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Ovarian cancer
1. Ovarian Cancer
Dr. Shazia Iqbal
Assistant Professor
Obstetrics and Gynaecology
Alfarabi College Of Medicine Riyadh KSA
2. Objectives
Learn how malignant diseaseof the ovary, Fallopian tube
and peritoneum presents.
Learn how ovarian cancer is investigated and staged
Learn how ovarian cancer is managed
3. What is Ovarian Cancer?
The most common type of Ovarian Cancer that starts from epithelial cells –
gland forming cells
Adenocarcinoma
* Other common adenocarcinomas are found in the breast, colon,
lung, prostate, uterus, sometimes cervix
Other types of Ovarian Cancer start in the:
“eggs”(germ cell tumors)
body of the Ovary (stromal tumors)
4. Burden of disease
Ovarian cancer is the second most common gynaecological
malignancy and the major cause of death from gynaecological
cancer in UK
There areapproximately 7,000 new cases and 4,000 deaths
from ovarian cancer per year
When detected in its early stages, ovarian cancer has an
excellent prognosis
The lifetime risk of developing ovarian cancer in the
general population is 1.4% (1 in 70), and themean ageof
presentation is 64 years.
5.
6. Epithelial tumors
Approximately 10% of epithelial tumours are classified as
borderline ovarian tumours (BOTs).
These tumours are well differentiated, with some features of
malignancy(nuclear pleomorphism, cellular atypia) but do not
invade the basement membrane.
BOTs spread to other abdominopelvic structures (peritoneum,
omentum) but do not often recur following initial surgery.
The majority of BOTsare serous tumours.
Mucinous BOTsmay actually arise from appendiceal
carcinomas of low malignant potentialand can be
associated with pseudomyxoma peritoneii.
7.
8. High-grade serous carcinomas account for around 75% of all
epithelial ovarian cancers; mucinous and endometrioid tumours
are less common,accounting for 10%, followed by clear cell
carcinomas.
High grade serous tumours are characterized histologically
by concentric rings of calcification,known as ‘psammomabodies’.
Mucinous carcinomas are generallylarge multiloculated
tumours associated with pseudomyxoma peritoneii.
9.
10. Endometrioid carcinomas are similarin histological appearance to
endometrial cancer, are associated with endometriosis in
approximately 10% of cases and also a synchronous separate
endometrial cancer in 10–15%.
They tend to be well differentiated and are associated with a
better survival than high-grade serous carcinomas.
Clear cell carcinomas can also arise from endometriosis and
arecharacterized histologically by clear cells, much like renal
cancer.
11. High-grade pelvic serous carcinomas
30% of high-grade pelvic serous cancers have BRCA
mutations, which has implications for themajority of women who
present with apparently sporadic disease.
The ‘incessant ovulation’ theory holds that therepeated damage to
theovarian surface epithelium that occursat ovulation increases
therisk of mutations that drive ovarian carcinogenesis.
Excess gonadotrophin secretion is also thought to drive
tumorigenesisthrough oestrogen-stimulated epithelial proliferation
and subsequent malignant transformation.
19. How does Ovarian Cancer Present?
Vague Symptoms
Bloating, Distention, Changes in Bowel and Bladder Function,
Pelvic / Abdominal Pain, Decreased Appetite
Symptoms persist and increase over time
>70% of women will present with
Advanced Stage Ovarian Cancer
Cancer has spread throughout the abdomen and
sometimes beyond (lungs, liver)
20. How do we treat Ovarian Cancer?
Current Approach -- Surgery and Chemotherapy
Primary Tumor Reductive Surgery
Chemotherapy
Neoadjuvant Chemotherapy (NACT)
Chemotherapy Surgery Chemotherapy
Goal of Surgery remove all visible disease
Goal of Chemotherapy kill all cancer cells
21. Significant Improvement in
Ovarian Cancer Outcomes
Tumor Reductive Surgery
Optimal Tumor Reductive Surgery -- No residual cancer > 1 cm
Suboptimal – Residual Cancer > 2 cm
Chemotherapy
Intraperitoneal + Intravenous Chemotherapy
Intravenous Chemotherapy Dose-Dense
High Volume Surgeons (Gynecologic Oncologists) and High Volume Facilities
Risk Reduction by identifying women with a genetic susceptibility to ovarian cancer
22. Important Questions at time of diagnosis
Will surgery remove all the visible cancer?
How much cancer is present to begin with?
How aggressive is the cancer?
How much skill and effort needed?
(Will chemotherapy kill the cancer?)
Is the cancer sensitive or resistant to “platinum”?
23.
24. Neoadjuvant Chemotherapy (NACT)
Chemotherapy given before surgery (usually 3 cycles)
NACT not inferior to Primary Tumor Reductive Surgery
NACT significantly improved the completeness of surgery with less
residual disease at time of surgery
Less post-operative morbidity and mortality with NACT
Increased rate of Blood Transfusions
25.
26. SEX CORD TUMOR (MALIGNANCY)
10% per cent of ovarian tumours, but almost 90% cent of all functional
(i.e. hormone-producing) tumours
low malignant potential with a good long -term prognosis.
Some morbidity may arise from the oestrogen (granulosa, theca or
Sertoli cell) or androgen production (Seroli–Leydig or steroid cell) characteristic
of these tumours, resulting in precocious puberty, abnormal menstrual bleeding
andan increased risk of endometrial cancer
most common subtype, accounting for over 70% of sex cord stromal
tumours
typically irregular menstrual bleeding,
postmenopausal bleeding
precocious puberty in young girls.
Granulosa cell tumours may present as a large pelvic mass or with pain
dueto torsion/haemorrhage.
Sertoli–Leydig cell tumours produce androgens in over 50% of cases.
27.
28. Treatment
Treatment is based on thepatient’s age and wish to preserve
fertility.
If thepatient is young, unilateral salpingo-oophorectomy,
endometrial sampling and staging is sufficient.
In theolder group, full surgical staging is recommended.
Granulosa cell tumours can recur many years after initial
presentation and long term follow-up is required.
Recurrence is usually well defined and surgery is the
mainstay of treatment as there is no effective chemotherapy
regime.
29. GERM CELL TUMOR
mainly in young women and account for approximately 10% of ovarian tumours
They are derived from primordial germ cells within the ovary
The emphasis of management is based mainly on fertility-preserving surgery and
chemotherapy.
common presenting symptom is a pelvic mass; 10% present acutely with torsion or
haemorrhage and due to the ageincidence, some present during pregnancy.
Seventy per cent of germ cell tumours are stage 1; spread is by lymphatics or
blood borne.
Dysgerminomas account for 50% of all germ cell tumours. They are bilateralin
20% of cases and occasionally secrete human chorionic gonadotrophin (hCG).
Endodermal sinus yolksac tumours are the second most common germ cell
tumours, accounting for 15% of the total. They are rarely bilateralandsecrete α-
fetoprotein (AFP).
Immature teratomas account for 15–20% of malignant germ cell tumours and
about 1% of all teratomas.
Non-gestational choriocarcinomas are very rare, usually presenting in young girls
with irregular bleeding andvery high levels of hCG.