Pathobiology of cancer and clinical biochemistry

Barreto, Stephany; Armstrong, Este; Doğan, Soner; Ray, Arunima

doi:10.1055/s-0036-1586447

Cited by 3 publications

(1 citation statement)

References 108 publications

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“…It has been estimated that among all cancers, approximately 5-10% are caused by genetic factors (i.e., inherited/hereditary cancers), brain cancers are accounting for 1-2%, and about 2% are pediatric cancers wherein genetic aberrations perhaps play a key role [1][2][3] . Unlike hereditary and pediatric cancers, primary brain cancers are probably associated with both genetic and environmental factors such as exposure to aromatic hydrocarbons, ionizing radiation, and pesticides [2,4] .…”

Section: Introductionmentioning

confidence: 99%

Cancer chemoprevention and healthy lifestyle

Gennaro¹,

Burke²,

Fecek³

et al. 2023

Int. J. Herb. Med.

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A growing body of evidence suggests that chronic low-grade inflammation and oxidative stress may lead to cancer development. These discoveries complement the usual focus of cancer prevention that primarily concentrates on carcinomas, i.e., ectodermal or endodermal (embryonic) tissue-derived cancers, which are more exposed to lifestyle/environment-related risk factors. Based on these findings, cancer preventive strategies can be formulated by using a number of dietary phytochemicals that display inhibitory effects on oxidative stress, inflammation, and other tumor-linked phenomena such as angiogenesis, cell proliferation, and DNA damage. Overall, a positive lifestyle and healthy food habits can reduce cancer risk.

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Section: Introductionmentioning

confidence: 99%

Cancer chemoprevention and healthy lifestyle

Gennaro¹,

Burke²,

Fecek³

et al. 2023

Int. J. Herb. Med.

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Extracellular matrix in obesity – cancer interactions

Barreto¹,

Hopkins²,

Bhowmick³

et al. 2015

Hormone Molecular Biology and Clinical Investigation

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Obesity or overweight is a risk factor for several health disorders such as type 2 diabetes, hypertension, and certain cancers. Furthermore, obesity affects almost all body systems including the extracellular matrix (ECM) by generating a pro-inflammatory environment, which are associated with abnormal secretions of several cytokines or hormonal substances, for example, insulin-like growth factors (IGFs), leptin, and sex hormones. These chemical mediators most likely have a great impact on the ECM. Accumulating evidence suggests that both obesity and ECM can influence tumor growth and progression through a number of chemical mediators. Conversely, cells in the connective tissue, namely fibroblasts and macrophages, support and aggravate the inflammatory situation in obesity by releasing several cytokines or growth factors such as vascular endothelial growth factor, epidermal growth factor, and transforming growth factor-beta (TGF-β). A wide range of functions are performed by TGF-β in normal health and pathological conditions including tumorigenesis. Breast cancer in postmenopausal women is a classic example of obesity-related cancer wherein several of these conditions, for example, higher levels of pro-inflammatory cytokines, impairment in the regulation of estrogen and growth factors, and dysregulation of different ECM components may favor the neoplastic process. Aberrant expressions of ECM components such as matrix metalloproteinases or matricellular proteins in both obesity and cancer have been reported by many studies. Nonstructural matricellular proteins, viz., thrombospondins, secreted protein acidic and rich in cysteine (SPARC), and Cyr61-CTGF-Nov (CCN), which function as modulators of cell-ECM interactions, exhibit protean behavior in cancer. Precise understanding of ECM biology can provide potential therapeutic targets to combat obesity-related pathologies.

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Tumor-linked HER2 expression: association with obesity and lipid-related microenvironment

Ray

2017

Hormone Molecular Biology and Clinical Investigation

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Abstract:Obesity is associated with the risk of several health disorders including certain cancers. Among obesity-related cancers, postmenopausal breast carcinoma is a well-studied one. Apart from an increase in certain types of lipids in obesity, excess adipose tissue releases many hormone-like cytokines/adipokines, which are usually pro-inflammatory in nature. Leptin is one of such adipokines and significantly linked with the intracellular signaling pathways of other growth factors such as insulin-like growth factor-1 (IGF-1), vascular endothelial growth factor (VEGF), human epidermal growth factor receptor 2 (HER2). In general, HER2 is overexpressed in roughly 30% of breast carcinomas; its presence indicates aggressive tumor behavior. Conversely, HER2 has certain effects in normal conditions such as differentiation of preadipocytes, cardiovascular health and vitamin D metabolism. HER2 has no known endogenous ligand, but it may form dimers with other three members of the epidermal growth factor receptor (EGFR) family and can activate downstream signaling pathways. Furthermore, HER2 is intimately connected with several enzymes, e.g. fatty acid synthase (FASN), phosphatidylinositol 3-kinase (PI3K), AKT and mechanistic target of rapamycin (mTOR), all of which play significant regulatory roles in lipogenic pathways or lipid metabolism. In obesity-related carcinogenesis, characteristics like insulin resistance and elevated IGF-1 are commonly observed. Both IGF-1 and leptin can modulate EGFR and HER2 signaling pathways. Although clinical studies have shown mixed results, the behavior of HER2+ tumor cells including HER2 levels can be altered by several factors such as obesity, leptin and fatty acids. A precise knowledge is useful in new therapeutic approaches against HER+ tumors.

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Pathobiology of cancer and clinical biochemistry

Cited by 3 publications

References 108 publications

Cancer chemoprevention and healthy lifestyle

Cancer chemoprevention and healthy lifestyle

Extracellular matrix in obesity – cancer interactions

Tumor-linked HER2 expression: association with obesity and lipid-related microenvironment

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