Endometrial carcinoma is the most common gynecologic malignancy in developed countries. It peaks between 50-70 years of age and is more common in postmenopausal women. The main risk factors are older age, obesity, diabetes, hypertension, early menarche, late menopause, and use of unopposed estrogen therapy. Endometrial carcinoma is classified into Type I and Type II tumors based on clinicopathological and molecular characteristics. Type I tumors are estrogen-dependent and usually endometrioid adenocarcinomas, while Type II tumors are not related to estrogen exposure and include serous and clear cell carcinomas. Endometrial hyperplasia is a precursor lesion where the endome

1. EndometrialCarcinoma
Associate Clinical Professor Dr. Aisha El-Bareg, MD, PhD.
Senior Consultantin (Obs & Gyn)/ Reproductive Medicine
Faculty of Medicine, Misurata University. LIBYA
aishaelbareg@med.misuratau.edu.ly

2.  Endometrial Carcinoma (EC) is the most common gynecologic
malignancy. The number of newly diagnosed cases in Europe
was nearly 100,000 in 2012. Cumulative risk for a diagnosis of
endometrial cancer is 1.71%.
 The incidence is increasing worldwide in recent years.
 Peak incidence 50 - 70 years (75% are postmenopausal with
median age of 62 years). Fewer than 5% under age of 40.
 4th most common malignancy in women after breast, lung &
colorectal cancer(in USA, accounting for 6% of cancers).
 In 2017, an estimated 61,380 women were diagnosed with EC,
and approximately 11,000 died from this disease.
 Twice as common as ovarian cancer and three times more
common than invasive carcinoma of the cervix.
 8th most common cause of death from malignancy.
 Family history of tumor is higher (12-28%).
Introduction & Epidemiology

3. Risk Factors
 Older age.
 Early menarche & Late menopause, 2-fold increased risk for EC.
 Unopposed estrogen therapy increases the risk for EC 10- to
30-fold if treatment continues 5 years or more.
 Nulliparity. Race- white.
 (Obesity, PCOS, HRT).
 Tamoxifen use (Risk increases with :duration of therapy &
Cumulative dose).
 Previous pelvic irradiation.
 Hypertension & Diabetes mellitus. Chronic liver diseases
 Lynch syndrome, an autosomal dominant inherited cancer
susceptibility accounts for 2–5% of EC, women have an
approximate 70% lifetime risk of developing EC.

4. Risk Factors
 Estrogen-producing tumours, or ovarian granulosa, and theca
cell tumours.
 Women with a high intake of animal fat and fried food have a
2.1-fold increased risk for endometrial carcinoma.
 Increased cancer risk was suggestively associated with butter
intake, even if this result was based on only two studies. There
was a significant negative association of dairy products intake
and EC risk among women with a higher BMI.
References: -( Xiaofan Li, et al. Nutrients 2018, 10, 25).
-Endometrial Cancer Consensus Conference Guidelines.
International Journal of Gynecological Cancer & Volume 26,
Number 1, January 2016

5. The risk for endometrial cancer is reduced by:
 Combined oral contraceptive pill. (50%).
 Smoking: It increases concentrations of sex-hormone-binding
globulin, thereby lowering levels of bioavailable estrogen.
 Increased coffee consumption is associated with decreased risk
of endometrial cancer.(Alessandra Lafranconi, et al. Nutrients
2017, 9).
 High vegetable intake are related to a lower EC risk
(Ricceri et al. BMC Cancer (2017) 17:757).
 Women with a high intake of complex carbohydrates,
predominantly breads and cereals, have a decreased risk (RR
= 0.6) after controlling for body mass.

6. Some of Common Risk Factors Explained:
 1-(PCOS):
 Women with PCOS have a nearly 3 times increased risk for EC.
 An association between PCOS and EC was first suggested
over fifty years ago.
 It is characterized by prolonged anovulation with consequent
exposure to estrogen unopposed by progesterone which may
explain why women with PCOS have an elevated risk of EC.
(an estrogen-sensitive disease).
 Hyperandrogenism:
 Is one major component of all 3 clinical diagnostic criteria for
PCOS, it is related to the chronic anovulation. Peripheral
conversion of androgens to estrogen leads to the chronic
exposure endometrium to estrogen and may result in
endometrial hyperplasia and EC.

