endometrial cancer

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Endometrial Cancer

• S.P CHUWA.
• For MD 3 2023

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Outline

• Introduction
• Epidemiology
• Etiology/Risk Factors
• Clinical presentation and examination
• Diagnosis and Staging
• Management
• Follow up
• Prevention

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Introduction

• Corpus cancer is the most frequently occurring
  female genital cancer in developed countries but
  with low death rate due to its early
  presentation.
• In developing countries the leading cause of
  death from genital malignancy is cervical cancer.
• Epidermic of obesity with its associated
  commorbidity diabetes and hypertension has
  increase the incidence of endometrial cancer in
  developed countries.

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Etiology

• The exact cause not clear-aetilogy has been
  associated with-
• Null parity 2-3-times compared with multiparity.
• Early menarche lt 12 years with Late menopause
  (aged gt52 y)
• Obesity (presence of fat appears to be
  responsible for the conversion of androstenedione
  by the ezyme aromatase to estrogen compounds at
  a much higher rate.

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Cont..

• Unopposed estrogen
• Unopposed estrogen-eg 1. granulosa cell tumor
• 2.
  polycystic ovarian disease
• Tamoxifen-for treatment of breast cancer.
• increased incidence of endometrial
  adenocarcinoma -
• tamoxifen-antestrogenic effect on the breast
  but has estrogenic effect on the
  endotrium-increase endometrial hyperplasia.

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Cont..

• Family history-
• Hereditary nonpolyposis colon cancer (HNPCC)
  Lynch syndrome autosomal dominant syndrome
  germcell mutation in mismatch repair genes MLH1
  and MSH 2 positive family history of this
  syndrome increases risk of colorectal,ovarian and
  endometrial cancer.

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• Diet-Risk increase with diet having high animal
  fat
• Coexisting Medical Condition-hypertension and
  diabetes mellitus.
• Estrogen replacement therapy after menopause.

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Protective Factors

• Smoking
• Apparently decreases the risk of developing
  endometrial cancer.
• effects- 1.Weight reduction
• 2.Smoker undergoes menopause 1-2
  years earlier than non smoker
• 3.Increase breakdown of estrogen
  by the liver.
• But the risk of lung cancer out weight this
  benefit.

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• Combined oral contraceptives
• decreases the risk of developing endometrial
  cancer.
• Protection occurs if used for at least 12/12 (one
  year), and protection continues for at least 10
  yrs after OC use.

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Phenotype characteristics/classification

• Classic phenotypic characteristic was thought to
  exist for a woman who would develop endometrial
  cancer.
• This phenotype included patients who were obese,
  nulliparous, and anovulatory in many instances.
• More recently, the existence of 2 pathogenic
  types of endometrial cancer was appreciated.

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Type-i

• Occurs in women who fall into classic category.
• Obese and have hyperlipidemia
• Signs of hyperestrogenism
• Uterine bleeding
• Infertility
• Late menopause
• Hyperplasia of (ovary, endometrium)
• They are white, obese, nulliparous, and have
  well-differentiated superficially invasive
  cancers that are sensitive to progesterone.
• Have favorable prognosis, extrauterine dss is
  unusual in this group of pts.
• Commonest endometrial cancer

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Type-ii

• Occurs in women who have none of the disease
  states present in the classic presentation.
• These individuals
• Poorly differentiated tumors
• Deep myometrial invasion
• High degree of metastasis to the lymph nodes and
  other sites
• Decreased sensitivity to progestin's
• Poor prognosis
• These patients tend to be thin, multiparous, and
  African American.

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Clinical Features

• 75 of endometrial cancer occurs in
  postmenopausal women.
• post menopausal bleeding.
• Premenopausal presents with irregular or
  excessive pv bleeding.
• Advance disease-Pelvic pain,dysuria,abdominal
  mass, weight loss
• Watery/offensive pv discharge-in case of
  pyometra.

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Physical examination.

• Pelvic examination
• Speculum examination- cervix healthy , blood or
  purulent offensive discharge escapes out of the
  external os.
• Bimanual examination/rectal vaginalexam-uterus is
  either atrophic, normal or enlarged due to
  spread of the tumor, associated fibroid or
  pyometra initially mobile but in late stage
  fixed.

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Diagnosis.

• Diagnostic approach-A.Hx and physical
  examination B.
• B.Histology C.Direct visualizatio(hysterescopy)
  D.Radilogy.
• E.Estrogen progesterone receptor assay.
• Post menopausal bleeding should considered
  endometrial cancer unless proved.
• Endometrial biopsy-can done as an out patient
  procedure.
• Transvaginal ultra sound.

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• HysteroscopyIt helps in direct visualization of
• endometrium and to take target biopsy.
• Computed Tomography (CT) scan of pelvis
• detect lymph node metastasis also distant
  metastasis-liver/lung.
• Magnetic Resonance Imaging (MRI) can detect
• myometrial invasion and cervical stroma
  involvement

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Endometrial Biopsy.

• Methods-A.Fractional Dilation and curratage
• B.Office biopsy- Pipelle,
  Novak Curet and Vabra aspirator .
• A.Fractional DC
• -Definitive procedure for diagnosis of
  endometrial carcinoma.
• -Patient should be under general anaesthesia.

