ovarian neoplasms. anita chudecka - głaz ovarian neoplasms

Ovarian neoplasms. Anita Chudecka - Głaz

Ovarian neoplasms.


• Human ovarian neoplasms (especially epithelial ovarian cancer) presents a major challenge to oncological research , because they are frequently diagnosed late and show poor prognosis and low survival despite the apparent success of chemotherapy in achieving remission with no evidence of disease.


Epithelial ovarian cancer is the fourth most common cause of death from cancer in women and the most lethal of gynaecologic neoplasms.

Epithelial ovarian cancer is the fourth most common cause of death from cancer in women

and the most lethal of gynaecologic neoplasms.


• The most important positive prognostic feature continues to be diagnosis at an early stage.

• BUT EARLY STAGE OVARIAN CANCERS DON’T PRODUCE

SYMPTOMS !!!


• The incidence of ovarian cancer is relatively high in Scandinavian (15/100000) countries , lower in western Europe and North America ( 10/100000 ) and low in Japan (3/100000).


ETIOLOGY

• Two hypotheses have been proposed to explain the biological mechanisms that increase the risk of ovarian cancer :

genetics

gonadotropin hypothesis


ETIOLOGY

The involvement of gonadotropins in human ovarian carcinoma is backed by a number of epidemiological and experimental studies showing:

increase occurrence of disease with exposure to high levels of LH , FSH during menopause , after ovariectomy or during fertility treatment


ETIOLOGY

reduced risk of cancer associated with multiple pregnancies, oral contraceptives , breast - feeding

LH and hCG receptors are expressed in 40% of epithelial ovarian cancer

LHRH receptors are expressed in almost 80% of EOC


ETIOLOGY

deficit of cases of ovarian cancer among women with diagnosis of alcoholism in

animals ovarian cancer may be induced by gonadal radiation or chemical toxins that cause premature oocyte death , but hypophysectomized animals do not develop ovarian tumours after oocyte depletion which suggests a specific role of gonadotropins


ETIOLOGY

other risk factors:

diettalcpelvic irradiationviruses age


ETIOLOGY

other risk factors:

PIDendometriosisblood grouplegal status education


SYMPTOMS

EOC oftenest are asymptomatic until advanced stage , when the prognosis is poor and 5 year survival less then 40%.

EOCoftenest are asymptomatic until advanced stage ,

when the prognosis is poor and 5 year survival less then 40%.


SYMPTOMS

Irrespective of histology , most ovarian neoplasms when they have large size in advanced stage cause symptoms by exerting pressure on contiguous structures (urinary frequency, pelvic discomfort and constipation).


SYMPTOMS

The most common :

abdominal swellingfatigueabdominal pain


SYMPTOMS

Upper abdominal metastases or ascites cause nausea, heart burn , bloating , weight loss and anorexia.

Acute abdominal pain secondary to haemorrhage , rupture or torsion can all result from tumour growth.


SYMPTOMS

Biologically active hormones , including estrogen, progesterone, testosterone , corticosteroids and hCG can be produce by a variety of ovarian neoplasms and cause the predicted symptoms associated with each compound.


DIAGNOSIS1. Physical examination-bimanual rectovaginal pelvic

examination

2. Ultrasound investigation

3. Tumour markers

4. Ascites puncture

5. Biopsy the tumour

6. Laparoscopy

7. CT

8. NMR

9. Chest X ray


ULTRASONOGRAPHY

abdominaltransvaginal TVS

colour Doppler CDI

ULTRASONOGRAPHY


TUMOR MARKERS

epithelial ovarian cancer

CA 125CA 125 CA 19-9 CEA


TUMOR MARKERS

endodermal sinus tumors

embryonal carcinomas

mixed germ cell tumorsrarely immature teratoma and polyembryoma

AFPAFP


TUMOR MARKERS

chorioncarcinoma

embryonal carcinoma

mixed germ cell tumors

polyembryoma

hCGhCG


TUMOR MARKERS

adult granulosa cell tumors

thecomas

ESTRADIOLESTRADIOL


TUMOR MARKERS

adult granulosa cell tumors

INHIBININHIBIN

PREMENOPAUSAL OVARIAN MASS

EXCLUDE NON-GYNAECOLOGICAL PROBLEM

Surgical evaluation

Solid or complex on US

OR > 6 cm

ORElevated

AFP/hCG/LDHOR

Elevated CA 125

Simple on USAND

< 6 cmAND

Normal CA 125

Observation for 6-8 weeksand

Gonadotrpopin suppression

Peristent on US

POSTMENOPAUSAL OVARIAN MASS

EXCLUDE NON-GYNAECOLOGICAL PROBLEM

SurgicalEvaluation

SymptomaticOROR

Complex on USOROR

> 3 cmOROR

Elevated CA 125

AsymptomaticANDAND

Simple on USANDAND

< 3 cmANDAND

Normal CA 125

Observe withFollow up

US


DIFFERENTIAL DIAGNOSIS

gynaecologic

tuboovarian abscessectopic pregnancyleiomyomafallopian tube neoplasialuteal or follicular cysts



gynaecologic

ovarian hyperthecosispregnancy luteomatheca-lutein cystsendometriomasimple cysts



nongynaecologic

diverticular diseaseappendiceal abscess Crohn’s diseaseprimary nongynaecological malignancypelvic kidney


