En Dome Trial Carcinoma

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, cmyc, 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.