7.  Hyperandrogenism, itself, also is a common finding in EC. It
has been shown that androgen receptor and 5a-reductases are
present in human endometrium. In some PCOS women, with
over expression of endometrial androgen receptors disordered
androgen action within the endometrium may result in EC.
(Dumesic and Lobo, 2013).
 PCOS and obesity are linked through their common symptom of
Insulin Resistance (IR), an important potential risk factor of EC.
 High levels of insulin induced by IR have direct and indirect
effects for the development of EC.
 Insulin directly stimulates endometrial cell proliferation and
activates mitogenic and anti-apoptotic signaling systems in
endometrium and also, the network among insulin estrogen
and IGF-1 enhances the risk of the development of EC.
Indirectly, insulin causes changes in sex hormone levels,
including increases in the levels of estrogen that promotes the
risk of EC.

8.  References:
 Ding et al. Medicine (2018) 97:39.
 Harris and Terry. Fertility Research and Practice (2016) 2:14.
 Aytekin Tokmak et al. Asian Pac J Cancer Prev, Vol 15, 2014,
7011-7014.

9. Pathophysiology of PCOS

13.  2- Obesity:
 Obesity is defined by WHO, as “abnormal or excessive fat
accumulation that may impair health.
 Excess weight by up to 22.7 kg have a threefold increased risk
for EC.
 The Most well-known cancer linked to obesity is EC. Obesity
has also been related to ovarian, breast colon cancers,
esophageal, pancreatic and kidney.
 EC excess risk is associated with endocrine and inflammatory
effects of adipose tissue. Adipocytes express aromatase that
converts ovarian androgens into estrogens, which induce
endometrial proliferation. SHBG are lower in obese women, so
level of unbound biologically active hormone is higher. level of
insulin-binding globulins is reduced and free insulin levels are
elevated. Insulin and insulin-like growth factors (IGF) also exert
a proliferative effect on the endometrium with other growth
factors.

14.  Adipose tissue secretes inflammatory factors called adipokines,
partly responsible for the IR that accompanies obesity and
therefore play a role in the augmented endometrial
proliferation. Adiponectin, produced by adipose tissue has an
inhibiting effect on the proliferation, but it is inversely
correlated with fat mass.

17. Tamoxifen:-3
 Tamoxifen, a nonsteroidal antiestrogen agent with a modest
estrogenic activity belongs to a group called selective estrogen
receptor modulators, is widely used as adjunctive therapy for
women with breast cancer. In standard dosages, it might be
associated with endometrial proliferation, hyperplasia, polyp
formation, invasive carcinoma, and uterine sarcoma.
 The increased relative risk of developing endometrial cancer for
women taking Tamoxifen is two to three times higher than that
of an age-matched population.
 Rate of endometrial cancer occurrence among Tamoxifen users
who were administered 20 mg/d was 1.6 per 1,000 patient
years, compared with 0.2 per 1,000 patient years among
control patients taking a placebo.
 The effect of progestin on the endometrium of women
receiving Tamoxifen is not known.

18.  Women taking Tamoxifen should be informed about the risks of
endometrial proliferation, endometrial hyperplasia, endometrial
cancer, and uterine sarcomas.
 Any abnormal vaginal bleeding, bloody vaginal discharge,
staining, or spotting should be investigated.
 Postmenopausal women taking Tamoxifen should be closely
monitored for symptoms of endometrial hyperplasia or cancer.
 Premenopausal women treated with Tamoxifen require no
additional monitoring beyond routine gynecologic care.
 Pretreatment screening of endometrial polyps in post-
menopausal women with transvaginal ultrasonography, and
sonohysterography when needed, or office hysteroscopy before
initiation of Tamoxifen therapy.
Reference: ACOG Committee opinion No.601(June 2014).

