BENIGN and

MALIGNANT OVARIAN
TUMORS

ALI MEHDI ROLL N0. 319

Learning Outcomes

• Anatomy and physiology of ovaries

• Classification of Ovarian tumors
• How Benign and Malignant ovarian tumors present?
• How to differentiate them clinically?
• What are specific tumor markers of B/M ovarian tumors
• How to investigate benign and malignant ovarian tumors
• How to treat them medically / surgically?
Anatomy

• Normal Size 5*3*3cm

• Variation in dimension can result from
• Endogenous Hormonal (Age/Menses)
• Exogenous Substances (OCPs,GnRH a.)
 Classification of Common Benign Tumors

TYPES EXAMPLES
Functional Follicular Cyst
Corpus Luteal
Theca Luteal

Inflammatory Tubo-ovarian Abcess

Endomertioma
Germ Cell Benign teratoma (dermoid cyst)
Epithelial Serous Cystadenoma
Mucinous Cystadenoma
Brenner Tumor
Sex Cord Stromal Fibroma
Thecoma
Presentation of Benign ovarian tumors?

• Age
• Pelvic Pain (Acute/Chronic)
• Abdominal mass
• Incidental finding
• Pelvic discomfort
• Pressure on Bowel/Bladder
Age

Functional Cysts Young girls(15-17),mid-adolescents

Germ Cell Tumor Young women

Benign Epithelial Tumors Older, post-menupausal

Sex Cord Stromal tumors

Inflammatory 15 to 25 years old

Pelvic Pain DD?
Adnexal Mass DD?
Investigations of Adnexal Masses

• Complete Physical Examination (Abdomen & Pelvis)

• Ultrasound Scan (TAUSS & TVUSS)
• CT Scan
• MRI
• Tumor Markers
• HCG
• Inflammatory Markers
• Laparoscopy / Laparotomy
Tumor Markers in investigation of Ovarian
cysts
Tumor Marker Ovarian Tumor Type Clinical Application
CA-125 Epithelial Ovarian Cancer Pre-op, Prognosis,
(Serous) & Borderline monitoring
Ovarian Tumors
Ca 19-9 Epithelial Ovarian Cancer Pre-op, Prognosis,
(Mucinous) & Borderline monitoring
Ovarian Tumors
Inhibin Granulosa cell tumor Follow-up
B-hcg Dysgerminoma, Diagnosis, staging,
Choriocarcinoma monitoring
AFP Endodermal Yolk sac tumor, Diagnosis, staging,
immature teratoma monitoring
Ovarian Torsion
• Refers to the rotation of vascular pedicle supplying the ovary
which compresses and cuts off its blood supply (decreased venous
and lymphatic outflow followed by arterial supply).
• Results in:
• Increase Size of ovary, oedema, ascites,
Haemorrage, Thrombosis, infarction, infection
• Associated with an adnexal mass
(functional cysts and demoid cysts)
Ovarian Torsion

Anatomical
Ovarian
Pedicle
Ovarian Torsion
Ovarian Torsion (Whirlpool sign/Knot sign)

The pedicle when twisted appears hyperechoiec with linear hypoechoic strands representing
vessels referred to as the ‘whirlpool’ sign (TVUSS) or ‘knot’ sign (Doppler). Most definitive sign
Of Ovarian torsion.
Ovarian Torsion

• Presentation:
• Acute Lower Abdominal Pain w/ Nausea & Vomiting
• History of Adnexal mass, functional cyts
• Diagnosis:
• Pelvic Ultrasonography w/ doppler measurement of blood flow
• Treatment:
• Laparocopic detorsion
• oopherectomy
Functional Ovarian Cysts

• Follicular Cyst
• Corpus Luteal Cyst
• Theca Luteal Cyst
• Most common clinically detectable enlargments of the ovary in
reproductive years
• All benign and usually asymptomatic
Follicular Cysts

• Cystic follicle is defined as Follicular cyst

of diameter >3cm (normally a follicle
measure upto 2.5cm)
• Most Common functional Cysts
• Rarely larger than 10cm
• Lined by granulosa cells
• Incidentally found on pelvic examinations
• Treatment> Expentant, OCPS
Corpus Luteal Cysts

• Occur following ovulation

• Less common than follicular cysts.
• Presents w/ pain due to rupture and
hemoperitoneum (mostly in females w/ bleeding
disorders/taking anto-coagulants)
• Treatment: Expectant with Analgesia, Surgical
washing of peritoneum & ovarian cystectomy.
Theca Luteal Cyst

