AKT1 E17 K pleckstrin homology domain mutation in urothelial carcinoma

Abstract The PI3 K/AKT pathway is frequently activated in human cancer. Recently, a G to A point mutation (E17 K) was found in the pleckstrin homology domain of AKT1. We aimed to explore this mutation in cases of urothelial carcinoma. Using chip-based matrix-assisted laser desorption-time-of-flight...

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Bibliographic Details
Published in:Cancer genetics and cytogenetics 2009-05, Vol.191 (1), p.34-37
Main Authors: Zilberman, Dorit E, Cohen, Yoram, Amariglio, Ninette, Fridman, Edward, Ramon, Jacob, Rechavi, Gideon
Format: Article
Language:English
Subjects:
Aged
Aged, 80 and over
Amino Acid Substitution
Carcinoma, Transitional Cell - enzymology
Carcinoma, Transitional Cell - genetics
Carcinoma, Transitional Cell - pathology
Demography
Female
Hematology, Oncology and Palliative Medicine
Humans
Male
Medical Education
Middle Aged
Mutation - genetics
Protein Structure, Tertiary
Proto-Oncogene Proteins c-akt - chemistry
Proto-Oncogene Proteins c-akt - genetics
Urothelium - enzymology
Urothelium - pathology
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Summary:Abstract The PI3 K/AKT pathway is frequently activated in human cancer. Recently, a G to A point mutation (E17 K) was found in the pleckstrin homology domain of AKT1. We aimed to explore this mutation in cases of urothelial carcinoma. Using chip-based matrix-assisted laser desorption-time-of-flight (MALDI-TOF) mass spectrometer, AKT1 E17 K mutation was searched in 26 total RNA samples obtained from 26 patients known to have urothelial carcinoma. Mutation was found in one out of 26 (3.8%) patients – a 46 year old female with a low grade transitional cell carcinoma located to the lamina propria (Ta disease). Our finding is in line with previous studies showing AKT1 E17 K mutation to be rare. Yet, further studies are required to determine whether this mutation is indeed related to less aggressive disease and carries better prognosis.
ISSN:0165-4608
1873-4456
DOI:10.1016/j.cancergencyto.2009.01.009