PMID- 22409860
OWN - NLM
STAT- MEDLINE
DCOM- 20120607
LR  - 20220321
IS  - 1471-2407 (Electronic)
IS  - 1471-2407 (Linking)
VI  - 12
DP  - 2012 Mar 13
TI  - Amphiregulin and Epiregulin mRNA expression in primary colorectal cancer and 
      corresponding liver metastases.
PG  - 88
LID - 10.1186/1471-2407-12-88 [doi]
AB  - BACKGROUND: Amphiregulin (AREG) and Epiregulin (EREG), ligands of EGFR, are 
      reported to be predictive biomarkers of colorectal cancer patients treated with 
      Cetuximab, an anti-EGFR antibody. The purpose of this study is to determine the 
      correlation of AREG and EREG expression between primary colorectal cancer and 
      corresponding liver metastases. METHODS: One hundred twenty colorectal cancer 
      patients with liver metastases (100 with synchronous metastases, 20 with 
      metachronous) were evaluated. No patients had ever received anti-EGFR antibody 
      agents. AREG and EREG mRNA expression from both the primary tumor and liver 
      metastases were measured using real-time RT-PCR. KRAS codon 12, 13 mutation 
      status was analyzed by direct sequencing. RESULTS: Modest, but significant, 
      correlations were observed between primary tumor and corresponding liver 
      metastases in both AREG mRNA expression (Rs = 0.54, p < 0.0001) and EREG mRNA 
      expression (Rs = 0.58, p < 0.0001). AREG and EREG mRNA expression was strongly 
      correlated in both the primary tumor (Rs = 0.81, p < 0.0001) and the liver 
      metastases (Rs = 0.87, p < 0.0001). No significant survival difference was 
      observed between low and high AREG or EREG patients when all 120 patients were 
      analyzed. However, when divided by KRAS status, KRAS wild-type patients with low 
      EREG mRNA levels in the primary site showed significantly better overall survival 
      rates than those with high levels (p = 0.018). In multivariate analysis, low EREG 
      expression was significantly associated with better overall survival (p = 0.006). 
      CONCLUSIONS: AREG and EREG expression showed a modest correlation between primary 
      tumor and liver metastases. As EREG mRNA expression was associated with decreased 
      survival, it is appeared to be a useful prognostic marker in KRAS wild-type 
      patients who never received anti-EGFR therapy.
FAU - Kuramochi, Hidekazu
AU  - Kuramochi H
AD  - Department of Chemotherapy and Palliative Care, Tokyo Women's Medical University, 
      8-1 Kawadacho, Shinjukuku, Tokyo, Japan. Kuramochi@chemo.twmu.ac.jp
FAU - Nakajima, Go
AU  - Nakajima G
FAU - Kaneko, Yuka
AU  - Kaneko Y
FAU - Nakamura, Ayako
AU  - Nakamura A
FAU - Inoue, Yuji
AU  - Inoue Y
FAU - Yamamoto, Masakazu
AU  - Yamamoto M
FAU - Hayashi, Kazuhiko
AU  - Hayashi K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120313
PL  - England
TA  - BMC Cancer
JT  - BMC cancer
JID - 100967800
RN  - 0 (AREG protein, human)
RN  - 0 (Amphiregulin)
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (EGF Family of Proteins)
RN  - 0 (EREG protein, human)
RN  - 0 (Epiregulin)
RN  - 0 (Glycoproteins)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (KRAS protein, human)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (RNA, Messenger)
RN  - 62229-50-9 (Epidermal Growth Factor)
RN  - EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras))
RN  - EC 3.6.5.2 (ras Proteins)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Amphiregulin
MH  - Biomarkers, Tumor/*genetics
MH  - Colorectal Neoplasms/*genetics
MH  - DNA Mutational Analysis
MH  - EGF Family of Proteins
MH  - Epidermal Growth Factor/*genetics
MH  - Epiregulin
MH  - Female
MH  - Glycoproteins/*genetics
MH  - Humans
MH  - Intercellular Signaling Peptides and Proteins/*genetics
MH  - Liver Neoplasms/*genetics/*secondary
MH  - Male
MH  - Middle Aged
MH  - Proto-Oncogene Proteins/genetics
MH  - Proto-Oncogene Proteins p21(ras)
MH  - RNA, Messenger/genetics
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Survival Analysis
MH  - ras Proteins/genetics
PMC - PMC3317853
EDAT- 2012/03/14 06:00
MHDA- 2012/06/08 06:00
PMCR- 2012/03/13
CRDT- 2012/03/14 06:00
PHST- 2011/10/11 00:00 [received]
PHST- 2012/03/13 00:00 [accepted]
PHST- 2012/03/14 06:00 [entrez]
PHST- 2012/03/14 06:00 [pubmed]
PHST- 2012/06/08 06:00 [medline]
PHST- 2012/03/13 00:00 [pmc-release]
AID - 1471-2407-12-88 [pii]
AID - 10.1186/1471-2407-12-88 [doi]
PST - epublish
SO  - BMC Cancer. 2012 Mar 13;12:88. doi: 10.1186/1471-2407-12-88.