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Endometrial cancer
INTRODUCTION
• In India, ranks IIIrd among gynaecological malignancies next to
cervix and ovary
• Incidence: 2 per 1 lakh
• Unlike cancer cervix, cost effective screening program is not
available
• Common in postmenopausal women
• Increasing incidence due to
 Increased screening
 Improved hysteroscopic diagnosis
 Increase in geriatric population
 Estrogen use
• SURGICO PATHOLOGICAL STAGING, as opposed to clinical staging
Epidemiology
• Most frequent genital cancer in rich countries
• MEAN AGE: 60 years
• PEAK INCIDENCE: 55-70 years
• 20-25% - perimenopausal
• 5% - <40 years
• 5 year survival for stage I disease more than
90%
• Overall 5 year survival for all stages: 60-70%
ENDOMETRIAL CANCER
ENDOGENOUS ESTROGEN
DEPENDENT
EXOGENOUS ESTROGEN HEREDITARY
Nulliparity, low parity Unopposed estrogen
therapy
LYNCH II / HEREDITARY
NON POLYPOSIS
COLORECTAL CANCER –
HNPCC SYNDROME
PCOD tamoxifen
Early menarche, late
menopause
Functioning ovarian tumours
Obesity
Hypertension
Diabetes
hyperlipidaemia
Protective factors / Prevention
• Oral contraceptive pills (combined pills with addition of
progesterone to HRT)
• Smoking (as it decreases level of estrogen, decreases
weight and associated with earlier age of menopause)
• Multiparity
• Phytoestrogens
• Green tea
• Coffee
• Physical exercise
• Treatment of PCOS
• MIRENA IUCD- effective in simple hyperplasia
• Early screening , while pt is on TAMOXIFEN
PATHOLOGY
• Localized/ diffuse
• App – nodule/ polyp/ diffuse lesion
• Involving entire uterine cavity
HISTOPATHOLOGY
• Adenocarcinoma / endometrioid 80%
• Adeno acanthoma
• Adenosqamous carcinoma 15%
• Papillary serous adenocarcinoma
• Mucinous adeno carcinoma
• Clear cell carcinoma
• Undifferentiated
• Mixed
SPREAD
• DIRECT EXTENSION – Most common
• Lymphatic spread - occurs to pelvic and para-
aortic nodes, fundus – para aortic nodes,
round ligament – supl inguinal nodes
• Hematogenous spread (usually to lungs, liver,
brain, bone) is rare
• Trans tubal – ovaries, pelvis, peritoneal cavity
GRADE 1 : The glandular pattern is maintained, but cells
show atypia
GRADE 222 : some glands show a papillary
pattern and are solid
GRADE 3
3
: glands are solid with cellular proliferation, and
glandular architecture is lost, endometrium is packed
with glands and little stroma
GRADING (FIGO)
Depends on differentiation , glandular architecture and anaplasia of cells
GRADE 1 GRADE 2
GRADE 3
Histological differences in endometrial cancer
FEATURES TYPE I ENDOMETRIOID
80%
TYPE II (NON
ENDOMETRIOID) 20%
Unopposed oestrogen present Absent
Menopausal status Pre and perimenopausal Postmenopausal
Hyperplasia present Absent
Race white Black
Grade low High
Myometrial invasion Minimal Deep
Specific subtypes Endometrioid
Adeno CA grade 1,2
Serous, clear cell, adeno CA
grade 3
Behavior stable Aggressive
Associated gene Pten/Kras p53
Good
prognosis
Poor
prognosis
Type I Type II
Clinical features
• Asymptomatic – 7 to 10%
• POST MENOPAUSAL BLEEDING
• irregular vaginal bleeding
• Discharge per vagina:
 brown , watery offensive discharge
 watery discharge free from blood-hydrorrhoea
• Past H/O PCOS, HRT
• Obesity/ HTN / DM – CORPUS CANCER
SYNDROME
pelvic pressure/ discomfort
Referred pain in hypogastrium / both iliac
fossa - simpson’s pain
Pain – not severe, tends to occur at the same
time each day, lasting for 1-2 hours
