ArticleCancer science2004
Integration of human T-cell leukemia virus type 1 in genes of leukemia cells of patients with adult T-cell leukemia.
Article in Cancer science, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 23 citations in OpenAlex.
- Methodological landscape in the field of integration site identification of retroviruses and retroviral vectors.Frontiers in bioengineering and biotechnology · 2025Review
- Review
- The host genomic environment of the provirus determines the abundance of HTLV-1-infected T-cell clones.Blood · 2011Article
- Expression profiles of adult T-cell leukemia-lymphoma and associations with clinical responses to zidovudine and interferon alpha.Leukemia & lymphoma · 2010Article
- High-throughput insertional mutagenesis screens in mice to identify oncogenic networks.Nature reviews. Cancer · 2009Review
- Proviral loads and clonal expansion of HTLV-1-infected cells following vertical transmission: a 10-year follow-up of children in Jamaica.Intervirology · 2009Article
- HTLV-1 integration into transcriptionally active genomic regions is associated with proviral expression and with HAM/TSP.PLoS pathogens · 2008Article
- Human T-cell leukemia virus type 1 integration target sites in the human genome: comparison with those of other retroviruses.Journal of virology · 2007Article
- A primate virus generates transformed human cells by fusion.The Journal of cell biology · 2005Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adult T-cell leukemia (ATL) occurs after a long latent period of persistent infection by human T-cell leukemia virus type 1 (HTLV-1). However, the mechanism of oncogenesis by HTLV-1 remains to be clarified. It was reported that the incidence curve of ATL versus age was consistent with a multistage carcinogenesis model. Although HTLV-1 is an oncogenic retrovirus, a mechanism of carcinogenesis in ATL by insertional mutagenesis as one step during multistage carcinogenesis has not been considered thus far, because the exact integration sites on the chromosome have not been analyzed. Here we determined the precise HTLV-1 integration sites on the human chromosome, by taking advantage of the recently available human genome database. We isolated 25 integration sites of HTLV-1 from 23 cases of ATL. Interestingly, 13 (52%) of the integration sites were within genes, a rate significantly higher than that expected in the case of random integration (P = 0.043, chi(2) test). These results suggest that preferential integration into genes at the first infection is a characteristic of HTLV-1. However considering that some of the genes are related to the regulation of cell growth, the integration of HTLV-1 into or near growth-related genes might contribute to the clonal selection of HTLV-1-infected cells during multistage carcinogenesis of ATL.
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