Publication: Molecular pathology of endometrial carcinoma, Transcriptional signature in endometrioid tumors
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Date
2006
Authors
Abal, M. ; Planaguma, J. ; Gil-Moreno, A. ; Monge, M. ; Gonzalez, M. ; Baró, Teresa ; Garcia, A. ; Castellvi, J. ; Ramón y Cajal, S. ; Xercavins, J. ; Alameda, F. ; Reventos, J.
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Publisher
Murcia : F. Hernández
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Description
Abstract
A dualistic model, which has been
established on a morphological basis and that
differentiates type I endometrioid from type II nonendometrioid
endometrial cancer, is widely accepted.
Molecular genetics have provided us with data
supporting the dualistic model of endometrial
tumorigenesis and with some clues to speculate about
the sequence of the molecular alterations defining the
tumorigenesis pathways. In type I endometrioid
endometrial cancer, PTEN gene silencing, microsatellite
instability associated with defects in DNA mismatch
repair genes, or mutations in the K-ras gene are the
known major alterations defining the progression from
normal endometrium to hyperplasia and then on to
carcinoma. Recently, cDNA microarray technology for
identifying the differences in gene expression patterns
between the histological types of endometrial cancer
have permitted the identification of differentially
expressed genes that could help us to understand
differences in the biology and the clinical outcome
between histiotypes. Genes involved in the mitotic
checkpoint as a major mechanism of carcinogenesis in
non-endometrioid endometrial cancer, or altered genes
associated with the initial steps of myometrial
infiltration in endometrioid endometrial cancer,
represent examples of how useful large genetic
screenings can be for understanding the tumorigenesis
process and the future directions in the molecular
pathogenesis of endometrial cancer.
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