CLASSIFICATION

1. Epithelial ovarian tumours - 70% of all ovarian neoplasms

2. Sex cord stromal tumours 5-10%

3. Germ cell tumours 15-20%

4. Metastatic 5 %

5. Other


Epithelial ovarian neoplasms

malignant

borderline

benign


serous

m ucinous

endom etrioid

clear cell

Brenner-transitional cell

m ixed m esoderm al

undifferentiated

unclassified

EOC(m alignant, borderline, benign)


SEX CORD STROMAL TUMOURS

1. Granulosa stromal cell granulosa cell thecoma-fibroma

2. Sertoli stromal cell

3. Lipid cell tumours

4. Gynanandroblastoma


GERM CELL TUMOURS

1. Dysgerminoma

2. Endodermal sinus tumour

3. Embryonal carcinoma

4. Polyembryoma

5. Chorioncarcinoma

6. Teratomas

7. Mixed forms

8. Gonadoblastoma


STAGE I

Growth limited to the ovaries


STAGE II

Growth involving one or both ovaries with pelvic extension


STAGE III

Tumour involving one or both ovaries with peritoneal implants outside the pelvis and/or positive retroperotoneal or inguinal nodes; superficial liver metastasis ; tumour is limited to the true pelvis but with histologically proven malignant extension to small bowel or omentum


STAGE IV

Tumour involving one or both ovaries with distant metastases; if pleural effusion is present , there must be positive cytology to allot a case to stage IV


Five - year survival rates for epithelial ovarian cancer

Stage

IA 82,3%

IB 74,9%

IC 67,7%

IIA 60,6%

IIB&IIC 53,8%

III 22,7%

IV 8 %


PREDICTORS OF SURVIVAL

stage grade age residual disease max. cytoreductive surgery histopathology others ( protein p53, CA 125, EGF-R)


TREATMENT

• surgical• chemotherapy• radiotherapy• hormonal treatment

postoperative

procedures

Nowotwory jajnika. Anita Chudecka - Głaz

SURGICAL TREATMENT

cytoreductive operation: hysterectomy bilateral oophorectomy omentectomy appendectomy lypmphadenectomy ??


CHEMOTHERAPY

• CT• PC• PAC

• Vepesid or

Ifosfamid with CDDP as II LINE CHT.

• Hycamptin or Gemzar as III LINE CHT.

I LINE CHEMOTHERAPY


SURGICAL TREATMENT - EOC

benignIn young women conservative surgery usually including

cystectomy or oophorectomy. In postmenopausal women TAH/BSO should be considered to avoid the risk of cancer in the future.

borderlineIn young women conservative surgery oophorectomy or USO

can be performed. In women who have completed their child bearing a TAH/BSO/Omentectomy is appropriate always with very precise surgical staging.


SURGICAL TREATMENT - EOC

malignantIn all cases we have to carry out cytoreductive

surgery. It includes TAH/BSO complete omentectomy with resection of any metastatic lesions. In some cases bowel resection and retroperitoneal lymphadenectomy are necessary in order to obtain optimum cytoreduction. Optimum cytoreduction is achieved when the largest residual tumour mass measures less then 1,5 cm.


POSTOPERATIVE TREATMENT - EOC

chemotherapy Platinum-based combination with paclitaxel chemotherapy is

now the standard postoperative treatment for patient with ovarian cancer

radiation therapyIt is useful method especially in patient who have positive

second-look laparoscopy or laparotomy after chemotherapy treatment but the residual mass are less than 2 cm.

hormonal treatment


FOLLOW - UP

second-look laparoscopy every year during first 5 year to detect early microscopic relapse

CA 125 every 3 to 4 month complete medical history physical examination rectovaginal pelvic examination


SCREENING

Screening is recommended in women with HOCS and HBOCS and include:

rectovaginal pelvic examination CA 125 determination TVS prophylactic TAH/BSO


MALIGNANT GERM CELL TUMOURS

Dysgerminoma most common germ cell malignancy , in 10-15% is bilateral , survival rate for early stage is 95% and even in advanced stage grater then 80% when appropriate adjuvant therapy is given. LDH is useful tumour marker. hCG levels is elevated in small number of patients. In young women and stage I unilateral oophorectomy is recommended with inspection and biopsy of opposite ovary and staging with retroperitoneal lymphadenectomy. In other women TAH/BSO. Adjuvant therapy should be given in all patients radiotherapy and/or chemotherpy.


