Update on Prognostic Markers for Endometrial Cancer

Pratibha S Binder; David G Mutch

Women's Health. 2014;10(3):277-288.

Abstract and Introduction

Abstract

Endometrial cancer is the most common gynecologic cancer in the USA and the second most common worldwide after cervical cancer. While common symptomatology of endometrial cancer leads to early diagnosis and favorable 5-year survival in most cases, there is a subset of cancers that have a poorer prognosis. The clinical and pathologic prognostic factors for endometrial cancer are well known and instrumental in determining the need for adjuvant therapy. Recently, research has been focused on the identification of molecular changes leading to different histologic subtypes to improve classification of endometrial cancer. The identification of novel mutations and molecular profiles should enhance our ability to personalize adjuvant treatment with genome-guided targeted therapy.

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Abstract and Introduction
Background
Clinical Prognostic Factors
Pathologic Prognostic Factors
Molecular Markers Associated With Prognosis & Targeted Therapies
Conclusion
Future Perspective
References
Sidebar

Table 1. Clinical–pathologic characteristics of type I and type II endometrial cancer.
Clinical–pathologic characteristics	Type I	Type II
Histology	Endometrioid	Nonendometrioid (serous, clear cell, undifferentiated)
Grade	1, 2	2, 3
Stage	I, II	III, IV
Hormone receptor	ER+/PR+	ER-/PR-
Mutations	PTEN	p53
Etiology	Unopposed estrogen	Sporadic
Survival	Favorable	Poor

Table 2. Five-year survival based on histology for each stage.
Histology	Stage I (%)	Stage II (%)	Stage III (%)	Stage IV (%)
Endometrioid	90.1	79.5	67.7	25.8
Serous	79.7	40.7	37.7	–
Clear cell	85.1	63.4	48.5	–

Data taken from [31].

Table 3. Five-year survival based on histologic grade for each stage.
Grade	Stage I (%)	Stage II (%)	Stage III (%)	Stage IV (%)
1	92.9	86.0	78.6	49.2
2	89.9	80.0	67.3	26.5
3	78.9	66.0	46.4	13.4

Data taken from [31].

Box 1. Prognostic factors for endometrial cancer.
Clinical Age Race Pathologic Histologic subtype FIGO stage Histologic grade Lymphovascular space invasion Molecular markers; mechanism Hormone receptor; cellular expression PTEN; loss-of-function mutation P13K/AKT/mTOR; pathway aberrations TP53; loss-of-function mutation HER2/neu; activating mutation MSI; MMR gene defects Angiogenesis markers; mediates VEGF MEK/ERK; activating mutation K/Ras; activating mutation Other DNA ploidy Metformin use
FIGO: International Federation of Gynecology and Obstetrics; MSI: Microsatellite instability.