21. 4-Diabetes:
 IR, hyperinsulinemia, and chronic inflammation associated
with diabetes are all associated strongly with cancer. Changes
in bioavailable ovarian steroid hormone occur in diabetes (the
increasing levels of estrogen and androgen and decreasing
level of progesterone) are also considered potentially
carcinogenic conditions for the breast, endometrium, and
ovaries. In addition, interaction among insulin, insulin-like
growth factors (IGFs), and estrogen & progesterone, could act
synergistically during cancer development.
 C-reactive protein (CRP), an inflammatory biomarker induced
by IL-6, increased by IR and associated with an increased risk
of EC in postmenopausal women, therefore, EC may be
associated with chronic inflammation in T2DM.
Reference:(Kyong Hye Joung, et al. BioMed Research
International, Volume 2015).

24. ENDOMETRIAL HYPERPLASIA(EH)
 EH is a pre-cancerous, non-physiological, non-invasive
proliferation of the endometrium that results in increased
volume of endometrial tissue, associated with prolonged
estrogen stimulation of the endometrium without
progesterone.
 EH usually occurs after menopause, when ovulation stops and
progesterone is no longer made. It also can occur during
perimenopause, when ovulation may not occur regularly.
 The most common sign is AUB.
 Molecular genetics : Mutation in PTEN genes ( 20% of
hyperplasia ).

25. ENDOMETRIAL HYPERPLASIA(EH):
 Since EH is a precursor to cancer, all risk-factors of EC
could be related to EH.
 Classification : According to architectural & cytological
factors endometrial, it is divided into :
1. Simple hyperplasia
2. Complex hyperplasia
3. Atypical hyperplasia

27. ENDOMETRIAL HYPERPLASIA

28. The endometrial cavity is opened to reveal lush fronds of hyperplastic
endometrium.
ENDOMETRIAL HYPERPLASIA

30. Endometrial cystic hyperplasia

31. Simple hyperplasia:
 Affect the glands and stroma equally
 Cystic glandular hyperplasia- is a variant, the glands
shows cystic dilatation (Swiss cheese) Epithelial growth
pattern and cytology are similar to those of proliferative
endometrium. Mitosis not prominent.
 Malignancy occur in 1%
Simple hyperplasia without atypia
Simple hyperplasia with atypia

32. 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. Malignancy occurs
in 3%
COMPLEX HYPERPLASIA WITH ATYPIA COMPLEX HYPERPLASIA WITHOUT ATYPIA

33. Atypical hyperplasia
 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.
 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.

37. The investigations and management schemes for endometrial hyperplasia

41. Ultrasound Evaluation of Endometrium

45. ENDOMETRIAL HYPERPLASIA

46. ENDOMETRIAL HYPERPLASIA

51. :Metformin for Endometrial Hyperplasia Treatment
 Metformin is anti-proliferative on the endometrium, directly
activates adenosine monophosphate (AMP)-activated protein
Kinase (AMPK), also promotes AMPK activation by liver kinase
B1. AMPK activation inhibits cancer incidence.
 Blocks the epidermal growth factor signaling pathway.
 Chemosensitizes to progestins.
 Reduces EC cell line invasion and metastasis.
 850 mg twice daily for 7 to 30 days results in reduction of
atypical EH (AEH) and endometrioid EC.
 Metformin use is limited by its gastrointestinal adverse effect
profile.
 Reference: Healthcare 2017, 5, 30

52.  In conclusion it leads to reversion of AEH to a normal histology
and decreased cell proliferation biomarkers staining, from
51.94% to 34.47%.
 Reference: Gynecological Oncology, October 2017,Volume 147, Issue 1.

54. EC.PATHOLOGY
 Most forms of cancer arising in the endometrium are
adenocarcinomas.
 Endometrioid adenocarcinomas are the most common.
 lesions may be papillary, secretory, or ciliated.
 Squamous differentiation is a common feature.
 Degree of carcinoma differentiation may be based on
cytological or architectural criteria.
 FIGO has established architectural criteria that may be
applied to most cell types(For endometrial carcinomas):
 Tumor grade predicts the biologic behavior of EC.
 Grade1: Well differentiated adenocarcinoma, less than 5%
solid growth, ( with easily recognizable glandular pattern ),
superficial invasion with little propensity for nodal spread.

