PMID- 16450333
OWN - NLM
STAT- MEDLINE
DCOM- 20060503
LR  - 20210103
IS  - 0022-3417 (Print)
IS  - 0022-3417 (Linking)
VI  - 208
IP  - 5
DP  - 2006 Apr
TI  - Tenascin C and annexin II expression in the process of pancreatic carcinogenesis.
PG  - 673-85
AB  - Tenascin C (TNC) is a component of the provisional extracellular matrix (ECM) 
      that characterizes solid tumours. Cell surface annexin II is a high-affinity 
      receptor for large TNC splice variants. The aim of this study was to analyse 
      whether TNC and annexin II play a role in the development of pancreatic ductal 
      adenocarcinoma (PDAC). PDAC is characterized by a rich ECM populated by 
      pancreatic stellate cells, which play a crucial role in pancreatic desmoplasia. 
      The mRNA and protein levels of TNC and of annexin II were analysed in pancreatic 
      tissues by DNA array, quantitative reverse transcriptase-polymerase chain 
      reaction (QRT-PCR) and immunohistochemistry. TNC large splice variants were 
      detected by RT-PCR. Enzyme linked immunosorbent assay (ELISA) was used to measure 
      TNC levels in serum and culture supernatants. TNC and annexin II mRNA levels were 
      significantly higher in pancreatic cancer tissues than in the normal pancreas. 
      TNC expression was detected with increased frequency in the progression from 
      PanIN-1 lesions to PDAC, and a parallel switch from cytoplasmic to cell surface 
      expression of annexin II was observed. Large TNC transcripts were found in 
      pancreatic cancer and in chronic pancreatitis, but not in the normal pancreas. 
      TNC expression was demonstrated in pancreatic stellate cells, where it could be 
      induced by tumour necrosis factor alpha (TNFalpha), transforming growth factor 
      beta1 (TGF-beta1) and by cancer cell supernatants supplemented with TGF-beta1. In 
      conclusion, the expression of TNC and cell surface annexin II increases in the 
      progression from low-grade PanIN lesions to pancreatic cancer. Pancreatic 
      stellate cells are identified as a source of TNC in pancreatic tissues, possibly 
      under the influence of soluble factors released by the tumour cells.
FAU - Esposito, I
AU  - Esposito I
AD  - Institute of Pathology, University of Heidelberg, Heidelberg, Germany. 
      irene_esposito@med.uni-heidelberg.de
FAU - Penzel, R
AU  - Penzel R
FAU - Chaib-Harrireche, M
AU  - Chaib-Harrireche M
FAU - Barcena, U
AU  - Barcena U
FAU - Bergmann, F
AU  - Bergmann F
FAU - Riedl, S
AU  - Riedl S
FAU - Kayed, H
AU  - Kayed H
FAU - Giese, N
AU  - Giese N
FAU - Kleeff, J
AU  - Kleeff J
FAU - Friess, H
AU  - Friess H
FAU - Schirmacher, P
AU  - Schirmacher P
LA  - eng
PT  - Journal Article
PL  - England
TA  - J Pathol
JT  - The Journal of pathology
JID - 0204634
RN  - 0 (Annexin A2)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Neoplasm)
RN  - 0 (TGFB1 protein, human)
RN  - 0 (Tenascin)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Adenocarcinoma/genetics/*metabolism
MH  - Annexin A2/genetics/*metabolism
MH  - Blotting, Western
MH  - Cell Transformation, Neoplastic/genetics/*metabolism
MH  - Gene Expression Regulation, Neoplastic/drug effects
MH  - Humans
MH  - Immunoenzyme Techniques
MH  - Neoplasm Proteins/genetics/metabolism
MH  - Pancreatic Neoplasms/genetics/*metabolism
MH  - Pancreatitis, Chronic/metabolism
MH  - RNA, Messenger/genetics
MH  - RNA, Neoplasm/genetics
MH  - Reverse Transcriptase Polymerase Chain Reaction/methods
MH  - Tenascin/genetics/*metabolism
MH  - Transforming Growth Factor beta/pharmacology
MH  - Transforming Growth Factor beta1
MH  - Tumor Cells, Cultured
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 2006/02/02 09:00
MHDA- 2006/05/04 09:00
CRDT- 2006/02/02 09:00
PHST- 2006/02/02 09:00 [pubmed]
PHST- 2006/05/04 09:00 [medline]
PHST- 2006/02/02 09:00 [entrez]
AID - 10.1002/path.1935 [doi]
PST - ppublish
SO  - J Pathol. 2006 Apr;208(5):673-85. doi: 10.1002/path.1935.