LUMP - Hematometra / pyometra in cervical
stenosis
• P/V : uterus bulky/normal
• Bulky uterus – growth / fibroid/
pyometra
• Adnexal mass – feminizing/ metastatic
ovarian tumours
• Advanced stage: cervix bulky, mass
protruding through the os, suburethral
vaginal nodule
INVESTIGATIONS
• PAP SMEAR
• Endometrial aspiration
• Fractional curretage
• Hysteroscopy and biopsy – GOLD STANDARD
• TVS – ET – irregular line / polyp / ovarian tumour
/ ovarian metastasis / extension to endocervix
• Doppler ultrasound- low RI 0.37 to 0.7 or below –
EC
• SALINE INFUSUION SONOGRAPHY
• CA 125
INVESTIGATIONS
• Contrast enhanced computerized tomography CECT – hypodensity in
myometrium – myometrial infiltration
• Pelvic and para aortic nodes >1cm
• CT IS SUPERIOR THAN MRI in detecting ascitis , bowel , and
omental metastasis
• MRI – superior to CT in detecting myometrial invasion, nodal
enlargement (90%)
• Endometrial and myometrial junction – low intensity zone exists – intact –
myometrial invasion ruled out
• MRI useful in endocervical stromal invasion
• XRAY CHEST – lung metastasis
• Bone and liver metastasis – RADIO ISOTOPE SCANNING – PET CT – reveal
metabolic activity in tissue and lymph node- helpful for staging
DIFFERENTIAL DIAGNOSIS
• Senile endometritis
• Tubercular endometritis
• Atypical hyperplasia
• Endometrial polyp
• Hyperplasia without atypia
• Atypical hyperplasia/ EIN (Endometrial intraepithelial
neoplasia)
• TREATMENT:
• endometrial hyperplasia without atypia –
progesterone oral / LNG IUS / MPA 10-20mg/day /
norethisterone 10-15mg/ day for 6 months
• ATYPICAL HYPERPLASIA – risk of EC = 8-29% - total
hysterectomy
• Young – high dose of progesterone with frequent
evaluation of endometrium - biopsy
New WHO classification of
endometrial hyperplasia - 2014
ENDOMETRIAL CANCER
TREATMENT
• SURGICO – PATHOLOGICAL STAGING
• ABDOMINAL HYSTERECTOMY
• BILATERAL SALPHINGO – OOPHRECTOMY
• OMENTECTOMY
• PELVIC AND PARA AORTIC NODE SAMPLING
Remain the CORNER STONE for
management of early endometrial carcinoma
STAGE WISE MANAGEMENT OF ENDOMETRIAL CANCER
Stagewise Management
Stage I A grade 1 Surgery only
Stage I A grade 2, 3
Stage I B grade 1, 2
Sugery + vaginal brachytherapy
Stage IB grade 3 Surgery + vaginal brachytherapy +external beam
radiotherapy to pelvis
Stage II Surgery + external RT + Vaginal brachytherapy
Stage III Surgery + external RT + Vaginal brachytherapy +
Chemotheraoy
Stage IV Palliative RT + Chemotherapy + high dose
progesterone
SURGERY
• TAH with BSO +omentectomy (non endometriod type)
• Vaginal hysterectomy- obese, DM, prolapse
 morbidity is less + LAP lymphadenectomy / post
operative radiotherapy
• Modified Wertheims hysterectomy- stage II
• Debulking surgery – stage III
• Laparoscopic surgery
 Definite role in incompletely staged patients to decide
for adjuvant therapy
• Robotic surgery gaining importance
RADIOTHERAPY
• Vaginal vault irradiation – vaginal ovoids – dose = high
dose rate Iridium / Low dose rate Cesium via
COLPOSTAT to deliver 6000 cGy/6 weeks
• EXTERNAL PELVIC IRRADIATION:
Stage IB G3, Stage II, III
Dose: 4500 – 5040 cGy – 5-6 weeks
• EXTERNAL FIELD RADIATION:
4500 – 5000 cGy- positive para aortic nodes
• WHOLE ABDOMEN IRRADIATION:
Papillary serous, clear cell, adnexal upper abdominal
disease excised
• PRIMARY RADIOTHERAPY: inoperable stage III,IV-
brachytherapy + External RT + uterine cavity packed
