UTERINE OR ENDOMETRIAL CANCER

WITH INCREASE OF OBESITY RATE, THIS CANCER IS ONE OF THOSE ON THE RISE
AFFECTING 46000 WOMEN A YEAR
WITH 8000 DYING EVERY YEAR

4 TYPES

1-ENDOMETRIOID (80%)

2.1-SEROUS
2.2-CLEAR CELL
2.3-MUCINOUS
2.4-MIXED

The Endometrioid type is preceded by Hyperplasia and is genErally localized and of good prognosis.
The serous type is preceded by atrophy and is of worse prognosis. 

 Of those with uterine inner third involvement,
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55% of Serous will have spread of disease
17% with Endometrioid will have spread of disease
Median survival is 12 months in metastatic disease

11 genetic alterations described:
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1,loss of function of PTEN: An early event see in 83 % of Endometriod cancer.
opening the door to MTOR inhibitor use
metformin seems to potentiate effect of Taxol through modulation of MTOR.

INHIBITION OF PTEN MAY PREDICT SENSITIVITY TO PARP INHIBITORS, SO OLAPARIB HAS BEEN TRIED.  PARP INHIBITOR TRIED IN THOSE POSITIVE FOR BRCA 1,2

2.PIK3CA Mutation

3.AKT mutation
4.Microsattelite instability
5.KRas Mutation : 26% of endometrioid cancer  (MEK Inhibition by Selumetinib trial)
6.Overexpression of EGFR (Avastin and Decoy Aflibercept with minimum response from Sutent, NEXAVAR, AND THALIDOMID)   Tarceva, Iressa,Erbitux

In non-endometrioid cancer, existence of ERBB2 poto-ocnocgen has led to trial of Trastuzumab, Lapatinib with minimal response
7.P53 mutation
8.Nuclear B Catenin
9.Her-2/Neu amplification
10.FGFR PRESENCE HAS LED TO TRIAL WITH DOVITINIB
11.P16 inactivation