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A comprehensive analysis of phosphatase and tensin homolog deleted on chromosome
10 (PTEN) loss in colorectal cancer
#MMPMID25986931
Lin PC
; Lin JK
; Lin HH
; Lan YT
; Lin CC
; Yang SH
; Chen WS
; Liang WY
; Jiang JK
; Chang SC
World J Surg Oncol
2015[May]; 13
(?): 186
PMID25986931
show ga
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.
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