with Heyman capsules
CHEMOTHERAPY
• High risk tumours to reduce and prevent extra pelvic
failure
• CYCLOPHOSPHAMIDE +ADRIAMYCIN + CISPLATIN – 6
cycles – 2 year progression free survival
HORMONE THERAPY
• MDPA 1g weekly or 200mg orally daily
• 17 α progesterone 1g weekly or northiesterone
• Tamoxifen 10mg twice daily
• Doxorubicin, platinum, taxane, carboplastin – under
trial
STAGE III
• Surgico pathological staging – TAH BSO / Radical
hysterectomy / debulking – SURGICAL
IRRADICATION, followed by RT / Chemo
• Stage III B, C – inoperable – pelvic radiation
followed by surgery or
• external beam RT or extended field RT followed
by intra uterine and intra vaginal brachytherapy
• STAGE IV – debulking surgery /
radiotherapy(whole abdomen irradiation)
FOLLOW UP
• First 3 years = every 3-4 months
• Next 3-5 years = every 6 months
• Annually thereafter
• Each visit
physical , pelvic examination
pap smear
USG
CA 125
CT, MRI – when indicated
Chest Xray
FNAC/ LAP/ Laparotomy – pelvic/ distant recurrences
Post operative management based on histopathological type , peritoneal cytology, grade, LVSI,
Cervix/isthmus invasion, node, adnexal metastases, intra abdominal and distinct metastases
Low risk:
 G1 without myoinvasion
 No cervix/isthmus
invasion, LVSI, METASTASIS
 Negative peritoneal
cytology
 Tumour < 2 cm
No further management
Intermediate risk:
 G1, G2 with <50%
myometrial invasion
 No cervix/isthmus
invasion, LVSI, METASTASIS
 Negative peritoneal
cytology
POST operative intra vaginal
ovoid brachytherapy
High risk:
 G3 tumours
 Myoinvasion >50%
Adnexal spread
cervical invasion
 Lymph node metastasis
 LVSI
 Clear cell , PSC histology
 Intra abdominal / distant
metastasis
 Whole pelvic RT
Extended field RT if aortic /
common iliac nodes have
metastases/ CT
PROGNOSTIC VARIABLES IN
ENDOMETRIAL CARCINOMA
• Age
• Histological type
• Histological grade
• Myometrial invasion
• LVSI
• Isthmus/ cervix extension
• Adnexal involvement
• Lymph node metastasis
• Intra peritoneal tumour
• Tumour size
• Peritoneal cytology
• Hormone receptor status
• DNA/ ploidy / proliferative index
• Genetic / molecular tumour markers
Pre operative evaluation:
• HISTORY, examination
• Fractional curretage/ hysteroscopy
• Imaging – USG, CT ,MRI , CHEST XRAY
• Serum CA 125
SURGICAL = vertical incision/ LAP
Peritoneal cytology/ exploration
Type I hysterectomy with BSO
Cut section: tumour sixe, grade, MI
ENDOMETRIOID, no adverse risk factors:
G1, MI <50%, Tumour <2cm
NO FURTHER SURGERY 
SURVEILLANCE
High risk / NON ENDOMETROID
ENDOMETRIAL CANCER DIAGNOSED
POST HYSTERECTOMY
• High risk factors identified: COMPLETE
SURGICAL STAGING
• ALTERNATE = external beam radiation to the
pelvis
Recurrent endometrial cancer
MC time of recurrence Within first two years
MC symptom of local recurrence Vaginal bleeding
MC symptom of pelvic recurrence Pelvic pain
MC site of recurrence Vagina and pelvis
MC site of extrapelvic recurrence Lung
LN (Aortic)
Liver
Brain
Bones
Management
• For patients with recurrent endometrioid
tumours with hormone receptors positive, initial
treatment is progestin
• Contraindication to progestin  TAMOXIFEN
• Hormone negative  local management
• If Operable – surgery to be done
• If inoperable – RT is given
• If local treatment cannot be given – palliative
chemotherapy is given
THANK YOU

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ENDOMETRIAL CANCER