MALIGNANT GERM CELL TUMOUR

Embryonal carcinoma is quite rare , rarely bilateral and trends to spread intraperitoneally , survival is slightly better then with EST using the same platinum based chemotherapy regiments . Both AFP and hCG can serve as tumour markers. Surgical treatment depend on age and stage . Adjuvant therapy ( chemotherapy) is recommended in all cases.



Immature teratoma represents approximately 20% of all malignant germ cell tumours and 25 % in girls under 10. After grade surgicopathologic stage is the most prognostic factors. Fortunately most patient are diagnosed with early stage. Occasionally immature carcinoma produce AFP as tumour marker but hCG is never produced. Surgical treatment depend on age and stage. Chemotherapy is kind of adjuvant therapy but only in immature teratoma of all malignant germ cell tumours chemotherapy in stage IA grade I does not benefit.



Endodermal sinus tumour also known as “yolk sac tumour” is an extremely aggressive malignancy. Almost never is bilateral. Intraperitoneal and hematogenous spread is common. Commonly patients present with acute abdomen secondary to spontaneous rupture and haemorrhagiae. Platinum based chemotherapy significantly improves the survival. AFP is useful tumour marker.



Chorioncarcinoma nongestational is extremely rare , 50% is diagnosed in prepuberatal females , produced hCG as tumour marker . Although gestsational chorioncarcinoma is treated successfully in most patients with platinum based chemotherapy , remission is less common in patients with nongestational type.

Polyembryoma Mixed


BENIGN GERM CELL TUMOURS Gonadoblastoma is almost always found in patients with

gonadal dysgenesis associated with chromosome Y. In 50% coexist with malignant germ cell tumours

Teratomas 25-40% of all ovarian neoplasms. The most common is cystic teratoma - “dermoid cysts”. Most cases diagnosed in premenopausal women . Most patients are asymptomatic and often dermoids are diagnosed by usg. This tumours can be bilateral in 15%. The risk of malignancy is 1-2% and most commonly occurs in postmenopausal women.

Struma ovarii it is dermoid where thyroid tissue comprises greater than 50% of teratomas. This is unusual and accounts for only 2,7% of ovarian teratomas.



Adult granulosa cell tumours (GCTs) excess estrogen production is often found causing

precocious puberty and menometrorrhagia in menstruating or postmenopausal. Endometrial hyperplasia or carcinoma is at 60% in patients with this tumour.50% occur in postmenopausal women and only 5% in prepubertal girls. It is interestin that this king of tumour may relapse after many years ( even above 20 ) after primary diagnosis. Estardiol and in nowadays inhibin are useful tumour marker.



Juvenile granulosa cell tumours in 50% occur in prebubertal girls , rare relapse after many years from diagnosis , typically is early recurrence. Rarely lethal as GCTs.

Fibroma unilateral , diagnosed in 5 decade of life. Hormone production is unusual , eventually estrogen. It is benign tumour, when 1 to 3 mitoses are present is called cellular fibroma, if greater then 3 it is considered as fibrosarcoma.

Thecoma very similar to fibroma but more commonly produce etsrogen which causes postmenopausal bleeding , menorrhagia, endometrial hyperplasia or cancer.



Sertoli stromal cell tumours 1 % of all ovarian neoplasms , many of these tumours androgen producing , many are hormonally inert and some occasionally may produce estrogen. Diagnosed of pure Sertoli tumours is unlikely in the presence of virilization. Rarely is malignant.

Sertoli-Leydig cell tumours are the most common in these group , 40% have evidence of estrogen or androgen production, unilateral and occur in 3 decade of life. Rather frequently is malignant.

Sex cord tumour with annular tubules (SCTAT) in 30% associated with Peutz-Jegers syndrome.



Lipid cell tumour are typically virilizing with increased serum levels of testosteron and androstendione. Occasionally produce estrogen, estron and cortisol and in 10% cases Cushing Syndrom in found. In 20 % develop metastases.

Gynanroblastoma is rare ovarian tumours which contain granulosa stromal cell and Sertoli stromal cell tumours.

Leydig cell tumours mean age is 50 and almost always behaves in benign fashion. Testosterone is commonly produced resulting in mild virilization.

ovarian neoplasms. anita chudecka - głaz ovarian neoplasms

Documents

ovarian tumours

risk of ovarian cancer

animals ovarian cancer

incidence of ovarian

human ovarian carcinoma

eoc slide

fertility treatment

advanced stage cause