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Ovarian Tumours

Dr Fida Al-Asali
Malignant disease of the ovary & fallopian
tube
Ovarian cancer is the second most common
gynecologic malignancy after uterine cancer.
5th most common cancer in women, after breast,
bowel, lung and uterine cancer
The majority of ovarian tumours are epithelial in
origin, with a significant number thought to
possibly originate from the fallopian tubes.
Ovarian cancer the silent killer
Overall 5-year survival rate is 35%
The silent killer: asymptomatic in early stages
75% diagnosed with advanced stage disease
Womans lifetime risk of dying from ovarian
cancer is 1.1%
Most common cause of death from gynaecological
malignancy(UK)
Types of Ovarian Tumors
Functional Malignant (or malignant
Follicle cyst potential)
Corpus luteum cyst EOC
Theca lutein cyst Malignant teratoma
Inflammatory Endometrioid carcinoma
Tubo-ovarian abscess Dysgerminoma
Benign tumors/cysts* Secondary ovarian tumor
Cystadenoma,
Endometriotic cyst
cystadenocarcinoma (>50% for
Brenner tumor serous, ~5% for mucinous)
Benign teratoma (dermoid Granulosa cell tumor (15-20%)
cyst)
Arrhenoblastoma (<20%)
Fibroma
Theca cell tumor (<1%)
*Rare or very rare potential
for malignancy
Classification of ovarian tumours
Ovarian tumors could be classified according
to their origin, biological behavior or clinical
manifestations.

WHO CLASSIFICATION:
Epithelial tumours 70-80%
A) Serous Tumors D)Clear Cell
Benign (Mesonephroid) Tumors
Borderline Benign
Malignant Borderline Malignancy
B) Mucinous Tumors Malignant
Benign Worst prognosis
Borderline and papillary
cystadenoma E)Transitional
Malignant
cell(Brenner) tumours
pseudomyxoma ovarii&peritoneii Benign usually
C)Endometroid Tumors F)Mixed epithelial
tumours
Benign
Borderline malignancy
G)Undifferentiated &
unclassified
Malignant
Sex Cord Stromal Tumours 10%
A) Granulosa-Stromal Cell C) Gynandroblastoma
Tumors
Granulosa cell tumour
Tumors in the Thecoma-
fibroma group Fibromas associated with
B) Androblastomas: ascites & hydrothorax=
Meigs syndrome
Sertoli_Leydig Cell Tumors
Well differntiated
Of Intermediate
differntiation
Poor differentiated
(sarcomatoid)
Germ Cell Tumours 5%
A) Dysgerminoma a.Struma ovarii
Abnormal gonads b.Carcinoid
B) Endodermal Sinus Tumors
(Yolk Sac Tumors) c.Struma Ovarii and
C) Embryonal Carcinoma Carcinoma
D) Polyembryoma d.Others
E) Choriocarcnoma G.Mixed forms
F) Teratomas GONADOBLASTOMA
Imature (A) Pure
Mature
a.Solid (B) Mixed with
b.Cystic Dysgerminoma or Other
c. Monodermal &highly Form or Germ Cell
specialized Tumors.
65% serous malignancies are bilateral
25-30% of benign and borderline bilateral
40% mucinous malignancies are bilateral
5-10% benign and borderline bilateral
40% clear cell and endometrioid bilateral
5% granulosa cell bilateral
50% metastatics bilateral
Primary Ovarian neoplasms are commonly
found 40-60 yrs.
Teratomas and Sex Cord Tumors mostly before
puberty
Borderline malignant frequently 30-50 yrs.
Invasive Carcinoma 50-70 yrs.
The challenge
Natural history of ovarian cancer not well
understood
No well-defined precursor lesion
Length of time from localised tumor to
dissemination is unknown
Multiple efforts underway to develop effective
screening method for early detection
Symptoms of Ovarian Cancer
Abdominal bloating, increased girth, pressure
Unusual fatigue
GI : nausea, indigestion, gas, constipation or diarrhea
Urinary frequency or incontinence
Unexplained weight loss or gain
Shortness of breath
GCT Often present more acutely& at an earlier stage
Typically-a rapidly enlarging abdominal/pelvic mass,
acute severe lower abdominal pain due to tumour
rupture, haemorrhage or torsion.
Risk factors
Most cases of EOC are sporadic and the
aetiology unknown
Most significant risk factor is genetic
predisposition(BRCA1/BRCA2&HNPCC groups)
Risk factors: Heredity
Up to 10% of epithelial ovarian cancer cases
are familial
3 familial syndromes: familial breast-ovarian
cancer syndrome, site-specific ovarian cancer,
and cancer family syndrome (Lynch type II)
Familial breast-ovarian cancer and site-specific
ovarian cancer syndromes both associated
with mutations of the BRCA1 and BRCA2
suppressor gene; account for 90% of familial
ovarian cancers
Additional Risk Factors
Age rare <30, peak 60yrs
Reproductive history
early menarche, nulliparity or age >30 at
first child-bearing, and late menopause
Fertility drugs
Personal history of breast cancer
Talcum powder
Protective factors
Multiparity: First pregnancy before age 30
Oral contraceptives: 5 years of use cuts risk
nearly in half
Tubal ligation
Hysterectomy
Lactation
Bilateral oopherectomy
Diagnostic tools
History
P/E look for pleural effusions/palpable lymph
nodes/hepatomegaly
distended abdomen, pelvic mass& ascites
Pelvic Exam (including rectal)
TA& TV scans detection of masses
& mass characteristics
Tumor markers CA-125, -FP,HCG,LDH
CT assess spread to LN, pelvic and abdominal
structures
MRI best for distinguishing malignant from
benign tumors
CBC, urea & electrolytes/liver function tests
The diagnosis of ovarian malignancy is almost
certain if a fixed, irregular pelvic mass is
associated with an upper abdominal mass or
ascites.
Tumour markers
Hormones produced by different tumours

