Progress in serrated adenoma.docVIP

 PAGE \* MERGEFORMAT 17 Progress in serrated adenoma Keywords: Colorectal cancer; serrated adenoma; adenocarcinoma 1BRAF and KRAS mutation is generally believed that the majority of sporadic colorectal cancer from the APC tumor suppressor genes such as deletion, mutation, and acquired chromosomal instability. The serrated pathway is different, the gene mutation is generally not involving the APC gene, and the KRAS mutation rate low, but relatively high frequency of p53, BRAF mutations in other genes [6  8], as well as the TGFβR Ⅱ, BAX, and IGF Ⅱ R and so on gene mutations. Recent studies have reported more concentrated in the proto-oncogene mutations in the BRAF and KRAS. We know, RAS proteins involved in growth factor activation of RAS  RAF  MEK  ERK  MAP kinase pathway-mediated cell growth response to signals, regulating cell differentiation, proliferation, and apoptosis escape. RAS gene mutations in somatic cells, resulting in the signal pathway activation and malignant transformation in human cancers are common. The BRAF gene belongs to RAF gene family, located in chromosome 7q34, (known to have three family members, namely, Raf  1, BRAF, and ARAF). Encoding a 67 ~ 99KD cytoplasmic serine / threonine kinase, the kinase in the mitogen-activated protein kinase / extracellular signal kinase (MAPK / ERK) pathway at the entrance, it will cell surface receptors and RAS proteins by MEK and ERK and nuclear transcription factor within the connected, thereby regulating cell growth, development. BRAF mutations can activate these signaling pathways in tumor occurrence and development play an important role. BRAF mutation is found in malignant melanoma, colorectal, ovarian borderline (low malignant potential) tumors, also seen in benign melanocytic nevi and lung cancer. In SA, the multi-information display cases showed BRAF and KRAS mutations are mutually exclusive phenomena [8, 9]. Tsun LC et al [9] studies have shown that, SA occurred BRAF mut