Τίτλος:
Role of environmental chemicals, processed food derivatives, and nutrients in the induction of carcinogenesis
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
In recent years it has been hypothesized that cancer stem cells (CSCs) are the actual driving force of tumor formation, highlighting the need to specifically target CSCs to successfully eradicate cancer growth and recurrence. Particularly, the deregulation of physiological signaling pathways controlling stem cell proliferation, self-renewal, differentiation, and metabolism is currently considered as one of the leading determinants of cancer formation. Given their peculiar, slow-dividing phenotype and their ability to respond to multiple microenvironmental stimuli, stem cells appear to be more susceptible to genetic and epigenetic carcinogens, possibly undergoing mutations resulting in tumor formation. In particular, some animal-derived bioactive nutrients and metabolites known to affect the hormonal milieu, and also chemicals derived from food processing and cooking, have been described as possible carcinogenic factors. Here, we review most recent literature in this field, highlighting how some environmental toxicants, some specific nutrients and their secondary products can induce carcinogenesis, possibly impacting stem cells and their niches, thus causing tumor growth. © Mary Ann Liebert, Inc. 2015.
Συγγραφείς:
Persano, L.
Zagoura, D.
Louisse, J.
Pistollato, F.
Περιοδικό:
Stem Cells and Development
Εκδότης:
MARY ANN LIEBERT INC PUBL
Λέξεις-κλειδιά:
acrylamide; aldehyde dehydrogenase; benzo[a]pyrene; breast cancer resistance protein; carcinogen; catalase; checkpoint kinase 1; checkpoint kinase 2; cholesterol; curcumin; cyanocobalamin; environmental chemical; erlotinib; glutathione; homocysteine; isoflavone derivative; Janus kinase 2; leptin; multidrug resistance associated protein 1; nitrosamine; polyphenol; somatomedin C; sorafenib; STAT3 protein; superoxide dismutase; very low density lipoprotein; carcinogen, Article; brain tumor; cancer risk; cancer stem cell; carcinogenesis; cell differentiation; cell metabolism; cell proliferation; clonal evolution; cooking; double stranded DNA break; environmental factor; food processing; gene expression; genomic instability; human; hyperhomocysteinemia; nonhuman; nutrient; phenotype; pluripotent stem cell; priority journal; therapy effect; therapy resistance; treatment failure; tumor growth; tumor microenvironment; upregulation; adverse effects; animal; cancer stem cell; carcinogenesis; chemically induced; cytology; drug effects; food; metabolism; pathology; physiology; tumor recurrence, Animals; Carcinogenesis; Carcinogens, Environmental; Cell Differentiation; Food; Humans; Neoplasm Recurrence, Local; Neoplastic Stem Cells
DOI:
10.1089/scd.2015.0081