Tumour -FP hCG LDH

Dysgerminoma (-)

Immature
teratoma
Yolk sac tumour +
(endodermal
sinus tumour)

Choriocarcinoma +
Diagnostic approach
Risk of Malignancy Index gives an estimate of
the risk of Ovarian Ca for women with adnexal
masses.
The RMI is calculated using ultrasound
findings (U), menopausal status (M) and
CA125 value (serum levels >30U/ml abnormal.
RMI
RMI = U x M x CA125 U = 0 (ultrasound score
of 0)
Ultrasound findings are U = 1 (ultrasound score
scored with one point for of 1)
each of the following: U = 3 (ultrasound score
Multi-locular cyst of 2 5)
Evidence of solid areas
Evidence of metastases Menopausal status is
scored as follows:
Presence of ascites Postmenopausal status
Bilateral Lesions is graded M = 3,
Pre-menopausal status
is graded M = 1
RMI
RISK RMI Risk of Cancer

Low <25 <3

Moderate 25-200 30

High >200 75
Ultrasound
Both tranabdominal and transvaginal
techniques identify enlarged ovaries or
abnormal morphology; TVS has better
resolution
Major limitations are poor PPV in
asymptomatic women and inability to detect
malignances when ovaries are normal size
Allows earlier stage detection.
Color-flow Doppler
Used in conjunction with TVS
Measures resistance in blood vessels
supplying the ovaries
May provide additional information to help
distinguish malignant from benign masses
CA-125
Sustained elevation in 82% of women with
advanced ovarian cancer, but fewer than 1%
of healthy women
Poor sensitivity (elevated in only 50% of
women with Stage I disease)
Poor specificity (elevated in many gynecologic
and non-gynecologic malignancies as well as
benign conditions)
CA-125
Malignant conditions Benign conditions
Cervical CA Endometriosis/Menses
Fallopian tube CA Uterine fibroids
Endometrial CA PID
Pancreatic CA Pregnancy
Colon CA Diverticulitis
Breast CA Pancreatitis
Lymphoma Liver disease
Mesothelioma Renal failure
Appendicitis
IBD
Benign vs Malignant Tumors on the
Basis of Ultrasound & Doppler
Benign Malignant
o More likely unilateral o More likely bilateral
o Unilocular o Multilocular
o Thin-walled o Thick walls
o No papillae o Papillae present
o No solid areas o Mixed echogenicity due
to solid areas
o Greater Angiogenesis
and Blood Flow
Spread of Ovarian malignancies
By seeding of cancer cells to the peritoneum,
omentum, tubes and ureters.
By lymphatics to the paraortic nodes, umblicus
and diaphragm.
By the bloodstream to the lower vagina and in
the case of sarcomas and teratomas to the
lungs and else where.
By direct spread to any neighbouring organ or
tissue
Treatment Options
Surgery
Chemotherapy
Radiotherapy
General surgical principles
Accurate staging information
Midline incision
Careful evaluation of all peritoneal surfaces
Washings of the peritoneal cavity: diaphragm,
right and left abdomen, pelvis
Infracolic omentectomy
lymphadenectomy of the pelvic& para-aortic
lymph nodes
optimal cytoreduction - may improve survival
FIGO ovarian cancer staging: 2014 update
Stage Tumour confined to ovaries
I IA: Tumour limited to one ovary, capsule intact, no tumour on surface, negative washings
IB: Tumour involves both ovaries otherwise similar to 1A
IC: Tumour limited to one or both ovaries 1 Surgical spill, 2 Capsule rupture before surgery or tumour on ovarian surface
3 Malignant cells in the ascities or peritoneal washings.