  • 2. INTRODUCTION • In India, ranks IIIrd among gynaecological malignancies next to cervix and ovary • Incidence: 2 per 1 lakh • Unlike cancer cervix, cost effective screening program is not available • Common in postmenopausal women • Increasing incidence due to  Increased screening  Improved hysteroscopic diagnosis  Increase in geriatric population  Estrogen use • SURGICO PATHOLOGICAL STAGING, as opposed to clinical staging
  • 3. Epidemiology • Most frequent genital cancer in rich countries • MEAN AGE: 60 years • PEAK INCIDENCE: 55-70 years • 20-25% - perimenopausal • 5% - <40 years • 5 year survival for stage I disease more than 90% • Overall 5 year survival for all stages: 60-70%
  • 5. ENDOGENOUS ESTROGEN DEPENDENT EXOGENOUS ESTROGEN HEREDITARY Nulliparity, low parity Unopposed estrogen therapy LYNCH II / HEREDITARY NON POLYPOSIS COLORECTAL CANCER – HNPCC SYNDROME PCOD tamoxifen Early menarche, late menopause Functioning ovarian tumours Obesity Hypertension Diabetes hyperlipidaemia
  • 6. Protective factors / Prevention • Oral contraceptive pills (combined pills with addition of progesterone to HRT) • Smoking (as it decreases level of estrogen, decreases weight and associated with earlier age of menopause) • Multiparity • Phytoestrogens • Green tea • Coffee • Physical exercise • Treatment of PCOS • MIRENA IUCD- effective in simple hyperplasia • Early screening , while pt is on TAMOXIFEN
  • 7. PATHOLOGY • Localized/ diffuse • App – nodule/ polyp/ diffuse lesion • Involving entire uterine cavity
  • 8. HISTOPATHOLOGY • Adenocarcinoma / endometrioid 80% • Adeno acanthoma • Adenosqamous carcinoma 15% • Papillary serous adenocarcinoma • Mucinous adeno carcinoma • Clear cell carcinoma • Undifferentiated • Mixed
  • 9. SPREAD • DIRECT EXTENSION – Most common • Lymphatic spread - occurs to pelvic and para- aortic nodes, fundus – para aortic nodes, round ligament – supl inguinal nodes • Hematogenous spread (usually to lungs, liver, brain, bone) is rare • Trans tubal – ovaries, pelvis, peritoneal cavity
  • 10. GRADE 1 : The glandular pattern is maintained, but cells show atypia GRADE 222 : some glands show a papillary pattern and are solid GRADE 3 3 : glands are solid with cellular proliferation, and glandular architecture is lost, endometrium is packed with glands and little stroma GRADING (FIGO) Depends on differentiation , glandular architecture and anaplasia of cells
  • 11. GRADE 1 GRADE 2 GRADE 3
  • 12. Histological differences in endometrial cancer FEATURES TYPE I ENDOMETRIOID 80% TYPE II (NON ENDOMETRIOID) 20% Unopposed oestrogen present Absent Menopausal status Pre and perimenopausal Postmenopausal Hyperplasia present Absent Race white Black Grade low High Myometrial invasion Minimal Deep Specific subtypes Endometrioid Adeno CA grade 1,2 Serous, clear cell, adeno CA grade 3 Behavior stable Aggressive Associated gene Pten/Kras p53 Good prognosis Poor prognosis
  • 14. Clinical features • Asymptomatic – 7 to 10% • POST MENOPAUSAL BLEEDING • irregular vaginal bleeding • Discharge per vagina:  brown , watery offensive discharge  watery discharge free from blood-hydrorrhoea • Past H/O PCOS, HRT • Obesity/ HTN / DM – CORPUS CANCER SYNDROME
  • 15. pelvic pressure/ discomfort Referred pain in hypogastrium / both iliac fossa - simpson’s pain Pain – not severe, tends to occur at the same time each day, lasting for 1-2 hours LUMP - Hematometra / pyometra in cervical stenosis
