Sister chromatid exchange and chromosome abnormalities in uremic patients

Cengiz, Kuddusi; Block, AnneMarie W.; Hossfeld, Dieter K.; Anthone, Roland; Anthone, Sidney; Sandberg, Avery A.

doi:10.1016/0165-4608(88)90075-1

Cited by 39 publications

(27 citation statements)

References 44 publications

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“…Elevated cancer risk after transplantation is thought to result from the interplay of several factors: the chronic uraemic state favors carcinogenesis and overall or cumulative exposure to immunosuppression disrupts both antitumor immunosurveillance and anti-viral activity, and may potentiate the carcinogenic effects of other agents such as sunlight (7,8). Additionally, some drugs promote carcinogenesis by mechanisms independent of their immunosuppressive effects (9).…”

Section: Introductionmentioning

confidence: 99%

Identifying High Risk Groups and Quantifying Absolute Risk of Cancer After Kidney Transplantation: A Cohort Study of 15 183 Recipients

Webster

Craig

Simpson

et al. 2007

American Journal of Transplantation

267

146

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Section: Introductionmentioning

confidence: 99%

Identifying High Risk Groups and Quantifying Absolute Risk of Cancer After Kidney Transplantation: A Cohort Study of 15 183 Recipients

Webster

Craig

Simpson

et al. 2007

American Journal of Transplantation

267

146

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“…[20] Some studies have demonstrated that blood and tissues of uremic patients present changes in DNA that may play an important role in the pathogenesis of this disease. [1][2][3]7,24] In addition, an increase in the incidence of these changes may increase the risk for developing cancer. [1,7] In regards to the increased risk, DNA damage should be a target for therapeutical interventions.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3]7,24] In addition, an increase in the incidence of these changes may increase the risk for developing cancer. [1,7] In regards to the increased risk, DNA damage should be a target for therapeutical interventions. In in vitro studies, the coincubation of tubular cells with various antioxidants as well as the angiotensin II receptor blocker, candesartan, suppressed the toxic action.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3] This damage has been detected by the micronuclei (MN) frequency test and the formation of so-called tails in the comet assay (CA), a single-cell gel electrophoresis assay. [4,5] Moreover, the increased frequency of structurally abnormal chromosomes, elevated rates of sister chromatid exchange, [6,7] and increased 8-hydroxy 2'-deoxyguanosine (8-OH-dG) in leukocyte DNA [3] were also found in uremic patients.…”

Section: Introductionmentioning

confidence: 99%

“…[4][5][6]8] In addition, the increase in the prevalence of these damages may increase the risk of developing cancer. [1,2,7] Mitochondrial DNA (mtDNA) is more susceptible to damage than is nDNA due to its lack of histone protection and poor repair mechanisms. [9] In addition, mtDNA is located on the inner membrane of mitochondria, the site of the principle intracellular source of reactive oxygen species.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Prevalence of 4977bp Deletion in Mitochondrial DNA from Patients with Chronic Kidney Disease Receiving Conservative Treatment or Hemodialysis in Southern Brazil

et al. 2008

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Base excision repair capacity in chronic renal failure patients undergoing hemodialysis treatment

Stoyanova

Pastor

Coll

et al. 2013

Cell Biochemistry & Function

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The aim of this study was to determine if the differences observed in the levels of DNA damage in a group of patients suffering from chronic renal failure are due to differences in the repair capability. DNA damage was initially measured with the comet assay in 106 hemodialysis patients. A selected group of 21 patients representing high (ten patients) and low (11 patients) levels of DNA damage were obtained for determination of base excision repair capacity. This was measured in an in vitro assay where protein extracts from lymphocytes were incubated with a substrate of DNA containing 8-oxoguanine, and the rate of incision was measured with the comet assay. Patients with high levels of genomic damage showed, as an average, significantly lower repair capacity (12·73 ± 1·84) in comparison with patients with low levels of genomic damage (18·13 ± 1·13). Nevertheless, the correlation coefficient between repair ability and levels of genomic damage was found to be only close to the significance value (r:-0·423, p: 0·056). Although DNA damage was clearly related to time on hemodialysis, base excision repair capacity was not. This is one of the few studies providing information on the repair capacity of chronic renal failure patients undergoing hemodialysis. As a summary, our results would indicate that DNA damage levels are in part associated to the repair capacity of the patients, and this repair capacity is not associated with the duration of hemodialysis treatment.

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Sister chromatid exchange and chromosome abnormalities in uremic patients

Cited by 39 publications

References 44 publications

Identifying High Risk Groups and Quantifying Absolute Risk of Cancer After Kidney Transplantation: A Cohort Study of 15 183 Recipients

Identifying High Risk Groups and Quantifying Absolute Risk of Cancer After Kidney Transplantation: A Cohort Study of 15 183 Recipients

Prevalence of 4977bp Deletion in Mitochondrial DNA from Patients with Chronic Kidney Disease Receiving Conservative Treatment or Hemodialysis in Southern Brazil

Base excision repair capacity in chronic renal failure patients undergoing hemodialysis treatment

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