• Associated with multiple pregnancies, hydantiform moles,

choriocarcionmas, GnRH analogs, clomephiene use
• Often bilateral
• Caused by Overstimulation of ovary by beta-hcg
• May be large multi-cystic, regress spotaneously
Inflammatory Ovarian Cysts

• Usually associated with PID

• Most common in young women
• Can involve tube, ovary, bowel
• Tubo-ovarian mass develops occasionally due to
infections like appendicitis
• Diagnosis: Inflammatory markers
• Treatment: Antibiotics, surgical drainage or excision
• Surgery is usually delayed until the infection is
resolved to avoid risk of systemic infection.
Germ Cell Tumors

• Most common ovarian tumors in young women aged

20-40 (peak incidence in 20s), 10% bilateral, 2% risk
for malignancy
• Most common benign form is MATURE DERMOID
CYST (CYSTIC TERATOMA)
• Derived from all three germ layers
• Composed of teeth, bone, hair, fat, skin muscle etc
• Example: Struma Ovarrii
Germ Cell Tumors

• Diagnosis: Ultrasonography, MRI

• Treatment: Surgical Ovarian cystectomy with indications
(symptomatic, >5cm+enlarging )
Epithelial Tumors

SEROUS CYSTADENOMAS MUCINOUS CYSTADENOMAS

20-30% 10%
Unilocular Multilocular
Unilateral Bilateral

BRENNER TUMORS
Small tumors, incidentally found,
urothelium, sometimes secrete
estrogens
Serous cystadenoma
Mucinous cystadenoma
Sex Cord Stromal Tumors (FIBROMAS)

• Most common sex cord stromal tumor

• Solid ovarian masses
• AGE> older women
• Associated with torsion
• Occasionly presents with MEIGS syndrome (Pleural effusion,
Ascites and Ovarian Fibroma)
Sex Cord Stromal Tumors (FIBROMAS)
Sex Cord Stromal Tumors (THECOMAS)

• Solid tumor with yellow/orange discoloration

• Benign estrogen secreting tumors
• Presents after menopause with excessive estrogen secretion and
post menopausal bleeding.
• Risk of endometrial carcinoma
Other Ovarian Cysts

• Non ovarian cysts can present as ovarian tumors

• Fimbrial Cysts
• Paratubal Cysts
• Paraovarian Cyst of Morgagni
Ovarian cancer
Epidemiology

• 225000 new incidence annually worldwide. Incidence stable since 1970s

• 1600 new cases in Australia in 2010
• Median age at diagnosis 64
• Fourth commonest cause of cancer death in women in developed
countries
• >60% of women diagnosed with Stage III/IV
• symptoms of abdo pain, bloating, distension, constipation, back pain usually
happen in advanced stage
• To date, no mortality benefit demonstrated with CA125 and TVUS
screening.
 Subtypes

TYPES EXAMPLES
Epithelial ovarian Tumors (80%) High grade serous 75%
Mucinous 10%
Endometrioid 10%
Clear cell
Low grade serous (borderline)

Sex Cord Stromal Tumors (10%) Granulosa Cell

Sertoli –Leydig
Gynandroblastoma
Germ Cell(10%) Dysgerminoma, Endometrial Sinus tumor,
Teratoma, Choriocarcinoma, Mixed
Metastatic Krukenberg Tumor
Epithelial Tumors

• High grade serous 75%

• Mucinous 10%
• Endometrioid 10%
• Clear cell
• Low grade serous (BOTs)
Epithelial Tumors ( High Grade Serous)

• Epithelial carcinoma of serous cell lineage with papillary, glandular

and solid growth patterns and high grade cytologic atypia
• Often bilateral, solid and cystic ovarian masses
• Solid, pseudoendometrioid, transitional cell carcinoma-like
appearance more common in BRCA1 mutations
• Necrosis is frequent
• Psammoma bodies are found
Epithelial Tumors ( High Grade Serous)
Epithelial Tumors ( Mucinous Carcinoma)

• Primary tumors are usually unilateral, > 10 cm, smooth capsule,

cystic and solid areas of tumor evenly distributed throughout ovary
without discrete nodularity
• Associated with pseudomyxoma peritonii
Epithelial Tumors (Endometroid Carcinomas)

• Ovarian carcinoma resembling endometrioid

adenocarcinoma of the endometrium
• Most common ovarian endometrioid tumor
• Usually low grade and diagnosed at early stages
• May be associated with endometriosis and
adenofibroma
• Usually unilateral; only 5% bilateral
• Cystic with solid component and areas of
hemorrhage
Epithelial Tumors (Clear Cell Carcinoma)