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cont

• Steps fractional DC
• 1. curettage of the endocervical canal
• 2. dilatation of the canal
• 3. circumferential curettage of the endometrial
  cavity.
• Sample should be kept in different container and
  labeled.
• Complication-perforation of the uterus it should
  performed gently and terminated after obtaining a
  sufficient sample.

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• B.Office Biopsy
• 1.Does not require general anaesthesia-can be
  performed by paracervical block
• 2.Reduce cost
• 3.Rerformed as an office procedure
• -Dis advantage-high false negative.
• -Formal DC should be performed in asymptomatic
  patient with negative biopsy.

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• Vaginal ultrasonography
• Endometrial thickness gt 5mm
• Hyperechoic endometrium with irregular outline
• Increased vascularity with low vascular
  resistance

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Imagine cont..

• Hydroultrasonography
• R/o false-positive result
• This is accomplished by placing a small volume of
  saline into the endometrial cavity and then
  repeating the vaginal ultrasonogram.
• Hysteroscopy /- Biopsy.
• hydrosonography/hysterescopy can lead to
  spillage of cancer cells through fallopian tube.

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Histological classification endometrial cancer
WHO 2003.
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• Endometrioid Adenocarcinoma-commonest
  endometrial cancer (75).
• Contains gland similar to normal endometrium.
• Glandular component determine the differentiation
  of tumour high glandular component less
  aggressive without myometrial involvement-decrease
  glandular component less diffentiated with
  metastasis-this occur in atrophic endometrium.

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• Serous Carcinoma.
• 5 to 10 of endometrial cancers.
• Highly aggressive arise from the atrophic
  endometrium of older women.
• Commonly referred as uterine papillary serous
  carcinoma-due to its papillary pattern
• Its resembles serous epethelian ovarian cancer
  30 demonstrate psammona bodies.
• Produce tomour marker CA -125.

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• Clear Cell Carcinoma.
• 5 endometrial cancers
• Endometrial clear cell adenocarcinomas are
  similar to those arising in the ovary, vagina,
  and cervix
• high-grade- deeply invasive tumors.
• often are diagnosed with advanced disease and
  have a poor prognosis.

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• Mucinous Carcinoma.
• 1 to 2 of endometrial cancer.
• have a glandular pattern
• Since endocervical epithelium merges with the
  lower uterine segment, the main diagnostic
  dilemma is differentiating this tumor from a
  primary cervical adenocarcinoma-thus can be
  differentiated with immunohistochemistry.

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Pre operative evaluation

• Blood Exam
• Urine Exam
• X-ray
• Pelvic Ultrasaund
• MRI
• Renal and Liver profile
• Streroid receptor status
• Serum Makers CA 125

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Modes of Spreads

• Local Spread- invasion of the myometrium and
  vaginal vault are the commonest
• Venous Spread- occurs late (lung, liver bones and
  brain)
• Lymphatic Spread- usually late and involves
  pelvic para aortic and rarely inguinal and
  femoral lymph nodes

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Endometrial cancer FIGO Staging 1988.
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• Staging of endometrial cancer should correspond
  with grading
• G 1-mild differentiated
• G2-Moderate Diffentiated
• G3-Severly diffentiated.

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Prognosis

• Prognostic factors
• Stage of the disease
• Myometrial invasion
• Degree of differentiation
• Ploidy status
• Age at diagnosis
• Morphometric assessment
• Tumor size gt2cm
• Hormonal receptor status
• Extension to the cervix
• Lymph nodes metastasis
• Peritoeal cytology

• Prognosis ( 5 year survival).
• Stage I82.9
• Stage II 70.8
• Stage III 39.2
• Stage IV 27.3
• All stages 78.1

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Management

• Stage I.
• Surgical treatment. (TAH BSO)
• Adnexae are removed bse the risk of containing
  subclinical tumour rather than to eliminate any
  hormonal influence they may have.
• Role of lympadenectomy is to identify those women
  without nodal disease who may not need
  radiotherapy complications.

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Stage II.

• If no obvious involvement of the cervix.
• Management is as in stage I.
• If there is obvious cervical involvement and if
  surgically fit-
• -radical hysterectomy
• -bilateral pelvic lympadenectomy
• -paraortic node sampling
• -radiotherapy

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Stage III.

• If the disease is confirmed to pelvic then
  radiotherapy is the treatment of choice.
• If adnexae involved, then do laparotomy and
  remove as much tumour as possible, remove the
  omentum.
• Stage IV.
• Lungs are the most site of metastases in patients
  with extra pelvic disease followed by peripheral
  lymph nodes and bladder.
• Mnx. Should be individualized and aim to-
• -symptom alleviation
• -local tumour control
• -radiation therapy, cytotoxic drugs and
  hormonal therapy may all be required.

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Recurrent dzz

• Majority(600) occurs within 2yrs of initial
  treatment
• Common sites are vaginal and the pelvis
• Extra pelvis are to the lungs, aortic lymph
  nodes, liver , and bones.
• Management Radiation therapy following surgery
• Hormonal and chemotherapy
• Extensive surgeries (have no value)

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Follow up

• Following initial therapy
• Examination every 4/12 (four monthes)for 2 years,
  6/12 (six monthes)for next 2 years and then
  annually
• (symptoms and clinical examination,
• Ivestigastions Cxr, Mamography, CT, and serum CA
  125)

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Prevention

• Strictly weight control beginning early in life
• Restrict use of estrogen after menopause
• Education on the irregular bleeding in post
  menopausal women
• Screening for the higher risk pts.