55.  Grade 2: Moderately differentiated adenocarcinoma with partly
solid growth <50%, showing well formed glands mixed with
solids sheets of malignant cells .
 Grade3: 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), often deeply invasive and metastatic.
 All non-endometrioid carcinoma classified as grade-3
irrespective of histological pattern.

56. EC Types:
A. According to the clinicopathological & molecular studies:
 1. Type - I
 2. Type – II
B. According to the histopathology:
 Endometrioid adenocarcinoma (80-85%).
 Adenocarcinoma with squamous differentiation(Squamous
differentiation is very common).
 Adenosquamous carcinoma (Pure squamous carcinomas of
endometrium are rare).
 Serous carcinoma.
 Clear cell carcinoma.
 Malignant mixed müllerian tumor(MMTs).

57. A. 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 endometrioid tumor
associated with atypical endometrial hyperplasia. Better
prognosis is better with superficial myometrial invasion.
Mutation in PTEN tumor suppressor gene – 80%. PIK3CA
mutation – 39%. Mutation in KRAS gene. Mutation in p53 gene
( upto 50% in poorly differentiated endometrioid carcinoma ).
 Type – II tumor: About 15% of EC, in the sitting of
endometrial atrophy, Not related to estrogen stimulation or
endometrial hyperplasia, poorly differentiated, high grade
tumor with poor prognostic cell type like - serous endometrial
carcinoma, clear cell tumor. Usually in older or postmenopausal
women and not related to obesity, HTN, DM. Aggressive in
behavior. Mutation in p53 gene. Aneuploidy. PIK3CA.

58. B. 1-Endometrioid carcinoma:
 EC either localized polypoid tumor or diffuse tumor involving
the endometrial surface.
 Endometrial adenocarcinoma formed well 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.
 Up to 20% of endometrioid carcinoma contain foci of squamous
differentiation.

59. This uterus is not enlarged, but there is an irregular
mass in the upper fundus that proved to be
endometrial adenocarcinoma

60. adenocarcinoma of the endometrium

61. Endometrioid carcinoma

62. Endometrioid carcinoma

63. 2-Serous carcinoma:
 Arise in the sitting of small atrophic uterus, often form large
bulky tumor or deep invasion in to the myometrium. Precursor
of serous carcinoma is endometrial intraepithelial carcinoma.
Lesion may have papillary growth pattern composed of cells
with marked cytological atypia (high nuclear to cytoplasmic
ratio, atypical mitotic figure, heterocromastia and prominent
nucleoli.
 Different from adenocarcinoma by marked cytological atypia.
 5 - 10 % of all endometrial carcinomas.
 Psammoma bodies often present.
 High tendency to invade lymphatics.

64. Serous carcinoma

65. Serous carcinoma

66. 3-Clear cell:
 4 % of all endometrial carcinomas.
 Aggressive.
 Often associated with an advanced stage of disease and thus,
poor prognosis.
 Solid, tubular or papillary patterns of growth.
 Nuclear grade is usually high.

67. Clear cell

68. Clear cell

69. 4-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.
 Occur in the post-menopausal women and present with post
menopausal bleeding. This is a highly malignant tumor.
 They are fleshier than adenocarcinomas, be bulky and polypoid
and sometimes protrude through the cervical os.
 On histology: tumor consists of adenocarcinoma mixed with
malignant mesenchymal elements ( striated muscle, adipose
tissue, bone).