• Large unilocular, mainly cystic, smooth marginated mass

• Mean age is 55 - 56 years
• Higher Incidence in Asia
Epithelial Tumors (Borderline)

• 10% of ovarian carcinomas

• Well differentiated with some features of malignancy but do not
invade basement membrane
• BOTs invade to peritoneum, omentum but do not recur after
surgery
• Majority of BOTs are serous tumors
• Mucinous BOTs arise from appendcieal carcinomas of low
malignant potential and are associated with pseudomyxoma
peritonii.
Aetiology

• Epithelial cancers affect ovary, fallopian tubes and peritoneum

• HIGH GRADE PELVIC SEROUS CA presents with advanced disease
difficult to identify primary site of origin. The term is used to
incorporate all high grade tumors airsing from ovary, tubes, &
peritoneum.
• Women with BRCA1 mutation who have undergone BSO suggest
tubal origin of HGPSC. These precursors are called Serous Tubal
Intraepithelial Carcinomas (STIC) characterized by mutations in
p53 in secretory cells of fallopian tubes.
 Aetiology

• ENDOMETRIOID, MUCINOUS, CLEAR CELL, BORDERLINE AND LOW-GRADE

SEROUS OVARIAN CARCINOMAS Inclusion cysts of the ovarian surface epithelium and
endometriosis give rise to neoplasms that are distinctly ovarian in origin, and can include mucinous,
endometrioid, clear cell, borderline and low-grade serous carcinomas.
• Endometriosis-associated ovarian cancers are usually of endometrioid or clear cell histological subtype.
The origin of these tumours involves driver mutations in KRAS, PTEN, BRAF and ARID1A rather than TP53.
The clinical distinction between high-grade pelvic serous carcinomas and other histological subtypes is
important because of differences in disease progression, response to chemotherapy and prognosis.
• BRCA mutation carrier status is a risk factor for high-grade serous ovarian cancer. Most ovarian cancers,
however, are sporadic and risk relates to reproductive factors that are associated with hormone
treatment, contraceptive use, ovulation and pregnancy.
• The ‘incessant ovulation’ theory holds that the repeated damage to the ovarian surface epithelium that
occurs at ovulation increases the risk of mutations that drive ovarian carcinogenesis. Excess
gonadotrophin secretion is also thought to drive tumorigenesis through oestrogen-stimulated epithelial
proliferation and subsequent malignant transformation.
Ovarian Cancer Risk Factors

• 50 years of age or older • Other potential risk factors

• Familial factors • Early menarche (younger than 12
years of age)
• Family history of breast, ovarian,
or colon cancer ?3x baseline risk • Late menopause (older than 52
years of age)
• Personal history of breast or
colon cancer • Hormone replacement therapy
• Familial cancer syndrome (10%) • First pregnancy at older than 30
• BRCA (breast cancer) gene years of age
mutation • Infertility, endometriosis
• Hereditary nonpolyposis colon • (fertility Rx does not increase
cancer (HNPCC) risk)
Factors with Decreased Risk

• Multiparity
• Combined oral contaceptives
• Tubal ligation
• Sapingectomy
• hysterectomy
Lifetime Risk of Cancers Associated With Specific
Genes

Cancer, % BRCA1 BRCA2 Lynch Syndrome*

Breast 35-60 30-55 0
Ovarian 35-45 15-25 6-20
Endometrial 0 0 40-60

*MMR (mismatch repair) = HNPCC.

Red Flags for Cancer Susceptibility:
BRCA1/BRCA2

• Multiple family members with ovarian or breast cancer

• Age of onset of breast cancer
• Younger than 50 years of age (premenopausal)
• Bilateral breast cancer
• Both breast and ovarian cancer in same patient
• Ashkenazi Jewish ancestry (2% chance of BRCA)
 Natural History

• Precise natural history is poorly understood

• There is no direct evidence for a premalignant lesion in ovarian
cancer.
• The entire peritoneum is at risk because peritoneal
carcinomatosis may develop after an oophorectomy
Prevention of Ovarian Cancer

• Women who test positive for a BRCA mutation are offered risk-
reducing prophylactic BSO when they have completed their
families. This can usually be performed laparoscopically.
• Prophylactic surgery reduces the risk of ovarian cancer (by 90%)
and premenopausal breast cancer (by 50%), although it does not
eliminate the risk of primary peritoneal cancer.
• It is important to carry out risk-reducing surgery prior to the age-
related surge in ovarian cancer observed in BRCA mutation
carriers, which is younger in BRCA1 (mid 30s) than BRCA2 patients
(early 40s).
Prevention of Ovarian Cancer