  • 16. • P/V : uterus bulky/normal • Bulky uterus – growth / fibroid/ pyometra • Adnexal mass – feminizing/ metastatic ovarian tumours • Advanced stage: cervix bulky, mass protruding through the os, suburethral vaginal nodule
  • 17. INVESTIGATIONS • PAP SMEAR • Endometrial aspiration • Fractional curretage • Hysteroscopy and biopsy – GOLD STANDARD • TVS – ET – irregular line / polyp / ovarian tumour / ovarian metastasis / extension to endocervix • Doppler ultrasound- low RI 0.37 to 0.7 or below – EC • SALINE INFUSUION SONOGRAPHY • CA 125
  • 18. INVESTIGATIONS • Contrast enhanced computerized tomography CECT – hypodensity in myometrium – myometrial infiltration • Pelvic and para aortic nodes >1cm • CT IS SUPERIOR THAN MRI in detecting ascitis , bowel , and omental metastasis • MRI – superior to CT in detecting myometrial invasion, nodal enlargement (90%) • Endometrial and myometrial junction – low intensity zone exists – intact – myometrial invasion ruled out • MRI useful in endocervical stromal invasion • XRAY CHEST – lung metastasis • Bone and liver metastasis – RADIO ISOTOPE SCANNING – PET CT – reveal metabolic activity in tissue and lymph node- helpful for staging
  • 19. DIFFERENTIAL DIAGNOSIS • Senile endometritis • Tubercular endometritis • Atypical hyperplasia • Endometrial polyp
  • 20. • Hyperplasia without atypia • Atypical hyperplasia/ EIN (Endometrial intraepithelial neoplasia) • TREATMENT: • endometrial hyperplasia without atypia – progesterone oral / LNG IUS / MPA 10-20mg/day / norethisterone 10-15mg/ day for 6 months • ATYPICAL HYPERPLASIA – risk of EC = 8-29% - total hysterectomy • Young – high dose of progesterone with frequent evaluation of endometrium - biopsy New WHO classification of endometrial hyperplasia - 2014
  • 22. TREATMENT • SURGICO – PATHOLOGICAL STAGING • ABDOMINAL HYSTERECTOMY • BILATERAL SALPHINGO – OOPHRECTOMY • OMENTECTOMY • PELVIC AND PARA AORTIC NODE SAMPLING Remain the CORNER STONE for management of early endometrial carcinoma
  • 23. STAGE WISE MANAGEMENT OF ENDOMETRIAL CANCER Stagewise Management Stage I A grade 1 Surgery only Stage I A grade 2, 3 Stage I B grade 1, 2 Sugery + vaginal brachytherapy Stage IB grade 3 Surgery + vaginal brachytherapy +external beam radiotherapy to pelvis Stage II Surgery + external RT + Vaginal brachytherapy Stage III Surgery + external RT + Vaginal brachytherapy + Chemotheraoy Stage IV Palliative RT + Chemotherapy + high dose progesterone
  • 24. SURGERY • TAH with BSO +omentectomy (non endometriod type) • Vaginal hysterectomy- obese, DM, prolapse  morbidity is less + LAP lymphadenectomy / post operative radiotherapy • Modified Wertheims hysterectomy- stage II • Debulking surgery – stage III • Laparoscopic surgery  Definite role in incompletely staged patients to decide for adjuvant therapy • Robotic surgery gaining importance
  • 25. RADIOTHERAPY • Vaginal vault irradiation – vaginal ovoids – dose = high dose rate Iridium / Low dose rate Cesium via COLPOSTAT to deliver 6000 cGy/6 weeks • EXTERNAL PELVIC IRRADIATION: Stage IB G3, Stage II, III Dose: 4500 – 5040 cGy – 5-6 weeks • EXTERNAL FIELD RADIATION: 4500 – 5000 cGy- positive para aortic nodes • WHOLE ABDOMEN IRRADIATION: Papillary serous, clear cell, adnexal upper abdominal disease excised • PRIMARY RADIOTHERAPY: inoperable stage III,IV- brachytherapy + External RT + uterine cavity packed with Heyman capsules
