Endometrial hyperplasia is an increased proliferation of endometrial glands relative to the stroma that can progress to endometrial carcinoma. It occurs most often in peri-menopausal women with elevated estrogen levels and is caused by prolonged, unopposed estrogen stimulation. Endometrial hyperplasia is classified as simple, complex, or atypical depending on architectural and cytological abnormalities. Endometrial carcinoma is the most common cancer of the female reproductive system, occurring most often in post-menopausal women. It is broadly classified into Type I and Type II tumors based on clinical and molecular characteristics and risk factors. Surgery is the primary treatment for early-stage disease while radiation and chemotherapy may be used

1. ENDOMETRIAL
HYPERPLASIA

2. ENDOMETRIAL HYPERPLASIA
• Endometrial hyperplasia is defined
as an increased proliferation of
endometrial glands, relative to
stroma resulting in increased gland
to stromal ratio than normal
endometrium.
• The proliferative glands vary in size
& shape and may shows cytological
atypia, which may progress or co-
exist with endometrial carcinoma.

3. ENDOMETRIAL HYPERPLASIA
Age :
Peri-menopausal women, if
estrogen level more than
progesterone.

4. ENDOMETRIAL HYPERPLASIA
Causes of endometrial hyperplasia :
Endometrial hyperplasia associated with prolonged
estrogen stimulation of the endometrium, which may be
due to-
1. Anovulation
2. Increased estrogen production from endogenous
source or exogenous estrogen.
3. Obesity
4. Polycystic ovarian disease
5. Functional granulosa cell tumors of ovary
6. Estrogen replacement therapy
7. Cortical stromal hyperplasia
8. Idiopathic.

5. ENDOMETRIAL HYPERPLASIA
Molecular genetics :
Mutation in PTEN genes ( 20% of
hyperplasia )

6. ENDOMETRIAL HYPERPLASIA
Classification :
According to architectural &
cytological factors endometrial
hyperplasia divided into four groups-
1. Simple hyperplasia
2. Complex hyperplasia
3. Atypical hyperplasia ( has more
change to developed malignancy )

7. ENDOMETRIAL HYPERPLASIA
Simple hyperplasia :
Glands are various size and irregular
shapes with cystic dilatation with mild
hyperplasia. Epithelial growth pattern
and cytology are similar to those of
proliferative endometrium.Mitosis are
not prominent.
1% chance of develop carcinoma.

8. ENDOMETRIAL HYPERPLASIA
Complex hyperplasia :
Increase in the number and size of the
glands, marked gland crowding and
branching occurs. Gland form finger
like projection but not invasion
towards stroma, epithelial cell
remains cytologically normal.
3% chance to develop carcinoma .

9. ENDOMETRIAL HYPERPLASIA
Atypical hyperplasia :
In simple atypical hyperplasia, there is
cytological atypia within the
glandular cells- such as loss of
polarity, vesicular nuclei, prominent
nucleoli, cells become rounded and
loss the normal perpendicular
orientation to the basement
membrane.
8% may progress to carcinoma.

10. ENDOMETRIAL HYPERPLASIA
In complex atypical hyperplasia
consists of back-to-back crowding of
glands lined by atypical cells. Lipid
laden “ foam” cells may be noted in
the intervening stroma.
23% to 48% women have the chances
to develop carcinoma.

11. ENDOMETRIAL
CARCINOMA

12. ENDOMETRIAL CARCINOMA
Endometrial carcinoma is the most
common invasive cancer of the
female genital tract.
It is about 7% of all invasive cancer in
women.

13. ENDOMETRIAL CARCINOMA
Age :
• Common in women >40 years of
age ( peri & post menopausal
women )
• Relatively unknown in young age.
• Peak incidence 55 to 65 years of
age.

14. ENDOMETRIAL CARCINOMA
Risk factor of endometrial carcinoma :
1. Obesity
2. Diabetes
3. Hypertension
4. Infertility
5. Unopposed estrogen stimulation
6. Family history
7. Endometrial atrophy

15. ENDOMETRIAL CARCINOMA
Classification :
A. According to the clinico-
pathological & molecular studies :
1. Type - I
2. Type - II

16. ENDOMETRIAL CARCINOMA
B. According to the
histopathology----
1. Endometroid adenocarcinoma
2. Adenocarcinoma with squamous
differentiation
3. Adenosquamous carcinoma
4. Serous carcinoma
5. Clear cell carcinoma

17. ENDOMETRIAL CARCINOMA
Type - I endometrial carcinoma :
 It is the most commonest type, about
80% of all cases. Usually occurs in 55-
65 years. The majority are well
differentiated and estrogen related,
present histologically as a
endometroid tumor associated with
atypical endometrial hyperplasia.
 Prognosis is better and have
superficial myometrial invasion.

18. ENDOMETRIAL CARCINOMA
Molecular genetics of Type-I :
1. Mutation in PTEN tumor suppressor
gene – 80%
2. PIK3CA mutation – 39%
3. Mutation in KRAS & beta catenin
oncogen
4. Mutation in KRAS gene
5. Mutation in p53 gene ( upto 50% in
poorly differentiated endometroid
carcinoma )

19. ENDOMETRIAL CARCINOMA
Type – II tumor :
 About 15% of endometrial carcinoma.
 It is arise in the sitting of endometrial
atrophy. Not related to estrogen
stimulation or endometrial hyperplasia.
They are poorly differentiated, high
grade tumor with poor prognostic cell
type like - serous endometrial
carcinoma, clear cell tumor.

