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PIK3CA, HRAS and KRAS gene mutations in human penile cancer
Division of Cell Biology, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Department of Pathology, Örebro University Hospital, Örebro, Sweden.
Department of Urology, Örebro University Hospital, Örebro, Sweden.
Department of Urology, Örebro University Hospital, Örebro, Sweden.
Vise andre og tillknytning
2008 (engelsk)Inngår i: Journal of Urology, ISSN 0022-5347, E-ISSN 1527-3792, Vol. 179, nr 5, s. 2030-2034Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Purpose: The knowledge of somatic mutations that arise in penile cancer is limited. We examined the dysregulation of components in the phosphatidylinositol 3-kinase and Ras pathways.

Materials and Methods: Using single stranded conformational analysis and direct sequencing we performed mutational analysis of the PIK3CA, PTEN, HRAS, KRAS, NRAS and BRAF genes in 28 penile tumors.

Results: We identified somatic missense mutations in 11 of the 28 penile cancer samples (39%). In the PIK3CA gene 8 mutations (29%) were identified that were E542K or E545K. In the HRAS gene a G12S and a Q61L mutation were found (7%). The KRAS gene contained 1 mutation (3%), that is a G12S change. PIK3CA mutations were found in all grades and stages, whereas HRAS and KRAS mutations were found in larger and more advanced tumors. The mutations were mutually exclusive, suggesting that dysregulation of either pathway is sufficient for the development and progression of penile carcinoma.

Conclusions: The high frequency of mutations in the PIK3CA, HRAS and KRAS genes leads us to believe that dysregulation of the phosphatidylinositol 3-kinase or Ras pathway is significant for the development and progression of penile carcinoma.

sted, utgiver, år, opplag, sider
New York, USA: Elsevier, 2008. Vol. 179, nr 5, s. 2030-2034
Emneord [en]
Penis, penile neoplasms, mutation, 1-phosphatidylinositol 3-kinase, carcinoma, squamous cell
HSV kategori
Identifikatorer
URN: urn:nbn:se:oru:diva-49500DOI: 10.1016/j.juro.2007.12.040ISI: 000255005300100PubMedID: 18355852Scopus ID: 2-s2.0-41749108849OAI: oai:DiVA.org:oru-49500DiVA, id: diva2:914917
Tilgjengelig fra: 2016-03-27 Laget: 2016-03-25 Sist oppdatert: 2017-11-30bibliografisk kontrollert

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