  • 26. CHEMOTHERAPY • High risk tumours to reduce and prevent extra pelvic failure • CYCLOPHOSPHAMIDE +ADRIAMYCIN + CISPLATIN – 6 cycles – 2 year progression free survival HORMONE THERAPY • MDPA 1g weekly or 200mg orally daily • 17 α progesterone 1g weekly or northiesterone • Tamoxifen 10mg twice daily • Doxorubicin, platinum, taxane, carboplastin – under trial
  • 27. STAGE III • Surgico pathological staging – TAH BSO / Radical hysterectomy / debulking – SURGICAL IRRADICATION, followed by RT / Chemo • Stage III B, C – inoperable – pelvic radiation followed by surgery or • external beam RT or extended field RT followed by intra uterine and intra vaginal brachytherapy • STAGE IV – debulking surgery / radiotherapy(whole abdomen irradiation)
  • 28. FOLLOW UP • First 3 years = every 3-4 months • Next 3-5 years = every 6 months • Annually thereafter • Each visit physical , pelvic examination pap smear USG CA 125 CT, MRI – when indicated Chest Xray FNAC/ LAP/ Laparotomy – pelvic/ distant recurrences
  • 29. Post operative management based on histopathological type , peritoneal cytology, grade, LVSI, Cervix/isthmus invasion, node, adnexal metastases, intra abdominal and distinct metastases Low risk:  G1 without myoinvasion  No cervix/isthmus invasion, LVSI, METASTASIS  Negative peritoneal cytology  Tumour < 2 cm No further management Intermediate risk:  G1, G2 with <50% myometrial invasion  No cervix/isthmus invasion, LVSI, METASTASIS  Negative peritoneal cytology POST operative intra vaginal ovoid brachytherapy High risk:  G3 tumours  Myoinvasion >50% Adnexal spread cervical invasion  Lymph node metastasis  LVSI  Clear cell , PSC histology  Intra abdominal / distant metastasis  Whole pelvic RT Extended field RT if aortic / common iliac nodes have metastases/ CT
  • 30. PROGNOSTIC VARIABLES IN ENDOMETRIAL CARCINOMA • Age • Histological type • Histological grade • Myometrial invasion • LVSI • Isthmus/ cervix extension • Adnexal involvement • Lymph node metastasis • Intra peritoneal tumour • Tumour size • Peritoneal cytology • Hormone receptor status • DNA/ ploidy / proliferative index • Genetic / molecular tumour markers
  • 31. Pre operative evaluation: • HISTORY, examination • Fractional curretage/ hysteroscopy • Imaging – USG, CT ,MRI , CHEST XRAY • Serum CA 125 SURGICAL = vertical incision/ LAP Peritoneal cytology/ exploration Type I hysterectomy with BSO Cut section: tumour sixe, grade, MI ENDOMETRIOID, no adverse risk factors: G1, MI <50%, Tumour <2cm NO FURTHER SURGERY  SURVEILLANCE High risk / NON ENDOMETROID
  • 32. ENDOMETRIAL CANCER DIAGNOSED POST HYSTERECTOMY • High risk factors identified: COMPLETE SURGICAL STAGING • ALTERNATE = external beam radiation to the pelvis
  • 33. Recurrent endometrial cancer MC time of recurrence Within first two years MC symptom of local recurrence Vaginal bleeding MC symptom of pelvic recurrence Pelvic pain MC site of recurrence Vagina and pelvis MC site of extrapelvic recurrence Lung LN (Aortic) Liver Brain Bones
  • 34. Management • For patients with recurrent endometrioid tumours with hormone receptors positive, initial treatment is progestin • Contraindication to progestin  TAMOXIFEN • Hormone negative  local management • If Operable – surgery to be done • If inoperable – RT is given • If local treatment cannot be given – palliative chemotherapy is given