This document summarizes information about endometrial cancer, including that it is the most common malignancy of the female genital tract, with most cases occurring in post-menopausal women aged 60-70 years. Risk factors include nulliparity, late menopause, obesity, diabetes, and use of unopposed estrogen therapy. Endometrial hyperplasia, especially when atypical, increases the risk. Prognosis depends on factors like histologic type, grade, depth of myometrial invasion, and whether the cancer has spread. Treatment may involve surgery, with radiation and chemotherapy also used in more advanced cases.

1. Moderator : Dr. V.V. Padhmalatha

2.  Most common malignancy of female
genital tract.
 4th most common cancer.
 Overall incidence – 2%- 3%
 80% - age of 60-70 years ; <5% under
40 years.

3. Exaggerated physiological state
Carcinoma in situ
 Due to protracted estrogen
stimulation in the absence of
progestin.

4.  Non Atypical hyperplasia ( without atypia)
Simple hyperplasia - 1%
Complex hyperplasia – 3%
(adenomatous hyperplasia)
 Atypical hyperplasia
Simple atypical hyperplasia – 8%
Complex atypical – 29%
(atypical adenomatous hyperplasia)

5. SIMPLE
HYPERPLASIA
(WITHOUT ATYPIA)
ATYPICAL
HYPERPLASIA

6.  Sporadic:
 Type 1 ( 75-85%)
estrogen dependant
 Type 2 ( 5%)
non- estrogen dependant
more in African – American , Asian women
 Hereditory:
HNPCC or Lynch II Syndrome
Autosomal Dominant
32- 60% risk

7. TYPE I TYPE II
MENOPAUSAL
STATUS
PERI-MENOPAUSAL
POST
MENOPAUSAL
ESTROGEN
RELATED
YES NO
ESTROGEN OR
PROGESTRONE
RECEPTOR
POSITIVE NEGATIVE
HISTOLOGY PROLIFERATIVE ATROPHIC

8. TYPE I TYPE II
BUILT OBESE THIN
GRADE LOW HIGH
HISTOLOGY
SUBTYPE
ENDOMTERIOD SEROUS/ CLEAR
CELL
CLINICAL
BEHAVIOUR
INDOLENT AGGRESSIVE

9. RISK FACTORS REALATIVE RISK
NULLIPARITY 2-3
LATE MENOPAUSE 2.4
OBESITY 3-10
DIABETES MELLITUS 2.8
UNOPPOSED ESTROGEN
THERAPY
4-8
TAMOXIFEN THERAPY 2-3
ATYPICAL
ENDOMETRIAL
HYPERPLASIA
8-29
LYNCH-II SYNDROME 20

10.  Tamoxifen:
- competitive inhibitor of estrogen binding to
ER.
- ACOG recommends:
• Benefits outweigh the risk
• Annual gynecologic examination
• Report any abnormal vaginal symptoms and
investigated
• Hysterectomy if atypical endometrial hyperplasia
• Classify as high and low risk grps prior to starting
therapy
• Tamoxifen not found to be benifical beyond 5
years

11.  Unopposed Estrogen:
• Endogenous
 functional ovarian tumor
 Obesity – androstenedione estrone
- SHBG
• Exogenous - HRT

12.  Protective Factors:
 OCPs
 Physical activity
 Smoking – stimulation of hepatic
metabolism of estrogens

13.  No role of routine screening.
 Routine Papanicolaou testing
- 30-50% have abnormal test
 Screening of high risk individuals
1. Lynch II syndrome – annual pevic
examination, TVS, EB beginning from
30-35 years of age.
2. risk with positive history in first degree
relative ( CASH study) – 3 fold

14.  Post menopausal bleeding with
exogenous estrogen
 Premenopausal with anovulatory cycles.

15.  75% pt older than 50 years.
 90% - vaginal bleeding or discharge.
 10% of PMB will have endometrial ca.
 Pelvic pressure or discomfort
 Presence of hematomtera or pyometra,
causing purulent vaginal discharge.
 5% are asymptomatic

16.  Premenopausal woman –
abnormal uterine bleeding
menometrorrhagia
oligomenorhea
cyclical bleeding beyond usual age

17. CAUSE PERCENTAGE
Endomterial
atrophy
60-80
estrogen
replacement therapy
15-25
Endometrial polyp 2-12
Endometrial hyperplasia 5-10
Endometrial cancer 10

