Establishment and biological characterization of an in vitro human cytomegalovirus latency model

Tanaka, Junji; Ogura, Tsutomu; Sato, Hiroshi; Hatano, Miyako

doi:10.1016/0042-6822(87)90171-1

Cited by 69 publications

(47 citation statements)

References 24 publications

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“…We retain this discrepancy only apparent since thyroid carcinoma cell lines, even deriving from differentiated tumours, cannot be completely compared to surgically removed tumours. In fact, these cell lines harbour p53 mutations that are rare in thyroid differentiated neoplasias (Tanaka et al, 1987;Estour et al, 1989;Pang et al, 1989;Ito et al, 1992;Dobashi et al, 1993;Donghi et al, 1993;Fagin et al, 1993;Zeki et al, 1993;Fabien et al, 1994;Matias-Guiu et al, 1994;Ain et al, 1997;Fiore et al, 1997;Basolo et al, 2002) and they have a high proliferation rate. However, this consideration does not exclude the validity of the use of the thyroid carcinoma cell lines as experimental model to draw new information that, however, need to be subsequently validated on fresh tumours.…”

Section: Discussionmentioning

confidence: 99%

“…The human thyroid carcinoma cell lines used in this study are: TPC-1 (Tanaka et al, 1987), WRO (Estour et al, 1989), NPA and ARO (Pang et al, 1989), FRO (Fagin et al, 1993), NIM 1 (Zeki et al, 1993), B-CPAP (Fabien et al, 1994), FB-1 (Fiore et al, 1997), FB-2 (Basolo et al, 2002), Kat-4 and Kat-18 (Ain et al, 1997). They were grown in DMEM (Gibco Laboratories, Carlsbad, CA, USA) containing 10% fetal calf serum (Gibco Laboratories), glutamine (Gibco Laboratories) and ampicillin/streptomycin (Gibco Laboratories) in a 5% CO 2 atmosphere.…”

Section: Cell Culture and Transfectionsmentioning

confidence: 99%

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UbcH10 overexpression may represent a marker of anaplastic thyroid carcinomas

et al. 2005

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The hybridisation of an Affymetrix HG_U95Av2 oligonucleotide array with RNAs extracted from six human thyroid carcinoma cell lines and a normal human thyroid primary cell culture led us to the identification of the UbcH10 gene that was upregulated by 150-fold in all of the carcinoma cell lines in comparison to the primary culture cells of human normal thyroid origin. Immunohistochemical studies performed on paraffin-embedded tissue sections showed abundant UbcH10 levels in thyroid anaplastic carcinoma samples, whereas no detectable UbcH10 expression was observed in normal thyroid tissues, in adenomas and goiters. Papillary and follicular carcinomas were only weakly positive. These results were further confirmed by RT -PCR and Western blot analyses. The block of UbcH10 protein synthesis induced by RNA interference significantly reduced the growth rate of thyroid carcinoma cell lines. Taken together, these results would indicate that UbcH10 overexpression is involved in thyroid cell proliferation, and may represent a marker of thyroid anaplastic carcinomas.

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Section: Discussionmentioning

confidence: 99%

Section: Cell Culture and Transfectionsmentioning

confidence: 99%

UbcH10 overexpression may represent a marker of anaplastic thyroid carcinomas

et al. 2005

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“…The human thyroid carcinoma cell lines studied were: TPC-1 (Tanaka et al, 1987), WRO (Pang et al, 1989), NPA (Estour et al, 1989), ARO (Pang et al, 1989), FRO (Fagin et al, 1993), NIM 1 (Zeki et al, 1991) and B-CPAP (Fabien et al, 1994). They were grown in Dulbecco's modi®ed Eagle's medium (DMEM) containing 10% fetal bovine serum.…”

Section: Cell Culture and Assay Of The Transformed Statementioning

confidence: 99%

Expression of the neoplastic phenotype by human thyroid carcinoma cell lines requires NFκB p65 protein expression

Visconti

Cerutti

Battista³

et al. 1997

Oncogene

167

111

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We have investigated the role of the NFkB complex in the process of thyroid carcinogenesis by analysing thyroid carcinoma cell lines. A signi®cant increase in p65 NFkB mRNA and protein expression, compared to normal thyroid cultures or tissue, was found in all of the cancer cell lines. Conversely, only a modest increase in the p50 NFkB mRNA and protein was found in most, but not all carcinoma cell lines. The block of p65 protein synthesis with speci®c antisense oligonucleotides greatly reduced the ability of two undierentiated carcinoma cell lines to form colonies in agar and reduced their growth rate. On the other hand, no eect was observed in the same cell lines when treated with p50 speci®c antisense oligonucleotides. These inhibitory eects seem to be mediated by the suppression of c-myc gene expression, since treatment with antisense oligonucleotides for p65 gene interfered negatively with c-myc gene expression. Our results indicate that activation of the NFkB complex by overexpression of p65 plays a critical role in the process of thyroid cell transformation.

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“…To check the ampli®cation sensitivity of each gene, we performed RT-PCR ampli®cation using RNA from TPC-1 and K562 cell lines. The TPC-1 cell, established from papillary adenocarcinoma of thyroid (Tanaka et al, 1987) and having a rearranged H4-RET oncogene (Ishizaka et al, 1989(Ishizaka et al, , 1990, and the K562 cell line having a BCR ± ABL gene derived from CML (Lozzio and Lozzio, 1975), were used as positive controls. PCR primers used in this study were obtained from Biologica (Nagoya, Japan) and their sequences are listed in Table 3.…”

Section: Reverse Transcription Pcr (Rt-pcr)mentioning

confidence: 99%

Continued expression of a tissue specific activated oncogene in the early steps of radiation-induced human thyroid carcinogenesis

et al. 1997

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Ionizing radiation is a well-known risk factor of cancer development, but the mechanism of radiation induced carcinogenesis is not clear. Chromosomal rearrangements induced by radiation most likely are one of the principal genetic alterations resulting in malignant transformation. The chimeric BCR-ABL associated with chronic myelogenous leukemia (CML) and H4-RET oncogenes associated with thyroid papillary carcinoma are the result of a translocation and inversion, respectively. In vitro studies showed these genes were induced by high-doses of X-irradiation in cell lines. Studies also show that therapeutic external X-ray doses as high as 60 Gy for treatment of various childhood cancers including Hodgkin's disease signi®cantly increase the risk of thyroid cancer. Therefore, we examined the induction and persistence of these chimeric genes in human thyroid tissues transplanted in scid mice after 50 Gy exposure as a function of time for 2 months to elucidate the early events of thyroid carcinogenesis. The H4-RET genes were detected on day 2 and throughout the 2 month period. On the other hand, BCR-ABL genes were detected on day 2 and were undetectable subsequently. These results suggest that ionizing radiation causes various oncogene activations, but cells with only speci®c gene alteration uniquely associated with thyroid carcinogenesis are selectively retained demonstrating one of the early events in the beginnings of radiation carcinogenesis in human thyroid tissues.

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Establishment and biological characterization of an in vitro human cytomegalovirus latency model

Cited by 69 publications

References 24 publications

UbcH10 overexpression may represent a marker of anaplastic thyroid carcinomas

UbcH10 overexpression may represent a marker of anaplastic thyroid carcinomas

Expression of the neoplastic phenotype by human thyroid carcinoma cell lines requires NFκB p65 protein expression

Continued expression of a tissue specific activated oncogene in the early steps of radiation-induced human thyroid carcinogenesis

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