70. -
MMTs

71. -MMTs

72. -MMTs

73. Mucinous:-5
 Primary adenocarcinoma of endometrium in which most of the
cells contain prominent intracytoplasmic mucin and resemble
colonic epithelium.
Mucinous Adenocarcinoma
Invasive Mucinous Adenocarcinoma

74. Staging:
 Over 80% of patients present with early stage disease due to symptoms of
AUB, with an overall excellent prognosis. EC is traditionally surgically staged
and the treatment varies by stage, grade, regional guidelines, and expertise.
 REVISED FIGO STAGING (2010)
 STAGE I: Tumour confined to the corpus uteri.
 Ia: No or less than half myometrial invasion.
 Ib: Invasion equal to or more than half of myometrium.
 Stage II: Cervical stromal invasion but not beyond the uterus.
 Stage III: Local and/or regional spread of the tumour.
 IIIa: Tumour invades the serosa of the corpus uteri and/or adnexa.
 IIIb: Vaginal and/or parametrial involvement.
 IIIc: Metastases to pelvic and /or paraaortic lymph nodes.
 Stage IV: Tumour invades bladder and/or bowel mucosa, and/or
distant metastases.
 IVa: Tumour invasion of bladder and/or bowel mucosa.
 IVb: Distant metastases, including abdominal metastases and/or
inguinal lymph nodes.

76. Routes of spread:
 1. Direct spread : slow growing (to the myometrium & serosa
of the uterus leading to perforation and peritonitis (commonest
cause of death). Downward spread to the cervix which if
blocked, pyometra results.
 2. Lymphatic : (Usually late. Three separate lymphatic
pathways: a- Paracervical and Parametrial – pelvic LN3, b-
Ovarian – para aortic LN, c-round ligament –inguinal LN).
 3. Heamatogenous spread : (Rare & late in carcinoma,
Common & early in sarcoma, to the lower part of the anterior
vaginal wall).
 4. Implantation : along the cervix to vaginal vault, along
fallopian tubes to the peritoneal cavity.

77. EC. Clinical presentation:

78. EC. 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.
 PATIENT PROFILE: usually nulliparous, postmenopausal or
h/o delayed menopause; Younger women with PCOD, infertility,
obese, hypertensive & diabetic.
 90% of patients with EC present with PMB.
 Watery & offensive, bloody or purulent discharge due to
pyometra.
 There may be ascites.
 Abdominal lump due to pyometra, fibroid, Hepatomegaly.

79. EC. Clinical presentation:
 Bimanual examination: Size of the uterus: small, normal or
large, usually mobile. In advanced cases it is fixed and
irregular. Adnexae : mass in case of simultaneous tumour or
secondary growth in ovary.
 Parametrium : for induration.
 Cul-de-sac : for nodularity.

80. Management: Pretreatment Evaluation:
 Investigations: CBC, LFTs, RFTs, Chest x-ray, Intravenous
pyelography.
 Transvaginal sonography: ET>4mm, a polypoid endometrial
mass or collection of fluid within the uterus requires further
evaluation.
 Pap’s smear
 Endometrial sampling: (D&C Gold standard, indicated in:
inadequate sample by aspiration biopsy, Cervical stenosis or
patient intolerance, bleeding recurs after a negative
endometrial biopsy), false negative : 10%.
 Hysteroscopy with curettage: office hysteroscopy is a
simple procedure that can provide a good visualization of the
whole uterine cavity without cervical dilation and usually
without anesthesia. Excellent method for targeted biopsy that
one may miss at D & C or endometrial aspiration.

81.  Combined use of hysteroscopy and histopathology gives 100%
accuracy. Identification of other uterine pathology as polyps
and submucous myomas. Highest accuracy in diagnosing end.
polyps with sensitivity & specificity of 95.3% and 95.4%,
respectively.
 In conclusion: hysteroscopy is highly accurate and clinically
useful in the diagnosis of endometrial cancer. In cases that EC
is suspected, peritoneal spilling through the fallopian tubes can
be reduced by a low intrauterine pressure of up to 70 mmHg.
Reference: (N. Koutlaki, et al. Gynecol Surg (2010) 7:335–341).
 Magnetic resonance imaging: The goal of MRI is to identify
patients preoperatively who would benefit from abdominopelvic
lymph node dissection and adjuvant therapy while avoiding
over treating early stage patients with unnecessary
lymphadenectomies, but (differentiating benign mimics of
Fibroid, Adenomyosis, Polyp & EH).

