PMID- 17990328
OWN - NLM
STAT- MEDLINE
DCOM- 20080916
LR  - 20151119
IS  - 1098-2264 (Electronic)
IS  - 1045-2257 (Linking)
VI  - 47
IP  - 2
DP  - 2008 Feb
TI  - Amplification of PRKCI, located in 3q26, is associated with lymph node metastasis 
      in esophageal squamous cell carcinoma.
PG  - 127-36
AB  - DNA amplification is one of the mechanisms to activate genes that are implicated 
      in neoplastic transformation and gain of chromosome band 3q26 is a common event 
      in squamous cell carcinomas. The aim of the present work was to identify the 
      specific target gene from four candidates (MDS1, PRKCI, ECT2, and PIK3CA) located 
      on 3q26 amplification in esophageal squamous cell carcinomas (ESCCs). To assess 
      the prevalence of copy number gains of putative genes, fluorescence in situ 
      hybridization (FISH) was applied on 108 ESCCs and 9 ESCC cell lines. Our data 
      showed that MDS1 and PRKCI were more frequently gained. Positive correlation was 
      found only for PRKCI between amplification and tumor size (P = 0.043), lymph node 
      metastasis (P = 0.015) and clinical stage (P = 0.002). PRKCI gene amplification 
      was highly correlated with protein overexpression (P = 0.009), suggesting that 
      gene amplification is one important mechanism involved in PRKCI overexpression. 
      To investigate further the role of PRKCI alteration in esophageal tumors, a 
      tissue microarray containing samples from 180 ESCCs was used for 
      immunohistochemistry analysis. Statistical analysis revealed that PRKCI 
      overexpression was correlated with lymph node metastasis (P = 0.002) and higher 
      stage (P = 0.004). Performing multivariate logistic regression analysis, a 
      significant association between PRKCI overexpression and presence of lymph node 
      metastasis was found, which was independent of T-stage of the primary tumors (P = 
      0.004). Our results indicate that PRKCI is an attractive target in the 3q26 
      amplicon and that it may serve as a molecular marker for metastasis and occult 
      advanced tumor stages in ESCC.
CI  - (c) 2007 Wiley-Liss, Inc.
FAU - Yang, Yi-Ling
AU  - Yang YL
AD  - State Key Laboratory of Molecular Oncology, Cancer Institute (Hospital), Peking 
      Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
FAU - Chu, Jia-You
AU  - Chu JY
FAU - Luo, Man-Li
AU  - Luo ML
FAU - Wu, Yu-Peng
AU  - Wu YP
FAU - Zhang, Yu
AU  - Zhang Y
FAU - Feng, Yan-Bin
AU  - Feng YB
FAU - Shi, Zhi-Zhou
AU  - Shi ZZ
FAU - Xu, Xin
AU  - Xu X
FAU - Han, Ya-Ling
AU  - Han YL
FAU - Cai, Yan
AU  - Cai Y
FAU - Dong, Jin-Tang
AU  - Dong JT
FAU - Zhan, Qi-Min
AU  - Zhan QM
FAU - Wu, Min
AU  - Wu M
FAU - Wang, Ming-Rong
AU  - Wang MR
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Genes Chromosomes Cancer
JT  - Genes, chromosomes & cancer
JID - 9007329
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Isoenzymes)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - EC 2.7.11.13 (protein kinase C lambda)
SB  - IM
MH  - Biomarkers, Tumor/biosynthesis/*genetics/metabolism
MH  - Carcinoma, Squamous Cell/*enzymology/genetics/pathology
MH  - Cell Line, Tumor
MH  - Chromosomes, Human, Pair 3/*genetics
MH  - Disease Progression
MH  - Esophageal Neoplasms/*enzymology/genetics/pathology
MH  - Female
MH  - *Gene Amplification
MH  - Gene Dosage
MH  - Humans
MH  - Isoenzymes/biosynthesis/*genetics/metabolism
MH  - Lymphatic Metastasis
MH  - Male
MH  - Middle Aged
MH  - Protein Kinase C/biosynthesis/*genetics/metabolism
EDAT- 2007/11/09 09:00
MHDA- 2008/09/17 09:00
CRDT- 2007/11/09 09:00
PHST- 2007/11/09 09:00 [pubmed]
PHST- 2008/09/17 09:00 [medline]
PHST- 2007/11/09 09:00 [entrez]
AID - 10.1002/gcc.20514 [doi]
PST - ppublish
SO  - Genes Chromosomes Cancer. 2008 Feb;47(2):127-36. doi: 10.1002/gcc.20514.