1 / 48

Endometrial Cancer

Endometrial Cancer. Speaker : Shinenoam Chen Department of OBS/GYN. VGHKS. Introduction. Endometrial carcinoma is the most common gynecologic malignancy in the United States. Most cases are diagnosed at an early stage when surgery alone may be adequate for cure. Introduction.

ssonia
Download Presentation

Endometrial Cancer

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Endometrial Cancer Speaker : Shinenoam Chen Department of OBS/GYN. VGHKS

  2. Introduction • Endometrial carcinoma is the most common gynecologic malignancy in the United States. • Most cases are diagnosed at an early stage when surgery alone may be adequate for cure.

  3. Introduction • Type I endometrial carcinoma is estrogen-related: 1. tends to be associated with endometrial hyperplasia. 2. low grade endometrioid tumor 3. risk factors such as obesity, nulliparity, endogenous or exogenous estrogen excess, diabetes mellitus, and hypertension.

  4. Introduction • Type II endometrial carcinoma appears unrelated to estrogen : 1. older , multiparous. 2. poor prognostic cell types, such as papillary serous or clear cell tumors.

  5. ERT • Estrogen Tx alone increases the risk for endometrial hyperplasia and carcinoma. • Endometrial hyperplasia: 20-50% of women receiving unopposed estrogen in one year. • RR: 3.1-15 (related to dose and duration)

  6. ERT • Risk can be reduced by the concomitant administration of progestins.

  7. Endogenous estrogen • Functional ovarian tumors • Endogenous conversion of adrenal precursors into estrogen by adipose cells (estrone hypothesis) • Higher circulating estrogen and androgen levels, and lower SHBG levels.

  8. Tamoxifen • Competitive inhibitor of estrogen binding to estrogen receptors. • adjuvant therapy in women with early stage breast cancer, as treatment for recurrent disease, and for reduction of breast cancer incidence in high-risk women. • partial agonist activity, stimulating the endometrial lining.

  9. Tamoxifen • 2-3fold increased risk of endometrial cancer. • ACOG:the benefits outweigh the risks. Recommendations : 1.Annually Gyn exam. 2.Report vagina bleeding 3.Tx limited to 5 years 4. Hysterectomy if atypical hyperplasia.

  10. Obesity • high levels of endogenous estrogen. • Conversion of androstenedione to estrone and the aromatization of androgens to estradiol, both of which occur in peripheral adipose tissue. • lower circulating levels of sex hormone binding globulin.

  11. Obesity • Increased risk of death from endometrial cancer. • BMI ( 40 kg/m2) was 6.25-fold higher than that of normal weight women.

  12. Diabetes and hypertension • Increased risk for endometrial cancer, associated with obesity. • The effects of hyperinsulinemia, insulin resistance, and insulin-like growth factors on endometrial proliferation are under investigation.

  13. Chronic anovulation(ex.PCOS) • Adequate estrogen since androgens can be converted peripherally to estrogens. • Lack the progesterone normally present in the luteal phase. • constant estrogenic stimulation leading to endometrial hyperplasia and endometrial cancer.

  14. Age • 12 % of all patients with endometrial adenocarcinoma were under 50 years of age. • Common features of these cases were obesity (56 percent had a BMI 30 kg/m(2)) and nulliparity (44 percent).

  15. Parity • Nulliparity • High frequency of anovulatory cycles in infertile (and thereby nulliparous) women.

  16. Menarche and menopause • Early menarche or late menopause was a risk factor for endometrial cancer. • Prolonged estrogen stimulation without the protection of progesterone is the presumed mechanism.

  17. Protective factors • Oral contraceptives-progestin component suppresses endometrial proliferation. The protective effect persisted for at least 15 years after cessation of use. • Physical activity-changes in endogenous sexual and metabolic hormone levels and growth factors, decreased obesity and central adiposity, and changes in immune function • Smoking-smoking stimulates hepatic metabolism of estrogens.

  18. HISTOPATHOLOGY • The most common type of endometrial cancer is endometrioid adenocarcinoma (75-80%). • Clear cell type(1-5%) and papillary serous carcinomas(5-10%): much poorer prognosis • Well differentiated (gade I) : proliferation of back-to-back endometrial glands without intervening stroma. There is no more than 5% solid growth.