82.  In addition, MRI is excellent in assessing tumor size and
extension, myometrial & parametrial/cervical invasion.
 Preparation:
 To minimize bowel motion: Fasting for 4-6 hours prior to the
study, anti-peristaltic medications prior to exam, empty bladder
to avoid motion artifact.
Basic Protocol:
 Torso or Cardiac Coil.
 Axial/ Sagittal T1-pre and -post contrast images.
 Axial/Sagittal T2-wt images with fat saturation.
 Dynamic contrast enhanced images - 40 and 90sec.
 Axial and sagittal diffusion weighted images.
 In most studies, more than 80% of patients with elevated
CA-125 levels are found to have extrauterine disease at the
time of exploratory laparotomy.

88. ENDOMETRIAL CANCER

90. Malignant mixed müllerian tumour of the Uterus

94. Treatments Summery:
 Surgery
 Chemotherapy
 Radiotherapy
 Hormonal therapy
 Based on tumour grade and depth of myometrial invasion.
 Surgical: Stage 1, Stages 2&3: TAH+BSO,
(Wertheim’s operation) and free pelvic fluid or saline
washings for cytological evaluation + biopsy specimens
(mesentery). Lymph node sampling should be strongly
considered for patients with presumed stage I, grade 3 lesions
or for lesions of any grade with significant myometrial invasion.
-Patients with stage II or III disease or with disease of an
unfavorable histologic type should also undergo para-aortic and
pelvic lymph node sampling.

95. Treatments Summery:
 Surgical: Stage 4: surgical option: Non
 Hormonal therapy: Progestins for recurrent disease.
 Chemotherapy: In advanced, recurrent, or metastatic
disease.
Platinum doublet chemotherapy remains the mainstay for first-
line systemic therapy in patients with advanced EC. Agents used:
doxorubicin, cisplatin, paclitaxel, ifosfamide, ixabepilone.
 Radiotherapy:Indications:
 Patient medically unfit for surgery.
 Surgically inoperable disease.
 Those with high risk of recurrence
 Stage III or IV disease.
 Contraindications: pelvic infections, previous pelvic
radiation, previous laparotomy/adhesions.

98. Treatments Summery:
 Other targeted therapies:
Bevacizumab is a recombinant humanized monoclonal antibody
and in 2004 it became the first clinically used angiogenesis
inhibitor(bevacizumab with cytotoxic agents has demonstrated a
potential survival benefit).
 Other anti-angiogenic agents: thalidomide, aflibercept,
sorafenib, and the small molecule tyrosine kinase inhibitors
(TKIs) dovitinib, nintedanib, brivanib, and sunitinib.
 Inhibitors of the PI3K/Akt/mTOR pathway.
 Metformin (oral biguanide agent). PARP inhibitors
 Immunotherapy, Pembrolizumab was granted FDA approval for
tissue or site agnostic use in the treatment of patients with
unresectable or metastatic solid tumors, including EC.
Reference: Makker et al. Gynecologic Oncology Research and
Practice (2017) 4:19.

103. Postoperative Care:
 Patients with EC should be examined at regular intervals with
complete physicals and Papanicolaou smears. Ultrasonic
thickness of more than 4 mm indicates the need for
endometrial sampling. Frequency of visits and duration of
follow-up must be based on the likelihood for disease
recurrence in each patient.
 CXR, Regular serum CA-125 estimation, Mammography, CT,
MRI: When indicated, Every 4 months for the first 2 years,
Every 6 months for the next 2 years, thereafter annually.
 Prognostic Factors: depth of myometrial invasion, histologic
type, original tumor volume, pelvic lymph nodes involvement,
extension to the cervix, adnexal metastasis, positive peritoneal
washings.

104. 5-years survival rate:
 Stage I : 83%
 Stage II : 71%
 Stage III: 39%
 Stage IV : 27%
 Prevention: Controlling obesity, blood pressure, and diabetes
help reduce risk. Restriction use of estrogen after menopause in
non-hysterectomised women. Estrogen + cyclical progesterone.
Report any abnormal vaginal bleeding or discharge. Screening of
high risk women in postmenopausal period. Treatment of
endometrial hyperplasia.

105. THANK YOU