TY - JOUR
T1 - A comprehensive analysis of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) loss in colorectal cancer
AU - Lin, Pei Ching
AU - Lin, Jen Kou
AU - Lin, Hung Hsin
AU - Lan, Yuan Tzu
AU - Lin, Chun Chi
AU - Yang, Shung Haur
AU - Chen, Wei Shone
AU - Liang, Wen Yi
AU - Jiang, Jeng Kai
AU - Chang, Shih Ching
N1 - Publisher Copyright:
© 2015 Lin et al.
PY - 2015/5/20
Y1 - 2015/5/20
N2 - Background: Alterations of PTEN, regulator of the PTEN/PI3K-AKT pathway, are common in several types of cancer. This study aimed to do comprehensive analysis of PTEN in colorectal cancer patients. Methods: Totally, 198 colorectal cancer patients who received surgery at Taipei Veterans General Hospital from 2006 to 2008 were enrolled. Mutations, loss of protein expression, promoter hypermethylation, and DNA copy number of PTEN were analyzed by sequencing, immunohistochemistry, methylation-specific polymerase chain reaction PCR, and quantitative (QPCR), respectively, and correlated with clinicopathological features and patients' outcome. Results: Genomic mutations, loss of protein expression, promoter hypermethylation, and decreased DNA copy number of PTEN were found in 4 (2.02 %), 68 (34.3 %), 54 (27.3 %), and 36 (18.2 %) tumors, respectively. Of these 68 tumors with loss expression of PTEN, 34 (50 %) tumors had promoter methylation and 18 (26.5 %) had decreased DNA copy number. All four tumors with PTEN mutations demonstrated loss of PTEN expression. In the stage I disease, frequency of loss of PTEN expression was 20 % and significantly increased to 56.9 % in stage IV disease. Either loss expression of PTEN, PTEN hypermethylation or decreased PTEN copy number was not associated with colorectal cancer (CRC) patients' outcome. Conclusions: PTEN alterations were found in up to one-third of colorectal cancers but did not impact CRC patients' prognosis.
AB - Background: Alterations of PTEN, regulator of the PTEN/PI3K-AKT pathway, are common in several types of cancer. This study aimed to do comprehensive analysis of PTEN in colorectal cancer patients. Methods: Totally, 198 colorectal cancer patients who received surgery at Taipei Veterans General Hospital from 2006 to 2008 were enrolled. Mutations, loss of protein expression, promoter hypermethylation, and DNA copy number of PTEN were analyzed by sequencing, immunohistochemistry, methylation-specific polymerase chain reaction PCR, and quantitative (QPCR), respectively, and correlated with clinicopathological features and patients' outcome. Results: Genomic mutations, loss of protein expression, promoter hypermethylation, and decreased DNA copy number of PTEN were found in 4 (2.02 %), 68 (34.3 %), 54 (27.3 %), and 36 (18.2 %) tumors, respectively. Of these 68 tumors with loss expression of PTEN, 34 (50 %) tumors had promoter methylation and 18 (26.5 %) had decreased DNA copy number. All four tumors with PTEN mutations demonstrated loss of PTEN expression. In the stage I disease, frequency of loss of PTEN expression was 20 % and significantly increased to 56.9 % in stage IV disease. Either loss expression of PTEN, PTEN hypermethylation or decreased PTEN copy number was not associated with colorectal cancer (CRC) patients' outcome. Conclusions: PTEN alterations were found in up to one-third of colorectal cancers but did not impact CRC patients' prognosis.
KW - Colorectal cancer
KW - Methylation
KW - Mutation
KW - Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) loss
UR - http://www.scopus.com/inward/record.url?scp=84929583828&partnerID=8YFLogxK
U2 - 10.1186/s12957-015-0601-y
DO - 10.1186/s12957-015-0601-y
M3 - Article
C2 - 25986931
AN - SCOPUS:84929583828
SN - 1477-7819
VL - 13
JO - World Journal of Surgical Oncology
JF - World Journal of Surgical Oncology
IS - 1
M1 - 186
ER -
