ADVANCES IN CANCER EPIDEMIOLOGY: Understanding Causal Mechanisms and the Evidence for Implementing Interventions

Schottenfeld, David; Beebe‐Dimmer, Jennifer L.

doi:10.1146/annurev.publhealth.26.021304.144402

Cited by 52 publications

(35 citation statements)

References 94 publications

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“…In chronic inflammation, NF-κB has a specific role in coupling inflammation to cancer. In total, >15% of all malignancies are initiated by chronic inflammatory disease; for example, skin inflammation initiates squamous cell carcinoma, viral hepatitis initiates liver cancer and inflammatory bowel disease (IBD) initiates CRC (31,(37)(38)(39)(40)(41). Previous studies have indicated that constitutive NF-κB activation in IBDs may be the cause of the increased risk of developing CRC (42)(43)(44).…”

Section: Discussionmentioning

confidence: 99%

Parthenolide induces apoptosis in colitis-associated colon cancer, inhibiting NF-κB signaling

et al. 2015

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Abstract. Recently, the nuclear factor (NF)-κB inhibitor parthenolide (PT) was identified as a promising anticancer agent for the promotion of cancer cell apoptosis. Additionally, our previous study demonstrated that PT administration suppresses tumor growth in a xenograft model of colorectal cancer cells via regulation of the B-cell lymphoma-2 (Bcl-2) family. However, the role of PT in the development of colitis-associated colon cancer (CAC) is poorly understood. Therefore, the aim of the present study was to investigate the effects of PT administration on CAC using a murine model. Azoxymethane (AOM) and dextran sulfate sodium (DSS) were administered to induce experimental CAC in the following three groups of treated mice: i) AOM and DSS plus vehicle; ii) AOM, DSS and 2 mg/kg PT; and iii) AOM, DSS and 4 mg/kg PT. It was demonstrated that the histological acuteness of AOM/DSS-induced CAC was significantly reduced following the administration of PT, resulting in decreased NF-κB p65 expression levels via a blockade of phosphorylation and subsequent degradation of inhibitor of κB-α (IκBα). Furthermore, PT administration appeared to enhance the process of carcinogenesis via the downregulation of the antiapoptotic proteins Bcl-2 and Bcl-extra large, mediated by inhibition of NF-κB activation. Apoptosis and caspase-3 expression were markedly increased in the PT-treated group. These findings indicate that PT inhibits IκBα phosphorylation and NF-κB activation, resulting in the initiation of apoptosis and the eventual suppression of CAC development. The beneficial effects of PT treatment observed in the experimental CAC model indicate the potential chemopreventive and therapeutic role of PT in CAC.

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Section: Discussionmentioning

confidence: 99%

Parthenolide induces apoptosis in colitis-associated colon cancer, inhibiting NF-κB signaling

et al. 2015

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“…31 However, environmental factors have also been shown to play an important role in the regulation of cancer initiation, development, and aggressiveness. 32 One such factor that is now well-recognized to play an important role in this process is the diet. 33 Dietary cholesterol has an important role in the regulation of plasma cholesterol metabolism.…”

Section: Diet Cholesterol and Cancermentioning

confidence: 99%

Role of Cholesterol in the Development and Progression of Breast Cancer

Llaverı́as

Danilo

Mercier

et al. 2011

The American Journal of Pathology

264

237

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Breast cancer is the most commonly occurring cancer in women in Western societies. 1 It is estimated that 207,090 new cases will be diagnosed and that in the United States, 39,840 women will die of the disease in 2010 (American Cancer Society, Cancer Facts & Figures 2010, http://www. cancer.org/Research/cancer-facts-and-figures-2010, last accessed November 15, 2010. Interestingly, the incidence is about 5 times higher in Western countries than in developing countries. 2 Moreover, relocation and migrational studies have demonstrated that migration from a region with low incidence to a region with high incidence increases breast cancer incidence in the immigrant population. 3 These observations suggest a strong environmental influence on breast cancer development.Diet and obesity are now considered important risk factors for cancer development. 4,5 However, despite major modifications of its metabolism during obesity development and its function in tissue pathogenesis, little is known about the metabolism and role of plasma cholesterol in cancer development. Epidemiological studies have demonstrated that patients with cancer have abnormal levels of high-density lipoprotein (HDL)-cholesterol and low-density lipoprotein (LDL)-cholesterol, 6,7 which are the major lipoprotein carriers of cholesterol in human plasma. In addition, numerous studies have established that transformed cells and tumors exhibit abnormal regulation of several genes that are under the control of cholesterol. The products of these genes include the LDL receptor (LDL-R), hydroxy-methyl-glutaryl coenzyme A reductase (HMG-CoA Reductase), and their regulators, the sterol regulatory element binding proteins. 8 -13 As a consequence, these genes are dysregulated at the transcriptional level during tumorigenesis. These data suggest that transformed cells may require or utilize more cholesterol than normal cells, and this may be associated with their increased rate of proliferation. More recent studies have implicated HDL during tumor formation in breast cancer. 14 -16 However, their precise function remains controversial. The present study was performed to test the hypothesis that dietary cholesterol and plasma cholesterol levels have an important role in the regulation of breast cancer onset and progression.

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“…It has been estimated that more than 15% of all malignancies are initiated by chronic inflammatory disease (40)(41)(42)(43)(44)(45). In Table 1, an outline is given of inflammation that has been associated with cancer development: skin inflammation with squamous cell carcinoma, viral hepatitis with liver cancer and inflammatory bowel disease with colorectal cancer.…”

Section: Nf-b Links Inflammation To Cancermentioning

confidence: 99%

NF-κB Signaling Pathway, Inflammation and Colorectal Cancer

et al. 2009

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There is growing evidence for a connection between inflammation and tumor development, and the nuclear factor kappa B (NF-B), a proinflammatory transcription factor, is hypothesized to promote tumorigenesis. Although the genetic evidence for the hypothesis has been lacking, recent papers have lent credence to this hypothesis. It has been reported that constitutive NF-B activation in inflammatory bowel diseases (

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ADVANCES IN CANCER EPIDEMIOLOGY: Understanding Causal Mechanisms and the Evidence for Implementing Interventions

Cited by 52 publications

References 94 publications

Parthenolide induces apoptosis in colitis-associated colon cancer, inhibiting NF-κB signaling

Parthenolide induces apoptosis in colitis-associated colon cancer, inhibiting NF-κB signaling

Role of Cholesterol in the Development and Progression of Breast Cancer

NF-κB Signaling Pathway, Inflammation and Colorectal Cancer

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