Relationship of SV40 T‐antigen expression in vitro to disorders of bone marrow function

Lubiniecki, Anthony S.; Wa, Blattner; Dosik, Harvey; McIntosh, Steven; Wertelecki, Wladimir

doi:10.1002/ajh.2830080407

Cited by 4 publications

(2 citation statements)

References 22 publications

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“…Several investigations have reported that FA fibroblasts are particularly sensitive to transformation by SV40 T-Ag (Todaro et al, 1966;Dosik et al, 1970;Lubiniecki et al, 1980). This phenomenon is directly linked to the primary defect in these cells since correction of FA-C cells by transduction with FANCC has been shown to reduce their transformation potential (Liu et al, 1996).…”

Section: Sv40 Transformation and Famentioning

confidence: 99%

SV40 large T-antigen disturbs the formation of nuclear DNA-repair foci containing MRE11

et al. 2002

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Section: Sv40 Transformation and Famentioning

confidence: 99%

SV40 large T-antigen disturbs the formation of nuclear DNA-repair foci containing MRE11

et al. 2002

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“…In cell transformation and tumorigenesis, the SV40 large antigen (LT) oncoprotein targets and inactivates the functions of key cellular products, such as the tumor suppressor p53 and the pRB family proteins. LT may also lead to transformation by inducing point mutations and chromosomal alterations, suggesting that the SV40 transforming properties depend on its ability to perturb tumor suppressor pathways, apoptotic processes and cell growth [10] , [11] .…”

Section: Introductionmentioning

confidence: 99%

Fanconi Anemia Patients Are More Susceptible to Infection with Tumor Virus SV40

et al. 2013

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Fanconi anemia (FA) is a recessive DNA repair disease characterized by a high predisposition to developing neoplasms. DNA tumor polyomavirus simian virus 40 (SV40) transforms FA fibroblasts at high efficiency suggesting that FA patients could be highly susceptible to SV40 infection. To test this hypothesis, the large tumor (LT) antigen of SV40, BKV, JCV and Merkel Cell (MC) polyomaviruses were tested in blood samples from 89 FA patients and from 82 of their parents. Two control groups consisting of 47 no-FA patients affected by other genetic bone marrow failure diseases and 91 healthy subjects were also evaluated. Although JCV, BKV and MC were not found in any of the FA samples, the prevalence and viral load of SV40 were higher in FA patients (25%; mean viral load: 1.1×102 copies/105cells) as compared with healthy individuals (4.3%; mean viral load: 0.8×101 copies/105cells) and genetic controls (0%) (p<0.005). A marked age-dependent frequency of SV40 was found in FA with respect to healthy subjects suggesting that, although acquired early in life, the virus can widespread more easily in specific groups of population. From the analysis of family pedigrees, 60% of the parents of SV40-positive probands were positive for the virus compared to 2% of the parents of the SV40-negative probands (p<0.005). It is worthy of note that the relative frequency of SV40-positive relatives detected in this study was the highest ever reported, showing that asymptomatic FA carriers are also more susceptible to SV40. In conclusion, we favor the hypothesis that SV40 spread could be facilitated by individuals who are genetically more susceptible to infection, such as FA patients. The increased susceptibility to SV40 infection seems to be associated with a specific defect of the immune system which supports a potential interplay of SV40 with an underlying genetic alteration that increases the risk of malignancies.

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Reduced uptake and incorporation of 3H-thymidine in fanconi anemia fibroblasts

Shoyab¹,

Gunnell²,

Lubiniecki³

1981

Hum Genet

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Uptake of 3H-thymidine and its incorporation into DNA was studied in fibroblastic cell lines derived from normal individuals, patients with Fanconi anemia, and those heterozygous for this genetic trait. Uptake and incorporation for the normal cells were about five and seven times higher, respectively, than for Fanconi anemia fibroblasts; mean values for heterozygotes were intermediate. This effect was dependent on the duration of cell exposure to 3H-thymidine and was not observed with other labeled compounds. Thus a genetically-determined metabolic defect may exist in Fanconi anemia patients which can be readily studied at the cellular level. This finding may be relevant to the observed clinical, cytogenetic, biochemical, and biologic properties related to expression of the Fanconi anemia gene.

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Relationship of SV40 T‐antigen expression in vitro to disorders of bone marrow function

Cited by 4 publications

References 22 publications

SV40 large T-antigen disturbs the formation of nuclear DNA-repair foci containing MRE11

SV40 large T-antigen disturbs the formation of nuclear DNA-repair foci containing MRE11

Fanconi Anemia Patients Are More Susceptible to Infection with Tumor Virus SV40

Reduced uptake and incorporation of 3H-thymidine in fanconi anemia fibroblasts

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