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Ovarian Cancer
Dr. Shazia Iqbal
Assistant Professor
Obstetrics and Gynaecology
Alfarabi College Of Medicine Riyadh KSA
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
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)
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.
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.
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.
 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.
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.
Different Types of Epithelial Ovarian
Cancer by Histology
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)
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
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
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”?
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
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.
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.
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.
Ovarian cancer
Ovarian cancer
Ovarian cancer
Ovarian cancer
Ovarian cancer
Ovarian cancer
Ovarian cancer
Ovarian cancer

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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.
  • 12.
  • 13.
  • 14.
  • 15.
  • 16. Different Types of Epithelial Ovarian Cancer by Histology
  • 17.
  • 18.
  • 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.