• Another suggestion for risk reduction builds on the theory that BRCA-associated ovarian
cancers actually originate in the Fallopian tube; hence performing bilateral
salpingectomy with delayed oophorectomy in the 30s and early 40s may offset the
morbidity associated with a surgical menopause in young women while reducing the risk
of cancer.
• This strategy has yet to be subjected to rigorous testing and its efficacy is unknown.
Recent data indicate that the opportunistic removal of the Fallopian tubes during
hysterectomy for benign indications also reduces ovarian cancer risk in women at
average lifetime risk of ovarian cancer.
• Other procedures associated with ovarian cancer risk reduction include tubal ligation
(sterilization) and hysterectomy with ovarian conservation. Chemoprevention using the
combined oral contraceptive pill (COCP) reduces ovarian cancer risk by up to 50% in both
BRCA mutation carriers and women at average risk of ovarian cancer.
Screening

Screening using transvaginal ultrasound scan (TVUSS) and CA125

measurement has not been shown to improve survival in women with a familial
predisposition to ovarian cancer. This is because the high-grade serous
tumours that are associated with BRCA mutation carrier status develop rapidly
and most are at an advanced stage before they can be picked up by screening.
The role of screening for women of average lifetime risk of ovarian cancer
remains unclear; further results from the population-based UKCTOCS
randomized controlled trial are awaited, as the 2015 initial data were
equivocal.
 Clinical Features

The difficulty with clinical diagnosis is the main reason that patients with ovarian cancer
present with late stage disease
The most common symptoms are:
• Increased abdominal girth/bloating.
• Persistent pelvic and abdominal pain.
• Difficulty eating and feeling full quickly.
Other symptoms such as change in bowel habit, urinary symptoms, back
ache, irregular bleeding and fatigue occur frequently and any women with
persistence of these symptoms should be assessed by their general practitioner
(GP).
 Clinical Features

• Pelvic and abdominal examination may reveal a fixed, hard mass arising from the pelvis.
• Early-stage ovarian cancer is difficult to diagnose due to the position of the ovary, but an adenexal
mass may be palpable in a slim woman.
• It should be noted that less than 20% of adenexal masses in premenopausal women are found to be
malignant; in postmenopausal women this increases to around 50%. Chest examination is important
to assess for pleural fluid and the neck and groin should be examined for enlarged nodes.
Examination
Investigations

• Ultrasound (TVUSS)
 Tumor Markers
• CA125 is a non-specific tumour marker that is elevated in over 80% of epithelial ovarian cancers. It is only
raised in approximately 50% of early-stage epithelial ovarian cancers and is also commonly raised in benign
conditions such as pregnancy, endometriosis and alcoholic liver disease.
Tumor Marker Ovarian Tumor Type Clinical Application
CA-125 Epithelial Ovarian Cancer Pre-op, Prognosis, monitoring
(Serous) & Borderline Ovarian
Tumors
Ca 19-9 Epithelial Ovarian Cancer Pre-op, Prognosis, monitoring
(Mucinous) & Borderline Ovarian
Tumors
Inhibin Granulosa cell tumor Follow-up
B-hcg Dysgerminoma, Choriocarcinoma Diagnosis, staging, monitoring

AFP Endodermal Yolk sac tumor, Diagnosis, staging, monitoring

immature teratoma
Others

• (CT) and/or magnetic resonance imaging

• (MRI) scans.
• The CT scan is particularly useful for assessment of extrapelvic disease and for staging. The MRI
scan helps define tissue planes and operability.
• Other investigations required for preoperative work-up include chest X-ray, electrocardiography
(ECG), full blood count, urea and electrolytes, and liver function tests.
 FIGO Staging of Ovarian Ca
Stage at diagnosis and 5-yr survival
Stage at diagnosis 5-yr OS

Stage I Confined to the Ovary 20% 85%

IA Growth limited to one ovary, no ascites, capsule intact, no extension
IB Same as IA but involves both ovaries
IC IA or IB but with positive washings or ruptured capsule
Stage II Extends to True Pelvis 5% 60%
IIA Involves fallopian tube or uterus
IIB Extension to other pelvic tissues
IIC Either IIA or IIB but with positive washings or ruptured capsule
Stage III Extends Beyond the True Pelvis 58% 26%
IIIA Tumor limited to true pelvis but microscopic positive biopsy outside the pelvis
IIIB Abdominal implants up to 2 cm
IIIC Positive lymph nodes or abdominal implants > 2 cm
Stage IV Distant Disease 17% 12%
Management of Ovarian Cancer
Management (SURGERY)

