Oxidative Damage and Cancer

Oberley, Terry D.

doi:10.1016/s0002-9440(10)64857-2

Cited by 169 publications

(130 citation statements)

References 36 publications

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“…Oxidative stress has long been implicated in carcinogenesis (29) and shown to correlate with the most important clinical variables of disease (30). It is known that reactive oxygen species activate signal transduction pathways, including activator protein and nuclear factor-nB (NF-nB), and cause oxidative DNA damage, increasing risk of cancer development.…”

Section: Discussionmentioning

confidence: 99%

Molecular mechanisms of the chemopreventive effect on hepatocellular carcinoma development in Mdr2 knockout mice

Katzenellenbogen¹,

Mizrahi²,

Pappo

et al. 2007

Molecular Cancer Therapeutics

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Dietary antioxidants and selenium compounds were shown to have a therapeutic effect against hepatocellular carcinoma in several mouse models. We tested the effects of tannic acid and selenomethionine on hepatocellular carcinoma development in Mdr2 knockout (Mdr2-KO) mice. Mdr2-KO and age-matched Mdr2 heterozygous control mice were fed with tannic acid or selenomethionine during the first 3 months of life. Then, several mice from each group were sacrificed, and liver tissue samples were removed for analysis. The remaining mice were fed a regular diet until the age of 16 months, at which time the number and size of liver tumors were determined. Liver tissue samples of 3-month-old mice were subjected to gene expression profiling analysis using cDNA macroarrays containing probes for 240 genes that regulate responses to oxidative stress and inflammation or lipid metabolism. Both tannic acid and selenomethionine had partial chemopreventive effect on development of hepatocellular carcinoma in Mdr2-KO mice: they reduced the incidence of large tumor nodules (diameter >1 cm) at age 16 months. Both agents inhibited gene expression and reversed up-regulation of many genes that control inflammation or response to oxidative stress in Mdr2-KO livers at age 3 months. This inhibitory effect on gene expression correlated with the ability of agents to reduce incidence of large tumors: selenomethionine was more active than tannic acid in both aspects. Understanding the molecular mechanism of chemoprevention effect could improve our therapeutic modalities while using these agents. [Mol Cancer Ther 2007;6(4):1283 -91]

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Section: Discussionmentioning

confidence: 99%

Molecular mechanisms of the chemopreventive effect on hepatocellular carcinoma development in Mdr2 knockout mice

Katzenellenbogen¹,

Mizrahi²,

Pappo

et al. 2007

Molecular Cancer Therapeutics

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“…The integrity of the DNA of these surface cells surrounding the ovarian rupture site is compromised during ovulation, and rapid growth of cells with mutated DNA may result in the initiation of carcinogenesis [36]. The role of inflammation and oxidative damage to the pathogenesis of cancer has gained much attention [37,38]. Our results which demonstrate the high expression of COX-1 in the first postovulatory follicle (POF-1) may contribute to the pro-carcinogenic microenvironment where the malignant transformation of the OSE originates.…”

Section: Histology Of the Normal Hen's Ovary Compared To Ovarian Cancermentioning

confidence: 99%

Cyclooxygenases expression and distribution in the normal ovary and their role in ovarian cancer in the domestic hen (Gallus domesticus)

Hales

Zhuge

Lagman

et al. 2008

Endocr

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Cyclooxygenase (COX) (PTGS) is the rate-limiting enzyme in the biosynthesis of prostaglandins. Two COX isoforms have been identified, COX-1 and COX-2, which show distinct cell-specific expression and regulation. Ovarian cancer is the most lethal gynecological malignancy and the © Humana Press Inc. 2008 Correspondence to: Dale Buchanan Hales, dbhale@uic.edu. HHS Public Access Author ManuscriptAuthor Manuscript Author ManuscriptAuthor Manuscript disease is poorly understood due to the lack of suitable animal models. The laying hen spontaneously develops epithelial ovarian cancer with few or no symptoms until the cancer has progresses to a late stage, similar to the human disease. The purpose of this study was to examine the relative expression and distribution of COX-1 and COX-2 in the ovaries of normal hens and in hens with ovarian cancer. The results demonstrate that COX-1 was localized to the granulosa cell layer and cortical interstitium, ovarian surface epithelium (OSE) and postovulatory follicle (POF) of the normal ovary. In ovarian cancer, COX-1 mRNA was significantly increased and COX-1 protein was broadly distributed throughout the tumor stroma. COX-2 protein was localized to the granulosa cell layer in the follicle and the ovarian stroma. COX-2 mRNA expression did not change as a function of age or in ovarian cancer. There was significantly higher expression of COX-1 mRNA in the first POF (POF-1) compared to POF-2 and POF-3. COX-2 mRNA expression was not significantly different among POFs. There was no difference in COX-1 or COX-2 mRNA in the OSE isolated from individual follicles in the follicular hierarchy. The results confirm previous findings of the high expression of COX-1 in ovarian tumors further supporting the laying hen as a model for ovarian cancer, and demonstrate for the first time the high expression of COX-1 in POF-1 which is the source of prostaglandins needed for oviposition.

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“…Adversely, low concentrations of ROS serve a variety of important cellular functions such as the activation and modulation of the signal transduction pathways (Monteino & Stern, 1996), modulation of the activities of the redox sensitive transcription factors Oberley, 2002) Oberley, 2002). Increased ROS production is well displayed in transformed cells (Toyokuni, et al, 1995;Burdon, 1995;Storz, 2005;Kryston, et al, 2011) and growing evidence suggests that ROS act as second messengers in intracellular signaling pathways (Liou & Storz, 2010).…”

Section: Introductionmentioning

confidence: 99%