cyclooxygenase/breast neoplasms

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Relationship between cyclooxygenase-2 and human epidermal growth factor receptor 2 in vascular endothelial growth factor C up-regulation and lymphangiogenesis in human breast cancer.

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Both cyclooxygenase (COX)-2 and human epidermal growth factor receptor (HER)-2 promote breast cancer progression; however, the relationship between the two molecules remains unclear. We utilized human breast cancer tissues and cell lines to examine whether COX-2 and HER-2 played independent or

Relationship between the expression of cyclooxygenase 2 and MDR1/P-glycoprotein in invasive breast cancers and their prognostic significance.

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BACKGROUND Recent reports suggest that expression of the cyclooxygenase 2 (COX-2) enzyme may up-regulate expression of MDR1/P-glycoprotein (MDR1/P-gp), an exponent of resistance to cytostatic drugs. The present study aimed at examining the relationship between the expression of COX-2 and of

Cyclooxygenase-2 and chemoprevention of breast cancer.

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This article discusses the role of cyclooxygenase-2 (COX-2) in the aetiology and progression of breast cancer. Renewed interest in chemoprevention using non-steroidal antiinflammatory drugs (NSAIDS) has come from observations that regular NSAID use is associated with a reduced incidence of some

Cyclooxygenase-2 predicts adverse effects of tamoxifen: a possible mechanism of role for nuclear HER2 in breast cancer patients.

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Cyclooxygenase-2 (COX-2) is associated with breast tumour progression. Clinical and molecular studies implicate human epidermal growth factor receptor 2 (HER2) in the regulation of COX-2 expression. Recent reports raise the possibility that HER2 could mediate these effects through direct

Cyclooxygenase-2, multidrug resistance 1, and breast cancer resistance protein gene polymorphisms and inflammatory bowel disease in the Danish population.

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OBJECTIVE Crohn's disease (CD) and ulcerative colitis (UC) are characterized by an impaired mucosal defence to normal constituents of the intestinal flora and a dysregulated inflammatory response. The purpose of the study was to investigate whether single nucleotide polymorphisms (SNPs) in genes

Polymorphisms in regulatory regions of cyclooxygenase-2 gene and breast cancer risk in Brazilians: a case-control study.

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BACKGROUND Cyclooxygenase-2 (COX-2) is up-regulated in several types of cancer, and it is hypothesized that COX-2 expression may be genetically influenced. Here, we evaluate the association between single-nucleotide polymorphisms (SNPs) in the COX-2 gene (PTGS2) and the occurrence of breast cancer

Evaluation of the contribution of cyclooxygenase 2 genotypes to breast cancer in Taiwan.

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Overexpression of cyclooxygenase 2 (COX-2) has been suggested to be associated with breast carcinogenesis. The aim of the present study was to evaluate the contribution of genotypic polymorphisms in COX-2 to breast cancer risk of Taiwanese females. In total, 1,232 breast cancer patients and 1,232

Association of the three common SNPs of cyclooxygenase-2 gene (rs20417, rs689466, and rs5275) with the susceptibility of breast cancer: an updated meta-analysis involving 34,590 subjects.

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Several single nucleotide polymorphisms have been identified in cyclooxygenase-2 (COX-2) genes (e.g., -765 G>C (rs20417), -1195G>A (rs689466), and 8473 C>T (rs5275)). The association of these SNPs with the risk of different cancer types is still controversial. This study aims to evaluate the

Cyclooxygenase-2 inhibition: effects on tumour growth, cell cycling and lymphangiogenesis in a xenograft model of breast cancer.

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Cyclooxygenase-2 (COX-2) is associated with poor-prognosis breast cancer. We used a nude mouse xenograft model to determine the effects of COX-2 inhibition in breast cancer. Oestrogen receptor (ER)-positive MCF7/HER2-18 and ER-negative MDAMB231 breast cancer cell lines were injected into nude mice

NFAT induces breast cancer cell invasion by promoting the induction of cyclooxygenase-2.

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The NFAT (nuclear factor of activated T cells) family of transcription factors plays a fundamental role in the transcriptional regulation of the immune response. However, NFATs are ubiquitously expressed, and recent evidence points to their important functions in human epithelial cells and

Prognostic impact of cyclooxygenase-2 in breast cancer.

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Cyclooxygenase (COX)-2, an inducible isoform of cyclooxygenases, regulates the rapid production of high levels of prostaglandins during inflammation. Cyclooxygenase-2 is overexpressed in a variety of malignant tumors. This review discusses epidemiologic and preclinical data on the role of COX-2 in

Modulation of Delta9-tetrahydrocannabinol-induced MCF-7 breast cancer cell growth by cyclooxygenase and aromatase.

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Delta(9)-Tetrahydrocannabinol (Delta(9)-THC), a major constituent of marijuana, has been shown to stimulate the growth of MCF-7 breast cancer cells through cannabinoid receptor-independent signaling [Takeda, S., Yamaori, S., Motoya, E., Matsunaga, T., Kimura, T., Yamamoto, I., Watanabe, K., 2008.

Association of cyclooxygenase-2 and matrix metalloproteinase-2 expression in human breast cancer.

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Expression of cyclooxygenase-2 (COX-2) and matrix metalloproteinase-2 (MMP-2) associates with reduced survival in human breast cancer. COX-2 may be directly involved with mammary carcinogenesis, since expression of COX-2 is sufficient for formation of breast tumors in transgenic mice, and COX-2

Cyclooxygenase-2 expression correlates with diminished survival in invasive breast cancer treated with mastectomy and radiotherapy.

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OBJECTIVE To evaluate the relationship between cyclooxygenase-2 (COX-2) expression and pathologic features and outcome in invasive breast cancer. METHODS Formalin-fixed, paraffin-embedded tumor specimens from 23 women with invasive breast cancer were stained for COX-2 expression. All women underwent

Expression of cyclooxygenase-2 and Bcl-2 in breast cancer and their relationship with triple-negative disease.

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OBJECTIVE Carcinogenesis is a multistep process with many factors being involved. The aim of this study was to investigate the role of cyclooxygenase-2 (COX-2) and Bcl-2 expression in patients with triple-negative breast cancer (TNBC) and, also whether any differences exist between TNBC and non-TNBC

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