Chromosome complement and SV40 transformation of cells from patients susceptible to malignant disease

Webb, T.; Harding, Margaret M.

doi:10.1038/bjc.1977.235

Cited by 10 publications

(4 citation statements)

References 21 publications

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“…family compared with the controls. This is in accordance with reports by WEBB and HARDING (1977) and RICCARDI and MARGOS (1981).…”

Section: Discussion Von Recklinghausen's Disease Is Transmitted Bysupporting

confidence: 94%

“…In neurofibromatosis, no consistent chromosomal abnormality has ever been reported. In a chromosome study of skin fibroblasts from a family with neurofibromatosis, WEBB and HARDING (1977) found no deviation from controls with respect to breaks and gaps. Neither have any convincing karyotypic abnormalities been revealed by cytogenetic analyses of skin and tumour fibroblasts with conventional staining or G-banding (RICCARDI and M A R C~S 1981).…”

mentioning

confidence: 92%

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Sister chromatid exchanges and chromosome aberrations in von Recklinghausen's disease-a family study

Granberg-Öhman¹,

Brismar²,

Lindholm³

2008

Hereditas

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Five members of a family with von Recklinghausen's disease (v.R.d.) were studied with respect to the occurrence of sister chromatid exchanges (SCE) and chromosomal aberrations. The frequency of gaps, breaks and other chromosomal aberrations in cells from the v.R.d. family did not differ from those in controls. In the controls, the frequency of aberrations increased three‐fold after treatment with mitomycin C, but in the v.R.d. family no response was observed. The frequency of spontaneous SCE was significantly lower in all but one of the members of the v.R.d. family than in the controls. Mitornycin C increased the rate of SCE in all the v.R.d. family members and also in the controls, the increase being small, however, in two members of the v.R.d. family. The low frequency of SCE may be specific to the disease.

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“…family compared with the controls. This is in accordance with reports by WEBB and HARDING (1977) and RICCARDI and MARGOS (1981).…”

Section: Discussion Von Recklinghausen's Disease Is Transmitted Bysupporting

confidence: 94%

mentioning

confidence: 92%

Sister chromatid exchanges and chromosome aberrations in von Recklinghausen's disease-a family study

Granberg-Öhman¹,

Brismar²,

Lindholm³

2008

Hereditas

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“…However, Young [8] found that only one of five obligate FA heterozygotes and two of five possible heterozygotes (unaffected sibs) showed some degree of abnormality However, his assay system differed in certain key details from that employed by Todaro. Similarly, Webb and Harding [6] found elevated transformation rates in only one of two FA heterozygotes. Using a system that measures T-antigen expression at three days, we found consistently high values in 12 FA cases (mean = 26.…”

Section: Discussionmentioning

confidence: 82%

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

Lubiniecki¹,

Dosik

et al. 1980

American J Hematol

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Skin fibroblasts from patients with a variety of hematologic disorders were infected with SV40 virus in vitro in attempts to discover the reason for increased susceptibility of Fanconi anemia cells to this transforming virus. The proportion of skin fibroblasts expressing SV40 T-antigen by immunofluorescent methods was elevated in 12 patients with Fanconi anemia and in seven of nine obligate heterozygous relatives. Elevated expression was also observed in three patients with other hematological disorders at high risk of acute non-lymphocytic leukemia, but was not apparent in seven sporadic aplastic anemia patients or four of their relatives. T-antigen expression was elevated in about one-half of patients with thrombocytopenia-absent radius syndrome and related conditions, with familial aplastic anemia, and in their normal relatives. In the conditions under study, elevated T-antigen expression seemed clearly correlated with predisposition to leukemia, which may be genetically determined, but it was not associated with cytogenetic or anemic manifestations.

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“…For instance, infection of normal human skin fibroblasts with SV40 was shown to give rise to a limited number of transformed colonies. However, with cells from Fanconi’s anaemia (FA) patients there was a 10–20-fold increase in the number of transformants, whilst transformation of cells from ataxia telangiectasia (AT) and Bloom’s syndrome patients occurred at normal levels (Todaro et al , 1966; Kersey et al , 1972; Webb et al , 1977; Webb & Harding, 1977).…”

Section: An Historical Perspectivementioning

confidence: 99%

DNA viruses and the cellular DNA-damage response

Turnell

Grand

2012

Journal of General Virology

135

141

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It is clear that a number of host-cell factors facilitate virus replication and, conversely, a number of other factors possess inherent antiviral activity. Research, particularly over the last decade or so, has revealed that there is a complex inter-relationship between viral infection and the host-cell DNA-damage response and repair pathways. There is now a realization that viruses can selectively activate and/or repress specific components of these host-cell pathways in a temporally coordinated manner, in order to promote virus replication. Thus, some viruses, such as simian virus 40, require active DNA-repair pathways for optimal virus replication, whereas others, such as adenovirus, go to considerable lengths to inactivate some pathways. Although there is ever-increasing molecular insight into how viruses interact with host-cell damage pathways, the precise molecular roles of these pathways in virus life cycles is not well understood. The object of this review is to consider how DNA viruses have evolved to manage the function of three principal DNA damage-response pathways controlled by the three phosphoinositide 3-kinase (PI3K)-related protein kinases ATM, ATR and DNA-PK and to explore further how virus interactions with these pathways promote virus replication. IntroductionThe DNA-damage response (DDR) is a general term employed to describe a complex series of cellular pathways that detect DNA damage, initiate cell-cycle arrest so that mutated DNA is not duplicated, and then go on to repair the lesion or, if damage is too great, trigger apoptosis. Infection by many virus species is sufficient to initiate a DDR, activating some or all of the repair pathways. Simplistically, this has been seen as recognition by the host cell of viral DNA as its own damaged DNA, but it is now considered that this could, at least to some extent, be an antiviral response, aimed directly at combating infection. Viruses have a complex series of mechanisms that, in turn, have evolved to combat and inactivate the cellular damage-response pathways.The aim of this review is to consider how and why different viruses affect the balance of these opposing pathways: for example, to what extent is an activated DDR directly required by particular virus species to facilitate or assist virus replication or, conversely, to what extent does the cellular damage response hinder replication. Additionally, it is often not clear whether activation of the DDR is a mere byproduct of infection or a direct result of 'intentional' action of viral protein activity. If DDR activation is an unwanted result of infection, a further point of interest is to understand what measures viruses take to circumvent the deleterious effects of the cellular pathways. Past experience would suggest that viruses are so highly evolved and their primary structures so tightly constrained that the selective activation of DDR pathways by some viruses might prove advantageous to them. Whether this is the case will only become evident after considerable further investigation.The r...

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Chromosome complement and SV40 transformation of cells from patients susceptible to malignant disease

Cited by 10 publications

References 21 publications

Sister chromatid exchanges and chromosome aberrations in von Recklinghausen's disease-a family study

Sister chromatid exchanges and chromosome aberrations in von Recklinghausen's disease-a family study

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

DNA viruses and the cellular DNA-damage response

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