4. OBJECTIVE
In the present study, Wdr13
knockout female mice developed benign
proliferative epithelium that progressed into EH at
around
one year of age accompanied by an increase in body
weight and elevated estradiol levels.
5. Interaction between antigen
and antibody
METHODS
Inmunohistochemistry
Identification of a tissue
Colored
KI-67
Cell proliferation marker
Basis Use
6. METHODS
Western blot
Proteins are identified
Reaction between
antigen and antibody
Electrophoresis
Basis
Use
Interaction of gene with
other proteins
13. DISCUSSION
Author Approach Agree or disagree
Gao, Y., Li, S. & Li, Q. “EH condition, characterized by
the presence of proliferative
epithelial glandular cells, is one
of the main risk factors for EC”2
Felix, A. S. “Anomaly in the expression of
cell cycle regulators is often
associated with hyperplastic
condition” 20
Fiorito, E., Katika, M.R. &
Hurtado, A.
“Estradiol is known to mediate
regulation of its target genes by
direct interaction with ERα”23.
14. CONCLUSIONS
1.The inhibition of the Wdr13 gene will cause endometrial hyperplasia of
the ephitelial glandular cells and to long-term endometrial cancer.
2.The obesity, hyperinsulinemia and high levels of estradiol have been
shown to have an important implication in the development of the
endometrial hyperplasia interfering with factors like receptors,fat pad
among others.
3. The expression of proteins like ERα, ERβ, PI3K, PAX2 that are involved in
human endometrial hyperplasia were also found in mutant mice indicating
similarity of the Wdr13 -/- mice with the human condition.
