Asset Details
Do you wish to reserve the book?
AKT1 Loss Correlates with Episomal HPV16 in Vulval Intraepithelial Neoplasia
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
AKT1 Loss Correlates with Episomal HPV16 in Vulval Intraepithelial Neoplasia
Do you wish to request the book?
AKT1 Loss Correlates with Episomal HPV16 in Vulval Intraepithelial Neoplasia
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
AKT1 Loss Correlates with Episomal HPV16 in Vulval Intraepithelial Neoplasia
2012
Overview
Anogenital malignancy has a significant association with high-risk mucosal alpha-human papillomaviruses (alpha-PV), particularly HPV 16 and 18 whereas extragenital SCC has been linked to the presence of cutaneous beta and gamma-HPV types. Vulval skin may be colonised by both mucosal and cutaneous (beta-, mu-, nu- and gamma-) PV types, but there are few systematic studies investigating their presence and their relative contributions to vulval malignancy. Dysregulation of AKT, a serine/threonine kinase, plays a significant role in several cancers. Mucosal HPV types can increase AKT phosphorylation and activity whereas cutaneous HPV types down-regulate AKT1 expression, probably to weaken the cornified envelope to promote viral release. We assessed the presence of mucosal and cutaneous HPV in vulval malignancy and its relationship to AKT1 expression in order to establish the corresponding HPV and AKT1 profile of normal vulval skin, vulval intraepithelial neoplasia (VIN) and vulval squamous cell carcinoma (vSCC). We show that HPV16 is the principle HPV type present in VIN, there were few detectable beta types present and AKT1 loss was not associated with the presence of these cutaneous HPV. We show that HPV16 early gene expression reduced AKT1 expression in transgenic mouse epidermis. AKT1 loss in our VIN cohort correlated with presence of high copy number, episomal HPV16. Maintained AKT1 expression correlated with low copy number, an increased frequency of integration and increased HPV16E7 expression, a finding we replicated in another untyped cohort of vSCC. Since expression of E7 reflects tumour progression, these findings suggest that AKT1 loss associated with episomal HPV16 may have positive prognostic implications in vulval malignancy.
Publisher
Public Library of Science,Public Library of Science (PLoS)
Subject
/ Animals
/ Biology
/ Carcinoma, Squamous Cell - metabolism
/ Carcinoma, Squamous Cell - virology
/ DNA
/ Female
/ Genes
/ Human papillomavirus 16 - genetics
/ Human papillomavirus 16 - metabolism
/ Human papillomavirus 16 - physiology
/ Humans
/ Medicine
/ Melanoma
/ Mice
/ Mucosa
/ Papillomavirus E7 Proteins - genetics
/ Papillomavirus E7 Proteins - metabolism
/ Papillomavirus Infections - metabolism
/ Papillomavirus Infections - virology
/ Protein-serine/threonine kinase
/ Proteins
/ Proto-Oncogene Proteins c-akt - metabolism
/ Skin
/ Tumors
/ Uterine Cervical Neoplasms - metabolism
/ Uterine Cervical Neoplasms - virology
/ Virology
