You are on page 1of 22

Endometrial

Carcinoma
General considerations
 Most occur in the sixth and seventh
decades.
 Incidence : 1.3%-2.4%
 Consequent: the overall prognosis is
better.
Etiology
 Unknown
 Estrogen ( diabetes mellitus,
hypertension, polycystic ovary
syndrome, obesity, tamoxifen. )
 Family history: ovarian, colon, or
breast cancer.
 Certain oncogenes: Ha-, K-, N-ras, c-
myc, Her-2/neu, p53, PTEN
Histopathologic
classification
 Endometrial hyperplasia: simple;
complex; atypia
 Hyperplasia without atypia: simple–
1% Ca. Complex– 3% Ca. -- not
considered premalignant.
 Hyperplasia with atypia: respectively
8%- simple and 29%- complex
become Ca.
 Carcinoma in situ:
Endometrial carcinoma
 Adenocarcinoma :
 Adenocarcinoma with squamous
differentiation:5%
 Adenosquamous carcinoma:10-20%,
prognosis is worse
 Serous carcinoma: spread early.
 Clear cell carcinoma:
 Miscellaneous subtypes:
Possible routes of spread
 Direct extension
 Lymphatic metastases
 Peritoneal implants after
transtubal spread
 Hematogenous spread
Surgical staging
 Stage I: 75% a—limited to
endometrium; b—less than ½; c—
invasion more than ½
 Stage II: 11% a—endocervical
glandular invovement only; b—
cervical stromal invasion
 Stage III: 11% a—serosa, adnexa,
peritoneal; b—vaginal metastases; c
—pelvic or aortic lymph nodes
 Stage IV: 3% a—bladder or bowel
mucosa; b—distant metastases.
Clinical findings
 Symptoms and signs: abnormal
bleeding; abnormal discharge;
( postmenopausal bleeding – 20%
underlying cancer; 12-15%
endometrial carcinoma; others–
sarcoma…>80ys ½ cancer ); lower
abdominal cramps and pain;
 Bimanual or rectovaginal
examination: enlarged, soft,
pyometra.
Clinical findings
 Laboratory
findings: anemia;
pap smear;
Clinical findings
 Special examination:
1. Fractional curettage.
2. Endometrial biopsy: aspiration
biopsy; aspiration curettage
3. Pelvic ultrasonography
4. Estrogen and progesterone
receptor assays: patients with
receptors positive have longer
survival than negative.
Differential diagnosis
 Abortion
 Leiomyoma, hyperplasia, polyps,
genital cancer. Ovarian neoplasms.
Metastatic cancers.
 Atrophic vaginitis; exogenous
estrogens; endometrial hyperplasia
and polyps; genital neoplasms.
 D and C negative – tubal and ovarian
cancer? –hysterectomy and bilateral
salpingo-oophorectomy
Complications
 Perforation
 Peritonitis
 Pyometra
 Anemia
Treatment
 Surgery and radiation
Surgical treatment
 Hysterectomy
 Radical hysterectomy
Radiation therapy
 Extrauterine extension
 Lower uterine segment or cervical
involvement
 Poor histologic differentiation
 Papillary serous or clear cell
histology
 Myometrial penetration greater
than1/3 of the full thickness
Hormone therapy
 Progesterone
 >3 months
Antitumor chemotherapy
 Doxorubicin
 Cisplatin
 Carboplatin
 Cyclophosphamide
 5- fluorouracil
General and supportive
measures
 Most patients with weak, anemia,
diabetes, hypertension, and so on.
Prognosis
 Worse – high age; higher pathologic
grade; clinical stage; greater depth
of myometrial invasion.
 5-year survival rates: 81-91% for
surgical stage I; 67-77% for stage II;
31-60% for stage III; 5-20% for stage
IV.
 No risk factors – TAH+ bilateral
salpingo-oophorectomy >95% at 5
years.
Prevention
 Estrogen + progesterone for one
cycle.
 Monitor high risk patients.