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Endometrial Cancer: Understanding Risks, Symptoms, Diagnosis & Treatment
- 2. DEFINITION Malignant tumor that arises in the lining of the uterus
- 3. EPIDEMIOLOGY • It is the most common gynaelogical cancer in developing countries, while in developed countries it is the second most common cancer, behind cervical cancer. • In year 2012 a total of 320,000 new cases were recorded. • Globally, it is the sixth most common cancer in women, fourteenth most common overall. • In Peninsular Malaysia, it is the seventh most common cancer in women, according to Malaysian cancer Registry 2006. • It is rare among women younger than 40 years. • Peak incidence occurring at age 60-69. • Majority are of Chinese ethnicity (47.5%), followed by Malays (41.6%) and Indian (10.9%).
- 4. TYPES • Type 1 (Endometrioid Carcinoma) is the most common (80%) • Type 2 (Serous Carcinoma) is less common (20%) TYPE 1 (Endometrioid Carcinoma) TYPE 2 (Serous Carcinoma) Age 50-60 70 Cause Related to estrogen Not related to estrogen Risk Factor Obesity, DM, Late Menopause, Nulliparity, Cancer, Unopposed Estrogen, Tamoxifen, Family History Atrophic endometrium/ polyp Precursor Lesion Atypical endometrial hyperplasia Intraepithelial carcinoma Example Endometrioid Adenocarcinoma Clear cell & papillary carcinoma Genetic PTEN mutation P53 mutation Metastasis Lymph node, ovarian involvement Peritoneum Prognosis Good Poor
- 5. RIK FACTOR • Remember OLD AUNT Type 1 Endometrioid Carcinoma Obesity Late Menopause DM Cancer Unopposed Estrogen Nulliparity Tamoxifen
- 6. • OBESITY ✓↑ body fat ✓↑ estrogen ✓↑ endometrial proliferation • LATE MENOPAUSE ✓↑ menstrual cycles during a woman's lifetime ✓↑ estrogen ✓↑ endometrial proliferation • DM ✓insulin ↑ the growth of endometrial stromal cells • CANCER ✓hereditary nonpolyposis colorectal cancer (HNPCC) syndrome is caused by a germline mutation in one of several DNA mismatch repair (MMR) genes ✓Carriers of MMR gene mutations are at increased risk of cancers of the colon and endometrium • UNOPPOSED ESTROGEN ✓Hormone replacement therapy in postmenopausal women ✓↑ secretion due to androgen- secreting tumor or stress • NULLIPARITY (never gave birth) ✓↑ ovulation cycles ✓↑ estrogen ✓↑ endometrial proliferation • TAMOXIFEN (drug for breast cancer) ✓it acts like an estrogen in the uterus ✓ ↑ estrogen ✓In women who have gone through menopause, it can ↑ endometrial cell growth
- 7. Type 2 Serous Carcinoma Endometrial Atrophy Occurs in post menopausal women Normally, when cells grow old or get damaged, they die, and new cells take their place. Old or damaged cells however do not die as they should. The buildup of extra cells often forms a mass of tissue called a growth or tumor. Smoking ↑ progesterone Endothelial cell proliferation
- 8. PATHOGENESIS • KEY WORDS PROTOONCOGENE • Involve in cell differentiation and proliferation ONCOGENE • Transform normal cell into cancerous cell ANTIONCOGENE • Suppress tumor cell
- 9. Both behave as a tumor suppressor gene (antioncogene) When mutated, loss of function Activation of protooncogene & oncogene Cancer cell formation PTEN • Located at chromosome 10 P53 • Located at chromosome 17
- 10. CLINICAL SYMPTOMS Clinical Symptoms Irregular vaginal bleeding, spotting, or discharge Painful and difficulty during urination Pain during sexual intercourse Pelvic pain Abdominal swelling due to the mass or due to fluid accumulation in the belly (called ascites) Persistent feeling of abdominal bloating with nausea or vomiting Changes in bowel movements, such as constipation Feeling full soon, after eating less Loss of appetite with weight loss Fatigue, feeling tired easily Frequent urination (polyuria)
- 11. MORPHOLOGY TYPE 1 (Endometrioid Carcinoma) TYPE 2 (Serous Carcinoma) Closely resemble normal endometrium Resembles ovarian serous carcinoma May be exophytic, infiltrative or villoglandular pattern May have glandular pattern and resemble villoglandular carcinoma on low power Mucinous, tubular ciliated and squamous (occasionally adenosquamous) differentiation. Usually well formed papillae (thick and thin) or tubules with "lobster claw" appearance Is graded I to III, based on the degree of differentiation Usually a high grade tumor and behave aggressively Exhibits atypical hyperplasia Exhibits endometrial atrophy Stroma present is usually desmoplastic Usually marked desmoplastic response resembling carcinosarcoma May have foamy cells due to tumor necrosis Psammoma bodies Tumor cells have moderate pleomorphism, prominent nucleoli Highly pleomorphic tumor cells containing prominent nucleoli, small detached buds and tufts Atypia with no intervening stroma Exhibit much greater cytologic atypia Vascular invasion is associated with chronic inflammation around lymphatics Prominent myometrial invasion, frequent mitotic activity and necrosis
- 12. STAGING • According to FIGO staging Stage 1 – Cancer is confined to the body of the uterus (corpus). • 1A: <50% of uterus 1B: >50% of uterus Stage 2 – Cancer has spread from the corpus to the cervix, but not beyond the uterus Stage 3 – Cancer has spread out locally/regionally3A: Tumor invades the serosa and/or adnexa • 3B: Vaginal and/or parametrial involvement 3C: Spread to pelvic and/or paraaortic lymph nodes 3C1: Pelvic lymph nodes only 3C2: Pelvic and/or paraaortic lymph nodes Stage 4 – Cancer has spread to the bladder and/or bowel mucosa, or beyond the pelvis to other parts of the body (distant metastasis) • 4A: Tumor invades bladder and/or bowel mucosa 4B: Distant metastasis
- 14. DIAGNOSIS Medical consultation Physical examination PAP smear Transvaginal ultrasound Endometrial biopsy (Preferred. More sensitive) Hysteroscopy Dilatation and curettage