  19. HISTOPATHOLOGY • Moderate differentiated (grade 2) tumors have 6-50% of the tumor composed of solid tumor without glands, as well as greater nuclear atypia. • Poorly differentiated (grade 3) tumors contain more than a 50% solid component.

  20. CLINICAL PRESENTATION • The classic symptom of endometrial carcinoma is abnormal uterine bleeding. • 20%of women with postmenopausal bleeding will have endometrial cancer. • Pre- and perimenopausal women with menometrorrhagia also should be evaluated.

  21. Endometrial cells on Pap smear • The presence of endometrial cells on a Pap smear of a woman 40 years of age can signify endometrial disease. • Endometrial disease was identified in 36%, including endometrial hyperplasia in 13% and adenocarcinoma in 11%. • Endometrial biopsy is recommended.

  22. DIAGNOSIS • Diagnosis of endometrial cancer is most easily made by office endometrial biopsy. • Hysteroscopy with dilation and curettage (D&C) remains the gold standard. • A higher grade based on the hysterectomy specimen may be assigned in as many as 30% of cases.

  23. DIAGNOSIS Transvaginal ultrasonography • measuring the endometrial wall thickness • In postmenopausal women, an endometrial thickness of less than 4 to 5 mm is associated with a low risk. • The mean endometrial thickness in 759 women with endometrial cancer is 20 mm.

  24. DIAGNOSIS Sonohysterography • Differentiate Polyp or cancer. • Biopsy or resection via the hysteroscope.

  25. Pre-operative survey • ECC • MRI- assess cervical involvement and depth of myometrial invasion. • Tumor marker: CEA, Ca125, Ca199- predicting extrauterine spread of endometrial cancer, and for following patients after initial treatment

  26. Deep invasion (>50% of the myometrial thickness) of endometrial carcinoma (arrow).

  27. TREATMENT • Surgery • Chemotherapy • Radiation therapy • Hormone therapy

  28. Surgery • ATH+BSO+BPLND+ Paraaortic LN sampling. • Washing cytology. • MRH if cervix involved. (proved by ECC) • Laparoscopic lymphadenectomy combined with vaginal hysterectomy, provide an acceptable alternative to traditional laparotomy in patients with early stage disease.

  29. Endometrial cancer with <1/2 myometrial invasion

  30. Surgical staging *Grade 1.2 *No or minimal myometrial invasion Ib or G3 IbG3 or Ic.II.III *Adnexal spread *Intraperitoneal dz completely resected Positive peritoneal cytology Observe Vagina radiaion Pelvic RT&vagina Boost(extended filed if positive Para-aortic LN) Whole abdominal radiation or C/T Observe or progestins Management of stage I and II endometrial cancer

  31. Treatment by stage • Stage Ib or G3 : vagina R/T • IbG3 or Ic: pelvic R/T. • Stage II: +C/T

  32. Radiotherapy • Intermediate risk- Ic, II adjuvant RT : vaginal cuff brachytherapy +/- external beam RT is controversial. *Reduction in the rate of vaginal or pelvic recurrence, but not the survival. • High risk- vaginal cuff brachytherapy, pelvic external beam RT, and whole abdominal irradiation (WAI). *Reduce the likelihood of local recurrence, and possibly prolong survival.

  33. Chemoherapy • Regimens: PEI – Cisplatin + Epirubicin + Holoxan ( q3w X6 courses). • GOG122- Chemotherapy versus RT -Stage III or IV -WAI vs (doxorubicin 60 mg/m2 plus cisplatin 50 mg/m2 q3w for 7 courses, followed by an additional course of cisplatin) -Chemotherapy was superior to WAI in terms of two-year overall survival. • Taxol+carboplatin • CCRT

  34. Hormone therapy • PR: PR(-) correlated to LN metastasis and poor survival rate. • ER: less predictive than PR. Absence of ER was predictive of recurrence for stage I tumors • Progestin (synthetic progesterone) may be used to help stop the cancer from spreading. • response rate :30%

  35. Decision tree concerning the treatment of recurrent endometrial carcinoma.Legend: ENCA = endometrial carcinoma; QoL = Quality of Life; RT = radiotherapy; HT = endocrine treatment; CHT = chemotherapy

  36. Prognosis • 5 year survival:

  37. Prognosis • LN metastasis rate: • Stage I: 10% ( stageII: 15%) • G1:3% G2: 9% G3:18% • <1/2M: 5% >1/2M: 20% • Prognostic factor: Stage, grade, cell type, LN.

More Related