• Surgery combined with platinum-based chemotherapy is the mainstay of treatment for

advanced ovarian cancer.
• The aim of surgery is complete or optimal cytoreduction (where <1 cm of residual
macroscopic disease is left behind).
• Tumour deposits on the bowel, spleen, peritoneal surfaces and diaphragm are usually
amenable to resection, while disease involving the porta hepatis and bowel mesentery are
not.
• ‘Supraradical ovarian cancer surgery’ is appropriate in previously well, fit women with
disseminated disease if complete cytoreduction is achievable; it is associated with
perioperative morbidity and mortality and women must be carefully counselled.
• Three cycles of neoadjuvant chemotherapy followed by interval debulking surgery is not
inferior to upfront surgery and has been shown to be associated with less morbidity.
 Steps in Surgical Staging
1. Obtain any free fluid for cytologic evaluation

2. If no free fluid is present, obtain washings by instilling saline and recovering the fluid. The fluid should irrigate the cul de sac, paracolic gutters, and area beneath
each diaphragm.

3. Systematically explore all intraabdominal organs and surfaces: bowel, liver, gallbladder, diaphragms, mesentery, omentum, and the entire peritoneum should be
visualized and palpated, as indicated

4. Suspicious areas or adhesions should be biopsied. If there are no suspicious areas, multiple biopsies should be obtained from the peritoneum of the cul-de-sac,
paracolic gutters, bladder, and intestinal mesentery when the disease appears confined to the ovary. These biopsies are not needed if the patient has advanced
disease.

5. The diaphragm should be biopsied or scraped for cytology. A laparoscope and biopsy instrument may be used.

6. The omentum should be resected from the transverse colon.

7. The retroperitoneum should be explored to evaluate pelvic nodes. Suspicious nodes should be removed and sent for frozen section examination.

8. The paraaortic nodes should be exposed and enlarged nodes removed. Nodes superior to the inferior mesenteric artery should also be resected.

9. In the absence of suspicious nodes, pelvic and paraaortic nodes should still be sampled to exclude the possibility of microscopic stage III disease.

10. A total abdominal hysterectomy and bilateral salpingo-ophorectomy is performed. (Fertility-conserving surgery may be an option for some women).
Chemotherapy

• Chemotherapy can be given as primary treatment, as an adjunct following surgery or for

relapse of disease.
• First-line treatment is usually a combination of a platinum compound with paclitaxel.
• Platinum compounds are the most effective chemotherapeutic agents in ovarian cancer.
They are heavy metal agents that cause cross linkage of deoxyribonucleic acid (DNA)
strands, thus arresting cell replication.
• Carboplatin is now the main platinum compound used as it is less renal toxic and causes
less nausea than cisplatin, but is equally as effective. The dose of carboplatin is
calculated according to the glomerular filtration rate (GFR) using the area under the
curve (AUC).
• Bevacizumab, a monoclonal antibody against vascular endothelial growth factor (VEGF),
inhibits angiogenesis.
Chemotherapy

• Following completion of chemotherapy, patients have a further CT scan to assess

response to treatment. This scan can be used for comparison in the future if there is
clinical or biochemical evidence of recurrence.
• Follow-up of patients includes clinical examination and CA125 measurement. Studies
have shown that levels of CA125 start to rise prior to onset of clinical evidence of
disease recurrence; however, treating isolated rising CA125 levels does not improve
survival. When disease recurs treatment is largely palliative. If the duration of remission
is more than 6 months, carboplatin may be used again; otherwise taxol can be given or
other chemotherapy agents, such as topotecan or liposomal doxyrubicin.
Prognosis

• Stage of disease
• Volume of residual disease post surgery
• Histological type and grade of tumour
• Age at presentation
Sex Cord Stromal Tumors

These tumours account for approximately 10% per cent of ovarian tumours, but
almost 90% cent of all functional (i.e. hormone-producing) tumours. Generally,
they are tumours of 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 and an
increased risk of endometrial cancer. The peak incidence is around the age of
the menopause, although juvenile granulosa cell tumour usually presents in
girls under 10 years of age, causing precocious puberty. Overall, granulosa
cell tumours are the most common subtype, accounting for over 70% of sex
cord stromal tumours.
Clinical Features

