Visit our Expo - Redox and Inflammation signaling 2012

Session XIV : Transcriptional and translational control Poster XIV, 31
Multiple isoforms of delta TA p73 transcripts accumulate in liver fluke related
cholangiocarcinoma
Patcharee Jearanaikoon1,5, Cheuypratoom P 1 Temduang Limpaiboon1,5 Banchob
Sripa2,5 Leelayuwat C,3,5,Vajarabhongsa Bhudhisawasdi4,5
1Department of Clinical Chemistry, Centre for Research and Development of Medical
Diagnostic Laboratories, Faculty of Associated Medical Sciences, 2Department of
clinical imunology , Faculty of Associated Medical Sciences , 3Pathology Department of
Pathology, 4Department of Surgery, 5Liver Fluke and Cholangiocarcinoma Research
Center, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand.
E-mail: patjea@kku.acth
Intrahepatic cholangiocarcinoma (CCA) is usually a fatal malignant neoplasm originating
from bile duct epithelium. It is the highest incidence cancer in Northeast Thailand which is
caused by liver fluke (Opisthorchis viverrrini) infection. No data describing the presence of
oncogenic delta transactivation p73 transcripts( &TAp73) which lacking N terminal in
correlation to the clinicopathological parameter has been reported in liver fluke related CCA.
We examined the p73 expression in 88 tumors using IHC staining with two monoclonal
antibodies specific to N and C terminal of TP73 in combination. Nearly to 80% (79/88cases)
reveal no p73 expression indicating down regulation during tumor development. About 15%
(13/88cases) of the IHC positive cases , demonstrate oncogenic( &TAp73) protein. To
improve the lower sensitivity for the oncogenic p73detection , Nested RT –PCR was firstly
established to investigate five TP73 (TAp73, p73 &ex2 , p73 &ex2/3, &Np73 and &N’p73)
in 23 frozen tumor specimen. The frequency of four p73 transcripts can be observed in wild
type TA p73, &Np73,p73 &ex2 and p73 &ex2/3 with 74%,74 %,26 %and 26% ,respectively.
The &Np73 oncogenic transcript is generated from the second promoter usage of p73 gene
whereas p73 &ex2 and p73 &ex2/3 created by the alternate splicing of the common promoter.
Our results demonstrate the accumulation of oncogenic isoforms simultaneously generating
from both p73 promoters in 4/23 cases . Although, no statistical significance has been shown
between the oncogenic transcript and patient survival. This might be depended on the reason
that most of patients were in advanced stage.
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