UNIVERSI
TÄ
TS-
BIBLIOTHEK
P
ADERBORN
Anmelden
Menü
Menü
Start
Hilfe
Blog
Weitere Dienste
Neuerwerbungslisten
Fachsystematik Bücher
Erwerbungsvorschlag
Bestellung aus dem Magazin
Fernleihe
Einstellungen
Sprache
Deutsch
Deutsch
Englisch
Farbschema
Hell
Dunkel
Automatisch
Sie befinden Sich nicht im Netzwerk der Universität Paderborn. Der Zugriff auf elektronische Ressourcen ist
gegebenenfalls
nur via VPN oder Shibboleth (DFN-AAI) möglich.
mehr Informationen...
Universitätsbibliothek
Katalog
Suche
Details
Zur Ergebnisliste
Ergebnis 7 von 426
Datensatz exportieren als...
BibTeX
Amplification and overexpression of the AKT2 oncogene in a subset of human pancreatic ductal adenocarcinomas
Molecular carcinogenesis, 1998-02, Vol.21 (2), p.81-86
Ruggeri, Bruce A.
Huang, Lingyi
Wood, Moira
Cheng, Jin Quan
Testa, Joseph R.
1998
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Ruggeri, Bruce A.
Huang, Lingyi
Wood, Moira
Cheng, Jin Quan
Testa, Joseph R.
Titel
Amplification and overexpression of the AKT2 oncogene in a subset of human pancreatic ductal adenocarcinomas
Ist Teil von
Molecular carcinogenesis, 1998-02, Vol.21 (2), p.81-86
Ort / Verlag
New York: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
1998
Quelle
Wiley Blackwell Single Titles
Beschreibungen/Notizen
AKT2, an oncogene encoding a protein serine‐threonine kinase implicated in phosphatidylinositol‐3‐OH kinase signaling, is amplified in some human ovarian and pancreatic carcinomas. We previously demonstrated that the tumorigenicity and invasiveness of pancreatic ductal adenocarcinoma (PDAC) cell lines with amplified AKT2 could be markedly reduced by transfection with antisense AKT2 constructs. To evaluate further the extent of AKT2 alterations in PDAC, DNA and immunohistochemical analyses were performed to assess amplification or overexpression of AKT2, respectively, in 72 PDACs. Thirty‐five PDACs were subjected to Southern analyses, and AKT2 amplification was detected in seven tumors (20%). Forty‐one formalin‐fixed PDAC specimens were examined immunohistochemically with an anti‐AKT2 monoclonal antibody, and moderate to intense staining was observed in eight tumors (20%). AKT2 immunostaining paralleled AKT2 genomic status in each of four cases in which both Southern and immunohistochemical analyses were performed. No obvious relationship was observed between AKT2 status and tumor TNM stage or grade. These observations suggest the utility of immunohistochemical analysis in assessing alterations of AKT2 in human cancers. Furthermore, the role played by the AKT2 kinase in the signaling pathways of various mitogenic growth factors implicated in the development of pancreatic cancer suggests that alteration of AKT2 may be an important component in the pathogenesis of a substantial subset of PDACs. Mol. Carcinog. 21:81–86, 1998. © 1998 Wiley‐Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 0899-1987
eISSN: 1098-2744
DOI: 10.1002/(SICI)1098-2744(199802)21:2<81::AID-MC1>3.0.CO;2-R
Titel-ID: cdi_proquest_miscellaneous_79720316
Format
–
Schlagworte
AKT2 oncogene
,
Carcinoma, Ductal, Breast - genetics
,
DNA, Neoplasm - genetics
,
Gene Amplification
,
Gene Expression Regulation, Neoplastic
,
Humans
,
immunohistochemistry
,
Oncogene Proteins - genetics
,
Oncogenes
,
Pancreas - metabolism
,
pancreatic cancer
,
Pancreatic Neoplasms - genetics
,
Protein-Serine-Threonine Kinases - genetics
,
Proto-Oncogene Proteins
,
Proto-Oncogene Proteins c-akt
,
Tumor Cells, Cultured
Weiterführende Literatur
Empfehlungen zum selben Thema automatisch vorgeschlagen von
bX