A significant percentage of these tumours present with manifestations of their

hormone production, typically irregular menstrual bleeding, postmenopausal
bleeding or precocious puberty in young girls. Granulosa cell tumours may present
as a large pelvic mass or with pain due to torsion/haemorrhage. Sertoli–Leydig cell
tumours produce androgens in over 50% of cases. Patients present with a pelvic
mass and signs of virilization. Common symptoms are amenorrhoea, deep voice and
hirsutism. Occasionally, this group of tumours produce oestrogen and rarely renin,
causing hypertension. Most sex cord stromal tumours present as unilateral ovarian
masses, measuring up to 15 cm in diameter. Macroscopically, the tumour is often
solid with areas of haemorrhage, and the cut surface may be yellow due to high
levels of steroid production. Granulosa cell tumours produce inhibin, which can be
used for follow-up surveillance; levels often rise prior to clinical detection of
recurrence.
Treatment

Treatment is based on the patient’s age and wish to preserve fertility. If the
patient is young, unilateral salpingo-oophorectomy, endometrial sampling and
staging is sufficient. In the older 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 Tumors
Malignant germ cell tumours occur mainly in young women and account for approximately 10% of ovarian tumours. They
are derived from primordial germ cells within the ovary and because of this may contain any cell type. The emphasis of
management is based mainly on fertility-preserving surgery and chemotherapy.
The most common presenting symptom is a pelvic mass; 10% present acutely with torsion or haemorrhage and due to the
age incidence, 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 bilateral in 20% of cases and occasionally secrete
human chorionic gonadotrophin (hCG).
Endodermal sinus yolk sac tumours are the second most common germ cell tumours, accounting for 15% of the total. They
are rarely bilateral and secrete α-fetoprotein (AFP). They present with a large solid mass that often causes acute
symptoms with torsion or rupture. Spread of endodermal sinus tumours is a late event and is usually to the lungs.
Immature teratomas account for 15–20% of malignant germ cell tumours and about 1% of all teratomas. They are classified
as mature or immature depending on the grading of neural tissue present. About one-third of teratomas secrete AFP.
Occasionally, there can be malignant transformation of a cell type within a mature teratoma. The most common cell type
to transform is the epithelium, usually squamous cell carcinoma.
Non-gestational choriocarcinomas are very rare, usually presenting in young girls with irregular bleeding and very high
levels of hCG.
Clinical Features

• Germ cell tumours should be suspected if a young woman presents

with a large solid ovarian mass that is rapidly growing. MRI is
helpful to assess morphology, particularly within teratomas. CT
scaning of the abdomen allows assessment of the liver and lymph
nodes. All patients should have a chest X-ray to exclude pulmonary
metastases.
 Treatment
• Surgery is tailored to suit the patient. As most women presenting with malignant germ cell
tumours are of reproductive age, fertility-sparing treatment may be preferred. An
exploratory laparotomy is performed to remove the tumour and assess contralateral spread to
the other ovary (20% in dysgerminoma). If there is a cyst present on the other ovary, this
should be removed. Careful inspection of the abdominal cavity is required with peritoneal
biopsies and sampling of any enlarged pelvic or para-aortic nodes performed. If metastatic
disease is found, it should be debulked at surgery. Intraoperative frozen sections may be
required to assess nodal status.
• Postoperative chemotherapy depends on stage of disease. Stage 1 dysgerminomas and low-
grade teratomas are treated by surgery alone and the 5-year survival is in excess of 90%. For
the remainder of tumours and for patients with disease outside the ovary, chemotherapy is
given. The most common regime used is a combination of bleomycin, etoposide and cisplatin
(BEP), given as a course of three to four treatments, 3 weeks apart. This regime gives long-
term cure rates of over 90% and also preserves fertility if required.
• If the patient has recurrent disease, 90% will usually present in the first year following
diagnosis; salvage chemotherapy has very good success rates.
KEY POINTS

• Ovarian cancer tends to present late, with advanced disease because symptoms
are non-specific.
• Screening has not proven effective using tumour markers or TVUSS.
• Treatment is based on removing all tumour surgically, combined with platinum-
based chemotherapy.
• Prognosis is stage dependent: stage 1 disease has a 80–90% 5-year survival,
whereas stage 3 disease has a 30% 5-year survival.
• Sex cord stromal tumours usually present with endocrine effects due to excess
secretion of oestrogen or androgens.
• Germ cell tumours affect young women and are often cured by fertility-
preserving surgery.
THANK
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