Cytogenetic studies of human T-cell leukemia virus type I carriers

Itoyama, Takahiro; Sadamori, Naoki; Tokunaga, Seiji; I, Sasagawa; Nakamura, Hideo; Yao, Ei-ichi; T, Jubashi; Yamada, Yasuaki; Ikeda, Shu‐ichi; Ichimaru, Michito

doi:10.1016/0165-4608(90)90137-y

Cited by 14 publications

(7 citation statements)

References 12 publications

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“…Although no common type of chromosomal damage has been associated with the development of ATL, HTLV-1-transformed lymphocytes isolated from patients or immortalized in cell culture demonstrate a large variety of chromosomal aberrations, including deletions, duplications, translocations, rearrangements, and aneuploidy [Miyamoto et al, 1983;Rowley et al, 1984;Itoyama et al, 1990]. Tax expression interferes with various processes involved in DNA metabolism, normal progression through the cell cycle, and apoptotic elimination of cells containing dangerous amounts of DNA damage.…”

Section: Impairment Of Cellular Dna Repair Pathways By Viral Oncoprotmentioning

confidence: 97%

Impact of transforming viruses on cellular mutagenesis, genome stability, and cellular transformation

Gatza

Chandhasin

Ducu

et al. 2005

Environ and Mol Mutagen

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It is estimated that 15% of all cancers are etiologically linked to viral infection. Specific cancers including adult T-cell leukemia, hepatocellular carcinoma, and uterine cervical cancer are associated with infection by human T-cell leukemia virus type I, hepatitis B virus, and high-risk human papilloma virus, respectively. In these cancers, genomic instability, a hallmark of multistep cancers, has been explicitly linked to the expression of oncoproteins encoded by these viruses. This review discusses mechanisms utilized by these viral oncoproteins, Tax, HBx, and E6/E7, to mediate genomic instability and cellular transformation.

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Section: Impairment Of Cellular Dna Repair Pathways By Viral Oncoprotmentioning

confidence: 97%

Impact of transforming viruses on cellular mutagenesis, genome stability, and cellular transformation

Gatza

Chandhasin

Ducu

et al. 2005

Environ and Mol Mutagen

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“…HTLV-I transformed lymphocytes isolated from patients, and those immortalized in culture, demonstrate a wide range of chromosomal abnormalities, including deletions, translocations, rearrangements, duplications, and aneuploidy (Chieco-Bianchi et al, 1988; Fujimoto et al, 1999; Itoyama et al, 1990; Kamada et al, 1992; Maruyama et al, 1990; Whang-Peng et al, 1985), however no specific type of chromosomal change has been associated with the development of HTLV-I associated malignancy. Based on the complexity and variability of karyotypic abnormalities found in ATL cells, a multistep oncogenic process is thought to drive the development of ATL (Okamoto et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

The HTLV-1 Tax oncoprotein represses Ku80 gene expression

2011

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The HTLV-I oncoprotein Tax interferes with DNA double strand break repair. Since non-homologous end joining (NHEJ) is a major pathway used to repair DNA double strand breaks we examined the effect of Tax on this pathway, with particular interest in the expression and function of Ku80, a critical component of the NHEJ pathway. Tax expression decreased Ku80 mRNA and protein levels, and repressed transcription from the Ku80 promoter. Conversely, Ku80 mRNA increased following siRNA knockdown of Tax in HTLV-I infected cells. Tax expression was associated with an elevated number of micronuclei and nucleoplasmic bridges, hallmarks of improper DNA double strand break repair. Our studies identified Tax as a transcriptional repressor of Ku80 that correlates with decreased DNA repair function. The reduction of Ku80 transcription by Tax may deplete the cell of an essential DNA break binding protein, resulting in reduced repair of DNA double strand breaks and accumulation genomic mutations.

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“…Both HTLV-I transformed lymphocytes isolated from patients and those immortalized in culture demonstrate a wide range of chromosomal abnormalities that include deletions, translocations, rearrangements, duplications, and aneuploidy (Whang-Peng et al, 1985;ChiecoBianchi et al, 1988;Itoyama et al, 1990;Maruyama et al, 1990;Tanaka et al, 1990;Sadamori, 1991;Kamada et al, 1992;Fujimoto et al, 1999;Kao et al, 2000). There is no current evidence linking a specific type of chromosomal damage to the development of ATL.…”

Section: Effects Of Htlv-i Tax On Genome Instability and Dna Repairmentioning

confidence: 99%

Impact of HTLV-I Tax on cell cycle progression and the cellular DNA damage repair response

2005

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Cytogenetic studies of human T-cell leukemia virus type I carriers

Cited by 14 publications

References 12 publications

Impact of transforming viruses on cellular mutagenesis, genome stability, and cellular transformation

Impact of transforming viruses on cellular mutagenesis, genome stability, and cellular transformation

The HTLV-1 Tax oncoprotein represses Ku80 gene expression

Impact of HTLV-I Tax on cell cycle progression and the cellular DNA damage repair response

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