Cytogenetic characterization of a T-cell line, ATN-1, derived from adult T-cell leukemia cells

Naoe, Tomoki; Akao, Yukihiro; Yamada, Kazumasa; Utsumi, Kazuhiko R.; Koike, Kenichi; Shamoto, Michihiro; Koie, Katsuo; Kurosawa, Yoshikazu; Kato, Koji; Abe, Masumi; Shiku, Hiroshi

doi:10.1016/0165-4608(88)90171-9

Cited by 22 publications

(13 citation statements)

References 26 publications

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“…The ATN-1 cell line used in this study has been described (Naoe et al 1988). The IL-2-dependent, ATLL cell lines OMT, KOB, KK-1, and ST-1 were obtained from Dr. Yamada of Medical School of Nagasaki University Maeda et al 1999;Yamada et al 1991Yamada et al , 1999.…”

Section: Cell Linesmentioning

confidence: 99%

Rapid isolation of viral integration site reveals frequent integration of HTLV-1 into expressed loci

et al. 2004

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Although there is tight association of the human T-cell leukemia virus type-1 (HTLV-1) with adult T-cell leukemia/lymphoma (ATLL), it has remained unresolved whether the HTLV-1 integration into the host genome has any role in the development of this disease. We isolated a total of 58 HTLV-1 integration sites using newly developed, adaptor-ligated PCR from 33 ATLL patients and five ATLL cell lines. We compared our data as well as the previously reported ones with the complete human genomic sequence for the location of its placement, structure, and expression of genes nearby the integration site. The chromosomal target for integration was selected at random, but the integration favorably occurred within the transcription units; more than 59.5% of total integration was observed within the transcriptional unit. All inserted genes by HTLV-1 integration were expressed in normal T cells. Upregulation of genes due to viral integration was found in two out of nine ATLL cases; about 4.4-and 102-fold elevated ankyrin-1 (ANK-1) and gephyrin (GPHN) gene expressions were observed, respectively. These data suggest that the preferential integration of HTLV-1 into an expressed locus occasionally causes deregulation of corresponding gene, which may lead to leukemogenesis of a fraction of ATLL.

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Section: Cell Linesmentioning

confidence: 99%

Rapid isolation of viral integration site reveals frequent integration of HTLV-1 into expressed loci

et al. 2004

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“…ATN-1, KK1, ST1, and KOB were established from ATL patients and kindly provided by Dr Yasuaki Yamada of Nagasaki University Graduate School of Biomedical Sciences; the patient origins of these cells were confirmed by concordance of the integration sites of HTLV-1 proviral DNA and/or rearrangement profiles of the T-cell receptor ␤-chain gene. [33][34][35] MT-1 was derived form a patient with ATL. 36 MT-2 was established by cocultivation of human cord blood lymphocytes from a normal subject with peripheral blood mononuclear cells (PBMCs) from an ATL patient.…”

Section: Cell Lines and Culture Conditionsmentioning

confidence: 99%

NK314 potentiates antitumor activity with adult T-cell leukemia-lymphoma cells by inhibition of dual targets on topoisomerase IIα and DNA-dependent protein kinase

Hisatomi

Sueoka‐Aragane

Sato

et al. 2011

Blood

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“…To examine the expression of BC040320 and GPC5 in detail, Northern blot analysis was also performed for several cell lines and patients. Northern blot hybridization was performed with a standard method (21). Each RT-PCR product was used as a specific probe labeled by PCR.…”

Section: Introductionmentioning

confidence: 99%

Identification and Characterization of a Novel Gene, C13orf25 , as a Target for 13q31-q32 Amplification in Malignant Lymphoma

et al. 2004

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The amplification at 13q31-q32 has been reported in not only hematopoietic malignancies but also in other solid tumors. We identified previously frequent amplification of chromosomal band 13q31-q32 in 70 cases of diffuse large B-cell lymphoma patients by conventional comparative genomic hybridization analysis. In an attempt to identify a candidate gene within this region, we used array comparative genomic hybridization and fluorescent in situ hybridization to map the 13q31-q32 amplicon. We then screened the 65 expressed sequence tags and Glypican 5 (GPC5) by reverse transcription-PCR and Northern blotting. As a result, we identified a novel gene, designated Chromosome 13 open reading frame 25 (C13orf25), which was overexpressed in B-cell lymphoma cell lines and diffuse large B-cell lymphoma patients with 13q31-q32 amplifications. However, GPC5, which has been reported to be a target gene for 13q31-q32 amplification, was truncated in one cell line, Rec1, possessing the amplification, and its expression in various cell lines with amplification at 13q31-q32 was not significantly different from that in other cell lines without amplification, suggesting that GPC5 is not likely to be the candidate gene. Additional analysis identified two major transcripts in the C13orf25 gene. The two transcripts A and B predicted open reading frames of 32 and 70-amino acid polypeptides, respectively. The former has been reported as bA121J7.2, which is conserved among species. Transcript-B also contained seven mature microRNAs in its untranslated region. These results suggest that the C13orf25 gene is the most likely candidate gene for the 13q31-q32 amplicon found in hematopoietic malignancies.

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Cytogenetic characterization of a T-cell line, ATN-1, derived from adult T-cell leukemia cells

Cited by 22 publications

References 26 publications

Rapid isolation of viral integration site reveals frequent integration of HTLV-1 into expressed loci

Rapid isolation of viral integration site reveals frequent integration of HTLV-1 into expressed loci

NK314 potentiates antitumor activity with adult T-cell leukemia-lymphoma cells by inhibition of dual targets on topoisomerase IIα and DNA-dependent protein kinase

Identification and Characterization of a Novel Gene, C13orf25 , as a Target for 13q31-q32 Amplification in Malignant Lymphoma

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