@article{TCR17512,
author = {Motoyuki Otsuka and Rei Ishibashi and Eri Tanaka and Takahiro Seimiya and Tatsunori Suzuki and Kazuma Sekiba and Mari Yamagami and Motoko Ohno and Takahiro Kishikawa and Kazuhiko Koike},
title = {A tiny but crucial player bridging microbes and colonic carcinogenesis},
journal = {Translational Cancer Research},
volume = {6},
number = {Suppl 9},
year = {2017},
keywords = {},
abstract = {Colorectal cancer (CRC) is one of the most common malignancies in the world (1). The probability of suffering from CRC is approximately 4–5%, and the risk of developing CRC is associated with characteristics such as age, chronic disease history, and lifestyle (2). CRC is caused by mutations in oncogenes, tumor-suppressor genes, and genes related to DNA repair mechanisms. The underlying pathogenic mechanisms are threefold; namely, chromosomal instability (CIN), microsatellite instability (MSI), and CpG island methylator phenotype (CIMP). In CRC, common mutations, chromosomal changes, and translocations reportedly affect important intracellular signaling pathways [WNT, mitogen activated protein kinase (MAPK)/phosphoinositide 3-kinase (PI3K), transforming growth factor (TGF)-β, and TP53] (2). In addition to genetic mutations, alterations in non-coding RNAs, such as microRNAs, also contribute to carcinogenesis.},
issn = {2219-6803}, url = {https://tcr.amegroups.org/article/view/17512}
}