TY - JOUR
T1 - Sequencing Analysis of BRAF Mutations in Human Cancers
AU - Wooster, Richard
AU - Futreal, Andrew P.
AU - Stratton, Michael R.
PY - 2006/1/1
Y1 - 2006/1/1
N2 - Cancers arise because of the accumulation of mutations in critical genes that alter normal programs of cell proliferation, differentiation, and death. The RAS-RAF-MEK-ERK-MAP kinase pathway mediates cellular responses to growth signals. RAS is mutated to an oncogenic form in approximately 15% of human cancer. The three RAF genes code for cytoplasmic serine/threonine kinases that are regulated by binding RAS. ARAF and c-RAF are infrequently mutated in human cancer. However, BRAF is mutated in a wide range of human cancers. Most mutations are within the kinase domain, with a single amino acid substitution (V600E) accounting for most mutations.
AB - Cancers arise because of the accumulation of mutations in critical genes that alter normal programs of cell proliferation, differentiation, and death. The RAS-RAF-MEK-ERK-MAP kinase pathway mediates cellular responses to growth signals. RAS is mutated to an oncogenic form in approximately 15% of human cancer. The three RAF genes code for cytoplasmic serine/threonine kinases that are regulated by binding RAS. ARAF and c-RAF are infrequently mutated in human cancer. However, BRAF is mutated in a wide range of human cancers. Most mutations are within the kinase domain, with a single amino acid substitution (V600E) accounting for most mutations.
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U2 - 10.1016/S0076-6879(05)07018-7
DO - 10.1016/S0076-6879(05)07018-7
M3 - Review article
C2 - 16757326
SN - 0076-6879
VL - 407
SP - 218
EP - 224
JO - Methods in enzymology
JF - Methods in enzymology
ER -