Incidence, mechanism and prognostic value of activated AKT in pancreas cancer
When activated, the serine/threonine kinase AKT mediates an antiapoptotic signal implicated in chemoresistance of various cancers. The mechanism(s) of AKT activation are unknown, though overexpression of HER-2/neu has been implicated in breast cancer. Therefore, we determined the incidence of activa...
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| Published in | British journal of cancer Vol. 89; no. 11; pp. 2110 - 2115 |
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| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Nature Publishing Group
01.12.2003
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| Subjects | |
| Online Access | Get full text |
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| Abstract | When activated, the serine/threonine kinase AKT mediates an antiapoptotic signal implicated in chemoresistance of various cancers. The mechanism(s) of AKT activation are unknown, though overexpression of HER-2/neu has been implicated in breast cancer. Therefore, we determined the incidence of activated AKT in human pancreatic cancer, whether HER-2/neu is involved in AKT activation, and if AKT activation is associated with biologic behaviour. HER-2/neu expression and AKT activation were examined in seven pancreatic cancer cell lines by Western blotting. The in vitro effect of HER-2/neu inhibition on AKT activation was similarly determined. Finally, 78 pancreatic cancer specimens were examined for AKT activation and HER-2/neu overexpression, and correlated with the clinical prognostic variable of histologic grade. HER-2/neu was overexpressed in two of seven cell lines; these two cell lines demonstrated the highest level of AKT activation. Inhibition of HER-2/neu reduced AKT activation in vitro. AKT was activated in 46 out of 78 (59%) of the pancreatic cancers; HER-2/neu overexpression correlated with AKT activation (P=0.015). Furthermore, AKT activation was correlated with higher histologic tumour grade (P=0.047). Thus, it is concluded that AKT is frequently activated in pancreatic cancer; this antiapoptotic signal may be mediated by HER-2/neu overexpression. AKT activation is associated with tumour grade, an important prognostic factor. |
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| AbstractList | When activated, the serine/threonine kinase AKT mediates an antiapoptotic signal implicated in chemoresistance of various cancers. The mechanism(s) of AKT activation are unknown, though overexpression of HER-2/neu has been implicated in breast cancer. Therefore, we determined the incidence of activated AKT in human pancreatic cancer, whether HER-2/neu is involved in AKT activation, and if AKT activation is associated with biologic behaviour. HER-2/neu expression and AKT activation were examined in seven pancreatic cancer cell lines by Western blotting. The in vitro effect of HER-2/neu inhibition on AKT activation was similarly determined. Finally, 78 pancreatic cancer specimens were examined for AKT activation and HER-2/neu overexpression, and correlated with the clinical prognostic variable of histologic grade. HER-2/neu was overexpressed in two of seven cell lines; these two cell lines demonstrated the highest level of AKT activation. Inhibition of HER-2/neu reduced AKT activation in vitro. AKT was activated in 46 out of 78 (59%) of the pancreatic cancers; HER-2/neu overexpression correlated with AKT activation (P=0.015). Furthermore, AKT activation was correlated with higher histologic tumour grade (P=0.047). Thus, it is concluded that AKT is frequently activated in pancreatic cancer; this antiapoptotic signal may be mediated by HER-2/neu overexpression. AKT activation is associated with tumour grade, an important prognostic factor. When activated, the serine/threonine kinase AKT mediates an antiapoptotic signal implicated in chemoresistance of various cancers. The mechanism(s) of AKT activation are unknown, though overexpression of HER-2/ neu has been implicated in breast cancer. Therefore, we determined the incidence of activated AKT in human pancreatic cancer, whether HER-2/ neu is involved in AKT activation, and if AKT activation is associated with biologic behaviour. HER-2/ neu expression and AKT activation were examined in seven pancreatic cancer cell lines by Western blotting. The in vitro effect of HER-2/ neu inhibition on AKT activation was similarly determined. Finally, 78 pancreatic cancer specimens were examined for AKT activation and HER-2/ neu overexpression, and correlated with the clinical prognostic variable of histologic grade. HER-2/ neu was overexpressed in two of seven cell lines; these two cell lines demonstrated the highest level of AKT activation. Inhibition of HER-2/ neu reduced AKT activation in vitro . AKT was activated in 46 out of 78 (59%) of the pancreatic cancers; HER-2/ neu overexpression correlated with AKT activation ( P =0.015). Furthermore, AKT activation was correlated with higher histologic tumour grade ( P =0.047). Thus, it is concluded that AKT is frequently activated in pancreatic cancer; this antiapoptotic signal may be mediated by HER-2/ neu overexpression. AKT activation is associated with tumour grade, an important prognostic factor. |
| Author | Schlieman, M G Beckett, L Bold, R J Ramsamooj, R Fahy, B N |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/14647146$$D View this record in MEDLINE/PubMed |
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| DOI | 10.1038/sj.bjc.6601396 |
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| SubjectTerms | Adenocarcinoma - enzymology Antibodies, Monoclonal - pharmacology Apoptosis Breast cancer Cancer research Chemotherapy Enzyme Activation Humans Medical prognosis Medical research Molecular and Cellular Pathology Pancreatic cancer Pancreatic Neoplasms - enzymology Pancreatic Neoplasms - pathology Prognosis Protein Serine-Threonine Kinases - metabolism Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-akt Receptor, ErbB-2 - immunology Receptor, ErbB-2 - metabolism Receptor, ErbB-2 - physiology Tumor Cells, Cultured Tumors |
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| Title | Incidence, mechanism and prognostic value of activated AKT in pancreas cancer |
| URI | http://dx.doi.org/10.1038/sj.bjc.6601396 https://www.ncbi.nlm.nih.gov/pubmed/14647146 https://www.proquest.com/docview/229973659 https://search.proquest.com/docview/17699505 https://search.proquest.com/docview/1875851663 https://pubmed.ncbi.nlm.nih.gov/PMC2376856 |
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