Levels of 5-hydroxymethyl-2′-deoxyuridine in DNA from blood as a marker of breast cancer

Djurić, Zora; Heilbrun, Lance K.; Simon, Michael S.; Smith, Daryn; Luongo, Domenico A.; LoRusso, Patricia; Martino, Silvana

doi:10.1002/(sici)1097-0142(19960215)77:4<691::aid-cncr15>3.0.co;2-w

Cited by 54 publications

(24 citation statements)

References 26 publications

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“…Class I isoenzymes of ADH are able to reduce aldehyde products generated from lipid peroxidation (e.g., 4-hydroxynonenal) [22]. Many studies suggest that there is a relationship between an excess of aldehyde products of lipid peroxidation and carcinogenesis of the breast gland [23,24]. The ADH isoenzymes perform a protective function by reducing the highly electrophilic products of lipid peroxidation to their less toxic alcohols.…”

Section: Discussionmentioning

confidence: 99%

The activity of class I, II, III and IV alcohol dehydrogenase isoenzymes and aldehyde dehydrogenase in breast cancer

et al. 2006

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Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) play a significant role in the metabolism of many biological substances. ADH participates in the metabolism of ethanol, retinoic acid, lipid peroxidation products, leukotriene and glutathione metabolism. ALDH is responsible for oxidation of acetaldehyde and other aldehydes and metabolism of histamine and retinoic acid. The aim of this study was to compare the metabolism in breast cancer cells and normal breast parenchyma by measuring ADH isoenzymes and ALDH activities in these tissues. Total ADH activity was measured by a photometric method with p-nitrosodimethylaniline (NDMA) as a substrate. For the measurement of the activity of ALDH and class I and II isoenzymes of ADH we employed the fluorometric methods, with class-specific fluorogenic substrates. The activity of class III alcohol dehydrogenase was detected by the photometric method with n-octanol and class IV with m-nitrobenzaldehyde as substrates. The samples were taken surgically during resection of breast carcinoma from 75 women. The activity of the class I ADH isoenzyme was significantly lower in breast cancer cells than in healthy tissues. The other tested classes of ADH had a tendency for higher levels of activity in cancer cells than in normal mammary tissue. The activity of total ADH and ALDH was also not significantly lower in the cancer cells. The decrease of activity of class I ADH isoenzyme in breast cancer tissues may be a factor of some disorders in metabolic pathways with participation of these isoenzymes that can lead to carcinogenesis.

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Section: Discussionmentioning

confidence: 99%

The activity of class I, II, III and IV alcohol dehydrogenase isoenzymes and aldehyde dehydrogenase in breast cancer

et al. 2006

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“…The increase in SOD 1 activities was not accompanied by a decrease in urinary contents of 8-deoxyhydroxyguanosine (Figure 2), a DNA oxidation product with relevance to breast cancer [52,53]. Ceruloplasmin activities and protein were unchanged by the soy product and placebo treatments ( Table 1).…”

Section: Resultsmentioning

confidence: 96%

“…Despite the increase in SOD 1 activities, there was no change in urinary contents of 8-deoxyhydroxyguanosine, a DNA oxidant product considered relevant to breast cancer risk [52,53]. Thus, it may be speculated that the increase in SOD 1 does not translate to an actual increase in antioxidant protection.…”

Section: Discussionmentioning

confidence: 99%

Soy isoflavone supplementation elevates erythrocyte superoxide dismutase, but not plasma ceruloplasmin in postmenopausal breast cancer survivors

DiSilvestro

Goodman

et al. 2005

Breast Cancer Res Treat

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Soy isoflavone antioxidant effects may help prevent breast cancer re-occurrence, but isoflavone estrogen-like actions may increase breast cancer risk. These isoflavone actions can be reflected by effects on two copper enzymes activities, superoxide dismutase 1 (SOD 1), which has antioxidant function relevant to breast cancer prevention, and ceruloplasmin, which has its synthesis up-regulated by estrogen, and for which high values are associated with high breast cancer risk. A soy isoflavone-rich concentrate supplement was examined for effects on these two copper enzyme activities in post-menopausal breast cancer survivors (n = 7) in a crossover design with a placebo (24 days on supplement or placebo; 14 day wash out). The soy concentrate, but not the placebo, increased erythrocyte SOD 1 activities, but not ceruloplasmin activities or protein. The effect on superoxide dismutase activities was not likely due to increased copper intake since analysis of the soy extract showed little copper. The effect on superoxide dismutase was not accompanied by a change in urinary contents of 8-deoxyhydroxyguanosine, a DNA oxidant product, though perhaps this would change with a longer intervention. In summary, in regard to two copper enzyme activities, an isoflavone-rich soy concentrate showed an antioxidant effect considered relevant to breast cancer, but not an effect associated with estrogenic activity and increased breast cancer risk.

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“…There is some evidence that oxidative stress in vivo is biologically important. DNA isolated from peripheral blood leukocytes of breast cancer patients yields evidence of oxidative damage [17]. We have detected 8-hydroxy-2'-deoxyguanosine, an indicator of oxidative DNA damage, in murine mammary tumors (unpublished data) confirming published reports of oxidative DNA damage in both human 1-18] and rodent [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19] breast tumors.…”

Section: Discussionmentioning

confidence: 99%

Sublethal oxidative stress inhibits tumor cell adhesion and enhances experimental metastasis of murine mammary carcinoma

1995

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We have postulated that murine mammary tumor progression is fueled, in part, by tumor-associated macrophages that deliver sub-lethal oxidative stress to tumor cells. In the present study, we determined whether oxidative stress would affect murine mammary tumor cell attachment to laminin and fibronectin, critical functions in the metastatic process. Sublethal oxidative stress generated by exposure of cells to hydrogen peroxide (H2O2, 1-1000 microM/L) inhibited tumor cell attachment to immobilized laminin or fibronectin. This oxidant effect was blocked in the presence of catalase which removes H2O2. The inhibitory effect on attachment was rapid, with significant inhibition occurring at 5 min; total inhibition was achieved at 60 min with 1 mM H2O2. The oxidative stress effect was partially reversible at 20 h post-treatment and occurred at concentrations of H2O2 that do not adversely affect cell viability or growth. Pretreatment of tumor cells with H2O2 or hypoxanthanine and xanthine oxidase (to generate superoxide radical and H2O2) prior to intravenous injection, enhanced experimental lung tumor colony formation. The enhancement of experimental metastatic potential with enzyme-generated oxidative stress was completely reversed by catalase; the H2O2-mediated enhancement was only partially reversed with catalase. Thus, treatments that inhibit tumor cell attachment to extracellular matrix proteins in vitro enhance experimental metastasis in vivo.

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Levels of 5-hydroxymethyl-2′-deoxyuridine in DNA from blood as a marker of breast cancer

Cited by 54 publications

References 26 publications

The activity of class I, II, III and IV alcohol dehydrogenase isoenzymes and aldehyde dehydrogenase in breast cancer

The activity of class I, II, III and IV alcohol dehydrogenase isoenzymes and aldehyde dehydrogenase in breast cancer

Soy isoflavone supplementation elevates erythrocyte superoxide dismutase, but not plasma ceruloplasmin in postmenopausal breast cancer survivors

Sublethal oxidative stress inhibits tumor cell adhesion and enhances experimental metastasis of murine mammary carcinoma

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