaDu (Rangan, 1972; American Type Culture Collection), the mouse hepatoma cell line Hepa-1 wild type (clone Hepa-1c1c7) and its derivative Hepa c4 (HIF-1β mutant; Hankinson, 1979) were utilised. Only cells tested negative for mycoplasma were used in the experiments, since it had been shown that mycoplasma interfered with transfection, especially under hypoxia (results not shown).…”

Section: Cell Lines and Growth Mediamentioning

confidence: 99%

Gene delivery to hypoxic cells in vitro

et al. 2000

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Summary Hypoxia in solid tumours has been correlated with poor prognosis and resistance to radiation and chemotherapy. Hypoxia is also a strong stimulus for gene expression. We previously proposed a gene therapy approach which exploits the presence of severe hypoxia in tumours for the induction of therapeutic genes. Hypoxic cells are known to have a reduced metabolic rate, transcription and translation. These facts may prevent gene transfer and therefore warranted further investigation. In this paper the feasibility of gene delivery in vitro under tumour conditions was demonstrated. DNA was delivered in vitro using a peptide-mediated non-viral system. Across a range of oxygen tensions and mammalian cell lines (including human tumour and endothelial cells) it was shown that hypoxic cells could be transfected. Transfection efficiencies varied depending on the level of hypoxia, cell characteristics and gene promoters used. An in vitro model of hypoxia/reoxygenation, designed to mimic the variable nature of tumour hypoxia, showed that hypoxic preconditioning and reoxygenation alone did not reduce transfection efficiency significantly; only chronic anoxia reduced transfection. The fact that neither intermediate hypoxia nor intermittent anoxia significantly reduced transfection is promising for future hypoxia-targeted gene therapy strategies. 662-667 © 2000 Cancer Research Campaign doi: 10.1054/ bjoc.2000.1318, available online at http://www.idealibrary.com on List of abbreviations: HIF-1, hypoxia inducible factor 1; CMV, cytomegalovirus; SV40, simian virus 40; AnO 2 , anoxia; GFP, green fluorescent protein; FACS, fluorescent activated cell sorting Transfection efficiencies of two commonly used marker genes and viral promoters were recorded in a range of cell lines under different oxygenation conditions. A simple in vitro model of hypoxia/reoxygenation was used to mimic the variable nature of tumour hypoxia. MATERIALS AND METHODS Cell lines and growth mediaThe human bladder carcinoma cell line T24 (European Collection of Cell Cultures; Bubenik et al, 1973;Dirks et al, 1999), the immortalized human microvascular endothelial cell line HMEC-1 (Ades et al, 1992), human squamous carcinoma cell line of the head and neck FaDu (Rangan, 1972; American Type Culture Collection), the mouse hepatoma cell line Hepa-1 wild type (clone Hepa-1c1c7) and its derivative Hepa c4 (HIF-1β mutant; Hankinson, 1979) were utilised. Only cells tested negative for mycoplasma were used in the experiments, since it had been shown that mycoplasma interfered with transfection, especially under hypoxia (results not shown). All cells were maintained in Dulbecco's MEM (DMEM, Life Technologies, UK) with 10% fetal calf serum and L-glutamine in a 5% CO 2 humidified incubator at 37°C.Cell proliferation was monitored by cell counting using a haemocytometer and trypan blue (0.2% final concentration, Sigma) to distinguish live and dead cells. Hypoxic conditionsCells were plated 16-24 h prior to the experiment in oxygen impermeable dishes (Permanox, Nunc, UK...

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Established cell line of urinary bladder carcinoma (T24) containing tumour‐specific antigen

Cited by 467 publications

References 9 publications

Morphology and DNA degeneration during autoschizic cell death in bladder carcinoma T24 cells induced by ascorbate and menadione treatment

Morphology and DNA degeneration during autoschizic cell death in bladder carcinoma T24 cells induced by ascorbate and menadione treatment

Impaired ΔNp63 expression associates with reduced β-catenin and aggressive phenotypes of urothelial neoplasms

Gene delivery to hypoxic cells in vitro

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