20. ENDOMETRIAL CARCINOMA
 Usually occurs in older or post
menopausal women and not related
to obesity, HTN, DM.
 Develop finger like papillary
projection.
 Aggressive in behavior.

21. ENDOMETRIAL CARCINOMA
Molecular genetics of Type-II :
1. Mutation in p53 gene
2. Aneuploidy
3. PIK3CA

22. ENDOMETRIAL CARCINOMA
Endometroid carcinoma :
 85% of endometrial carcinoma.
 Endometrial carcinoma either localized
polypoid tumor or diffuse tumor
involving the endometrial surface.

23. ENDOMETRIAL CARCINOMA
 Endometrial adenocarcinoma formed
well differentiated to poorly
differentiated glandular structure mixed
with solid sheet of malignant cells. Poorly
differentiated type have barely
recognizable glands and greater degree
of nuclear atypia and mitotic activity.
 Upto 20% of endometroid carcinoma
contain foci of squamous differentiation.

24. ENDOMETRIAL CARCINOMA
Serous carcinoma:
Generally arise in the sitting of small
atrophic uterus, often form large bulky
tumor or deep invasion in to the
myometrium.
The precursor of serous carcinoma is
endometrial intraepithelial carcinoma.

25. ENDOMETRIAL CARCINOMA
• Lesion may have papillary growth
pattern composed of cells with marked
cytological atypia, including high nuclear
to cytoplasmic ratio, atypical mitotic
figure,heterocromastia and prominent
nucleoli.
• They can also have predominantly
glandular pattern, different from
adenocarcinoma by marked cytological
atypia.

26. ENDOMETRIAL CARCINOMA
Malignant mixed mullarian tumor :
MMTs consist of endometrial
adenocarcinomas with malignant changes
in the stroma.The stroma tends to
differentiate into a verity of malignant
mesodermal components, including
muscle, cartilage and even osteoid.
MMTs occur in the post-menopausal
women and present with post menopausal
bleeding. This is a highly malignant tumor.

27. ENDOMETRIAL CARCINOMA
In gross appearance: MMTs are
fleshier than adenocarcinomas, may
be bulky and polypoid and sometimes
protrude through the cervical os.
On histology: the tumor consist of
adenocarcinoma mixed with
malignant mesenchymal
elements(striated musce,adipose
tissue, bone)

28. ENDOMETRIAL CARCINOMA
Grading :
The step-grading system applied to
endometroid tumor –
G1 : Well differentiated adenocarcinoma,
less than 5% solid growth.( with easily
recognizable glandular pattern )
G2 : Moderately differentiated
adenocarcinoma with partly solid
growth <50% ( showing well formed
glands mixed with solids sheets of
malignant cells .

29. ENDOMETRIAL CARCINOMA
G3 : Poorly differentiated adenocarcinoma
with predominantly solid growth >50%
( solid sheets of cell with barely
recognizable gland with greater degree
of nuclear atypia and mitotic activity )
All non-endometroid carcinoma classified
as grade-3 irrespective of histological
pattern.

30. ENDOMETRIAL CARCINOMA
Staging :
Stage I :Carcinoma is confined to the corpus
uteri itself.
Stage II :Carcinoma involves the corpus and
the cervix.
Stage III :Carcinoma extends outside the true
but not outside the true pelvis.
Stage IV :Carcinoma extends outside the
true pelvis or involves the mucosa of
the bladder or rectum.

31. ENDOMETRIAL CARCINOMA
Route of spread :
1. Direct spread
2. Lymphatic spread and
Transtubal spread
3. Heamatogenous spread

32. ENDOMETRIAL CARCINOMA
Clinical presentation :
1. Asymptomatic
2. Abnormal uterine bleeding
3. Abnormal menstrual cycle &
Menorrhagia
4. Lower abdominal pain & pelvic
pain
5. Vaginal discharge in post
menopausal women.

33. ENDOMETRIAL CARCINOMA
How to diagnosed :
1. Pelvic examination
2. TVS
3. Pap’s smear
4. Endometrial sampling
5. D & C

34. ENDOMETRIAL CARCINOMA
Complications :
1. Anemia may result, caused by
chronic loss of blood.( This may occur if
the women has ignored symptoms of
prolonged or frequent abnormal menstrual
bleeding.)
2. Perforation of the uterus may occur
during D & C or an endometrial biopsy.

35. ENDOMETRIAL CARCINOMA
Management :
Surgery and Radiation therapy are the
only methods of successful
treatment.

36. ENDOMETRIAL CARCINOMA
Women with the early stage-I disease
treatment with surgical hysterectomy
either abdominal or vaginal.
Women with late stage-I disease and
stage-II disease are often offered
surgery in combination with Radiation
therapy.

37. ENDOMETRIAL CARCINOMA
Prognosis :
Stage-I & well differentiated
endometrial carcinoma – 75% to 80%
prognosis
Stage-II & III : < 50% prognosis

38. ENDOMETRIAL CARCINOMA
Prevention :
1. All women should have regular
pelvic examination and pap’s smear
( beginning at the onset of sexual
activity or at the age of 20 if not
sexually active ) to help detect signs
of any abnormal development.

39. ENDOMETRIAL CARCINOMA
2. Women with estrogen replacement
therapy should report immediately to the
doctor if any of the following symptoms
arise
I. Bleeding or spotting after intercourse
or douching
II. Bleeding that lasts longer than 7 days
III. Reappearance of blood or staining
after 6 months or more of no
bleeding at all.

40. THANK YOU