BMI and the risk of colorectal adenoma in African‐Americans

Ashktorab, Hassan; Paydar, Mansour; Yazdi, Shahla; Namin, Hassan Hassanzadeh; Sanderson, Andrew; Begum, Rehana; Semati, Mohammad; Etaati, Firoozeh; Lee, Edward; Brim, Hassan; Zenebe, Anteneh; Nunlee-Bland, Gail; Laiyemo, Adeyinka O.; Nouraie, Mehdi

doi:10.1002/oby.20702

Cited by 30 publications

(29 citation statements)

References 38 publications

(65 reference statements)

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“…Obesity has been strongly associated with precancerous lesions and conditions such as colon adenomas [68][69][70][71][72][73][74][75][76][77][78][79][80][81][82][83][84][85][86], monoclonal gammopathy [87][88][89][90][91][92][93][94][95][96][97][98], chronic pancreatitis [99][100][101][102], or inflammatory bowel disease (IBD) [103][104][105][106]. Observed risks of cancers associated with obesity include breast [107][108][109][110][111], colorectal [112][113][114][115], pancreatic [99]…”

Section: Morbid Obesitymentioning

confidence: 99%

Microbiome and morbid obesity increase pathogenic stimulus diversity

Brücher

Jamall

2019

4open

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The microbiome, the relationship between environmental factors, a high-fat diet, morbid obesity, and host response have been associated with cancer, only a small fraction of which (<10%) are genetically triggered. This nongenetic association is underpinned by a worldwide increase in morbid obesity, which is associated with both insulin resistance and chronic inflammation. The connection of the microbiome and morbid obesity is reinforced by an approximate shift of about 47% in the estimated total number of bacteria and an increase from 38,000,000,000,000 in a reference man to 56,000,000,000,000 in morbid obesity leading to a disruption of the microbial ecology within the gut. Humans contain 6,000,000,000 microbes and more than 90% of the cells of the human body are microorganisms. Changes in the microflora of the gut are associated with the polarization of ion channels by butyrate, thereby influencing cell growth. The decrease in the relative proportion of Bacteroidetes together with a change in the fermentation of carbohydrates by bacteria is observed in morbid obesity. The disruption of homeostasis of the microflora in the obese changes signaling and crosstalk of several pathways, resulting in inflammation while suppressing apoptosis. The interactions between the microbiome and morbid obesity are important to understand signaling and crosstalk in the context of the progression of the six-step sequence of carcinogenesis. This disruption of homeostasis increases remodeling of the extracellular matrix and fibrosis followed by the none-resolvable precancerous niche as the internal pathogenic stimuli continue. The chronic stress explains why under such circumstances there is a greater proclivity for normal cells to undergo the transition to cancer cells.

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Section: Morbid Obesitymentioning

confidence: 99%

Microbiome and morbid obesity increase pathogenic stimulus diversity

Brücher

Jamall

2019

4open

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“…Epidemiological data indicate that the risk of colon cancer is strongly associated with increasing body mass index (BMI) [110]. Similar to smoking and a history of colon polyps, a BMI value >25 also significantly increases the risk of colon cancer [111]. In addition to human data, several rodent models have been utilized to demonstrate a link between obesity and increased colon cancer.…”

Section: Link Between Obesity and Colon Cancermentioning

confidence: 99%

Mechanisms by Which Pleiotropic Amphiphilic n−3 PUFA Reduce Colon Cancer Risk

Chapkin

DeClercq

Kim

et al. 2014

Curr Colorectal Cancer Rep

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Colorectal cancer is one of the major causes of cancer-related mortality in both men and women worldwide. Genetic susceptibility and diet are primary determinants of cancer risk and tumor behavior. Experimental, epidemiological, and clinical data substantiate the beneficial role of n–3 polyunsaturated fatty acids (PUFA) in preventing chronic inflammation and colon cancer. From a mechanistic perspective, n–3 PUFA are pleiotropic and multifaceted with respect to their molecular mechanisms of action. For example, this class of dietary lipid uniquely alters membrane structure/ cytoskeletal function, impacting membrane receptor function and downstream signaling cascades, including gene expression profiles and cell phenotype. In addition, n–3 PUFA can synergize with other potential anti-tumor agents, such as fermentable fiber and curcumin. With the rising prevalence of diet-induced obesity, there is also an urgent need to elucidate the link between chronic inflammation in adipose tissue and colon cancer risk in obesity. In this review, we will summarize recent developments linking n–3 PUFA intake, membrane alterations, epigenetic modulation, and effects on obesity-associated colon cancer risk.

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“…Obesity is associated with the activation of insulin-like growth factor (IGF), oxidative stress and inflammatory pathways that increase the risk of adenoma and CRC [24, 25]. Ochs-Balcom et al [25] reported statistically significant association of IGF-1 with colorectal adenoma among African Americans.…”

Section: Introductionmentioning

confidence: 99%

Genetic Basis for Colorectal Cancer Disparities

Nayani

Ashktorab

Brim

et al. 2015

Curr Colorectal Cancer Rep

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African Americans suffer the highest burden from colorectal cancer (CRC) in the USA. Studies have suggested that healthcare access and poorer utilization of preventive services may be playing more of a role in this disparity. However, African Americans also tend to develop CRC at younger ages and are more likely to have proximal cancers. This raises the possibility of higher genetic predisposition to CRC among African Americans and this has not been well studied. In this article, we reviewed possible genetic basis underpinning biological differences in CRC burden in the USA.

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BMI and the risk of colorectal adenoma in African‐Americans

Cited by 30 publications

References 38 publications

Microbiome and morbid obesity increase pathogenic stimulus diversity

Microbiome and morbid obesity increase pathogenic stimulus diversity

Mechanisms by Which Pleiotropic Amphiphilic n−3 PUFA Reduce Colon Cancer Risk

Genetic Basis for Colorectal Cancer Disparities

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