2. INCIDENCE
The incidence is higher amongst the
white population of the United States
and lowest in India and Japan.
In India, it ranks third amongst genital
malignancy next to cervix and ovary.
Mean age of presentation is 60 years
.Peak incidence occurs from 55- 70
years.
Majority are diagnosed early.
3. Risk factors
• Family Has OLD AUNTIS
1. F : Family history ( HNPCC.All first degree relatives have increased chances).
2. H: Hypertension.
3. O: Obesity.
4. L: Late menopause or early menarche.
5. D: Diabetes.
6. A: Atypical endometrial hyperplasia.
7. U: Unopposed estrogen or increased estrogen in the body as in HRT, Fibroid , PCOD and
feminizing ovarian tumors.
8. N: Nullaparity.
9. T: Therapy(Tamoxifen and Radiation therapy).
10. I: Infertility/ Menstrual irregularity.
11. S: Senile endometritis.
4. Protective factors
Oral contraceptive pills.
Smoking(as it decreases levels of estrogen , decreases weight and is associated
with earlier age menopause).
Multiparity.
Physical exercise.
6. A. Simple hyperplasia
2 types:
• Simple hyperplasia without atypical cells.
• Simple hyperplasia with atypical cells.
Results from circumstances , in which there is prolonged , increased
estrogen production:
• Follicular cyst of ovary.
• PCOD
• Granulosa and Theca cell tumor of ovary.
• Hormone replacement therapy.
7. B. Complex
hyperplasia
2 types:
• Complex hyperplasia without atypical cells .
• Complex hyperplasia with atypical cells .
Less obviously connected with
increased estrogen.
Mostly , cause is unknown, can be a/w
• PCOD
• Glucose intolerance.
10. On TVS
Endometrial thickness
in premenopausal
female
≥12mm
Endometrial thickness
in postmenopausal
female
≥5mm
Endometrial cancer is
suspected or
hyperplasia is
suspected
Endometrial
aspiration biopsy
12. On histological and
biological behavior,
endometrial
cancer can be
classified into 2
types
Features Type I(Endometrioid-80%)
Type II(
Nonendometrioid- 20%)
Specific subtypes Endometrioid,
Adenocarcinoma grade 1,2
Papillary serous, clear cell ,
Adenocarcinoma grade 3
Prognosis Good Bad
Unopposed estrogen Present Absent
Menopause status Pre and perimenopausal Post menopausal
Race White Black
Hyperplasia Present Absent
Grade Low High
Behavior Stable Aggressive
Associated gene
alteration
pTEN/Kras P53, HER2/neu
Body weight Obese females Thin females
13. SPREAD
Direct spread(most common)
• Lymphatic spread involves pelvic, paraaortic (through
infundibulopelvic ligament), and rarely inguinal and
femoral (through lymphatics of round ligament) nodes.
• Lymph node metastasis is the most important
prognostic factor.
• The tubes and ovaries are involved (3–5%) either by
direct spread or by lymphatics.
• The vagina is involved in about 10–15% cases.
Lymphatic spread:
• The common sites of metastases are lungs, liver,
bones, and brain.
Hematogenous spread:
18. FIGO staging of
Ca
Endometrium
Stage Characteristics
Stage I Tumor confined to corpus uteri
Stage IA No or less than half myometrial invasion
Stage IB Invasion equal to or more than half of the myometrium
Stage II Tumor involves cervical stroma but does not extend beyond the uterus
Stage III Local and/or regional spread of the tumor
Stage IIIA Tumor invades the serosa of the corpus uteri and/or adnexae
Stage IIIB Vaginal and/or parametrial involvement
Stage IIIC Metastases to pelvic and/or paraaortic lymph nodes
Stage IIIC1 Positive pelvic nodes
Stage IIIC2 Positive paraaortic lymph nodes with or without positive pelvic lymph
nodes
Stage IV Tumor invades bladder and/or bowel mucosa, and/or distant metastases
Stage IVA Tumor invasion of bladder and/or bowel mucosa
Stage IVB Distant metastases, including intraabdominal metastases and/or inguinal
lymph nodes
19. Management
• Strict weight control.
• Strict the use of unopposed estrogen in non hysterectomized
patient.
• Prophylactic surgery in high risk women(Lynch II syndrome)
• Education
• Screening of high risk women in menopausal period
Preventive:
• In cancer endometrium , staging is surgical.
Principle of management
• TAH + BSO done till stage I
• Wertheim’s hysterectomy is done when cervix is involved i.e
in stage 2
• Debulking surgery is done in stage 3 & 4.
In surgery:
20. For Lymph node dissection
• In type II varieties always pelvic & para-aortic lymph node dissection.
• On type I , if cancer spreads outside uterus i.e from stage II onwards always
do Pelvic + para- aortic L.N dissection.
• If cancer is limited to uterus and ≥ 50% of myometrium is involved i.e.
stage IB then pelvic & para-aortic L.N dissection is done.
• If <50% of myometrium is involved i.e. stageIA
• Size of tumor ≥ 2cm : pelvic L.N dissection.
• If < 2cm size : No L.N dissection.
21. Postoperative management
• The post operative management of choice is Radiotherapy.
• 2 exceptions to this is :
• In stage IA grade I and II : No postoperative therapy is given .
• In stage III/IV : Postoperative therapy of choice is chemotherapy +
Radiotherapy( Paclitaxel + Adriamycin or Doxorubicin + Platinol or
Cisplatin)
22. Recurrent
Endometrial
cancer
Mostly occurs within 2 years and most
common sites are vagina> pelvis.
Most common extra pelvic recurrence site:
Lungs, aortic L.N, Liver , Brain and bones.
Management:
• Hormone receptor positive: Progestin.
• Hormone receptor negative: Local management(Palliative
chemotherapy)
• If contraindications to progesterone then Tamoxifen.
• If patient is operable – surgery
• If inoperable- Radiotherapy
23. Follow-up of
Patients
• Following initial therapy,
• patient is examined every 4 months for the first
2 years,
• Every 6 months for next 3 years and
• Thereafter, annually (ACOG 2005).
• Evaluation of symptoms, thorough clinical
examination and X-ray chest (annual) are
essential.
• Other investigations are: mammography
(annual) and CT, MRI when clinically indicated.
• Regular estimation of serum CA 125 may be
helpful in cases with uterine papillary serous
carcinoma (UPSC).