18.  Local
- endometritis
- cervical polyp
- cervicitis
- senile atrophic vaginitis
- vulval dystrophy
-submucous fibroid
- ca cervix
 Systemic – bleeding disorders,
endogenous estrogen

19.  Associated constitutional factors- obesity,
hypertension, diabetes – corpus cancer
syndrome.
 Physical examination:
site of metastasis – peripheral lymph node,
breast
abdominal examination- ascites, hepatic or
omental metastasis
 Pelvic Examination:
vaginal and cervical examination
suburetheral area

20.  Bimanual rectovaginal examination
-uterine size and mobility
-adnexa for masses
- parametrium
- POD for nodularity

23.  DIRECT :
cavity to cervix
fallopian tube ovaries, peritoneal
cavity.
invading endometrium serosal surface,
parametrium and pelvic wall
rarely to pubic bone
 HEMATOGENOUS :
to lung, live
occurs with recurrent ca.

26.  CLINICAL STAGING:
- for patient not fit for surgery
- due to gross cervical invovement,
parametrial spread,invasion to bladder
and rectum
- distant metastsis- liver, lung,
virchow’s node.

27. PATHOLOGICAL
CLASSSIFICATION
A. Endometrioid
adenocarcinoma
(80%)
- villoglandular or
papillary(2%)
- secretory
-with squamous
differentiation(15-
25%)

28. SQUAMOUS
DIFFERENTIATION
VILLOGLANDULAR

29. B. Mucinous carcinoma: (5%)
-cells with intracytoplasmic mucin
- should be differentiated from
endocervical carcinoma.
-positive immunohistochemical
staining with vimentin.

30. C.Papillary serous
carcinoma
-3-4%
-similar to ca
of ovary and
fallopian tube
-psammoma
bodies
- high- risk
lesion

31. D. Clear Cell
Carcinoma
-< 5%
-Cells arrange in
hobnail
configuration
- Poor prognosis

32.  E. Squamous carcinoma of endometrium
- rare
-associated with cervical stenosis, chronic
inflammation, pyometra.
- poor prognosis
 F. Synchronous tumor of the endometrium and
ovary
- 1.4 – 3.8%
- well diff. adenocarcinoma – good prognosis

34. FACTORS PROGNOSIS
AGE Increase recurrence by 7%
for every 1 year inc. in age
HISTOLOGIC TYPE Non- endometrioid
HISTOLOGIC GRADE Tumor with grade 3
TUMOR SIZE Size > 2cm

35. HORMONE RECEPTOR
STATUS
Estrogen and
progesterone + ve tumors
( better prognosis)
DNA Ploidy and
Proliferative index
Inc. aneuploid cells – bad
prognosis
Myometrial invasion Inc. depth of invasion – inc.
spread and recurrence
Lymph-Vascular
invasion
Present – poor prognosis

36. Isthmus and cervix
extension
Increased recurrence
Peritoneal cytology Recurrence when present
other poor prognostic factors
Adnexal or uterine
serosal involvement
Poor prognosis
Lymph node metastasis 90% - without l.n
54%- with l.n
Intraperitoneal
metastasis
Poor prgnosis

37.  Rare tumor of meodermal origin.
 2-6% of uterine malignancies
 Increased incidence after radiation therapy for
ca cervix or bening condition.
 Most common histologic variants:
- leiomyosarcoma and
cacinosarcoma(40%)
-endometrial stromal sarcoma(15%)

40.  Endometrial Stromal Tumor
- perimenopausal women
- symptoms – abnormal uterine bleeding, pain
and pressure
-3 types
I. Endometrial stromal nodule
II. Endometrial stromal sarcoma
III. Undifferentiated sarcoma

41.  Leiomyosarcoma
43- 53 years
short duration of symptoms
variants-
I. Myxoid lieomyosarcoma
II. Leiomyoblastoma
III. Intravenous leiomyomatosis
IV. Benign metastasizing leiomyomatosis
V. Disseminated peritoneal leiomyomatosis

42.  Carcinosarcoma / malignant mixed
mullerian tumor :
- mixture of glandular and sarcomatous
elements
- median age of 62 years
- post menopausal bleeding(80-90%)
- highly malignant extension beyond
uterus in 40-60%

44.  Berek’s and Novak’s gynecology -15 th ed.
 Clinical gynecology, Berek’s and Novak’s
 Histopathology of endometrial ca, Lars-
Chrisitan Horn et al
 ACOG – Tamoifen and uterine ca, June 2006