Stage Tumour involves one or both ovaries with pelvic extension (below the pelvic brim) or
II primary peritoneal cancer
IIA: Extension and/or implant on uterus and/or fallopian tubes
IIB: Extension to other pelvic intraperitoneal tissues

Stage Tumour involves one or both ovaries with cytologically or histologically confirmed
III spread to the peritonium outside the pelvis and/or metastasis to the retroperitoneal
lymph nodes
IIIA: Positive retroperitoneal lymph nodes and/or microscopic metastasis beyond the pelvis
IIIA1: Positive retroperitoneal lymph nodes only
IIIA1(i): Metastasis 10 mm
IIIA1(ii): Metastasis >10 mm
IIIA2: Microscopic, extrapelvic (above the brim) peritoneal involvement positive retroperitoneal lymph nodes
IIIB: Macroscopic, extrapelvic, peritoneal metastasis 2 cm positive retroperitoneal lymph nodes
IIIC: Macroscopic, extrapelvic, peritoneal metastasis > 2 cm positive retroperitoneal lymph nodes. Includes
extension to capsule of liver/spleen without parenchymal involvement of either organ.
Stage Distant metastasis excluding peritoneal metastasis
IV IVA: Pleural effusion with positive cytology
IVB: Hepatic and/or splenic parenchymal metastasis, metastasis to extra-abdominal organs (including inguinal lymph nodes and
lymph nodes outside of abdominal cavity)
Grading by FIGO for ovarian cancer
Epithelial tumours of the ovary are also further
sub-classified by grading. This is important
because histological grading is proportional to
prognosis. This grading system does not apply to
non-epithelial tumours.
Gx Grade cannot be assessed
G1 Well differentiated
G2 Moderately differentiated
G3 Poorly differentiated
Types of Surgery
Total abdominal hysterectomy and bilateral
salpingo-oopherectomy (TAHBSO)
Unilateral salpingo-oopherectomy (if fertility has to
be preserved)
Cytoreductive or debulking
Infracolic omentectomy
Peritoneal metastasis reduction
Second look laparotomy
Laparoscopic surgery
Conservative surgery
Chemotherapy-Ovarian cancer is a chemosensitive
solid tumour
Adjuvant: Chemotherapy employed after the initial
tumor has been removed after some other methods.
Combination: several agents given simultaneously
to enhance their effectiveness.
Induction: as an initial treatment for patients
presenting with advanced cancer that cant be
treated by other means
Neo-adjuvant: as an initial therapy in patients with
localized cancer to decreased tumor burden prior to
other treatments
Regional: administered as a regional perfusion
Chemothearaputic Agents
Alkalyting agents: Cyclophosphamide, Cisplatin,
Carboplatin, Melphalan, Altretamine

Plant alkaloids: Paclitaxel, Vincristine, Etoposide,


Topotecan

Anticancer antibiotics: Bleomycin, doxorubicin

Antimetabolites: Fluorouracil, Gemcitabine


Side effects of chemotherapy
Side effects Carboplatin Paclitaxel
Alopecia No Yes
Thrombocytopenia Yes No

Nausea and vomiting Yes Yes

Neurotoxicity No Yes
Adverse cardiac effects No No

Arthralgia No Yes
Myalgia No Yes
Hypersensitivity reaction No Yes

Diarrhoea No No
Nephrotoxicity Yes Yes
Neutropenia Yes Yes
Side effects of chemotherapy
nausea and vomiting
fatigue
sore mouth
high-tone hearing loss/tinnitus (ototoxicity; due to
cisplatin)
peripheral neuritis
nephrotoxicity (exacerbated by dehydration)
myelosuppression with risk of infection (neutropenic
sepsis)/bleeding (thrombocytopenia) & anaemia
pulmonary toxicity (bleomycin). Any new-onset
cough/shortness of breath should be investigated urgently
to exclude pneumonitis or fibrosis.
EOC-Surgery
TAH &BSO & infracolic omentectomy & peritoneal
cytology
Fertility-conserving surgery
Advanced disease is considered as disease that
has progressed beyond the ovaries, stage 1c &
above---require both surgery and chemotherapy
Aim of surgery is to leave no residual disease----
Optimal cytoreduction with maximum residual
tumour deposits being no more than 1 cm
MOGCT-Surgery
Fertility-preserving surgery via mid-line incision
(unilateral salpingo-ophorectomy &surgical staging)
is accepted standard of care in early-stage disease.
Biopsy of a contralateral normal ovary is not
recommended (might impair fertility).
In advanced stage, chemotherapy is recommended
as primary treatment followed by completion
surgery to resect residual masses.
In recurrence, surgical removal is recommended,
followed by chemotherapy if adverse features were
found in the histological specimen.
MOGCT-Chemotherapy
Chemotherapy is standard of care for all MOGCTs.
Decision to treat is based on the type of GCT, the grade of
differentiation and disease stage.
Stage IA are managed safely w/o immediate adjuvant
chemotherapy (reserved for relapse), but an intensive
surveillance protocol must be in place (e.g. tumour
markers, chest x-ray and abdomino-pelvic MRI).
The woman should be counselled to avoid pregnancy for
first 2 years following treatment.
Adjuvant chemotherapy is the accepted standard for
most cases with greater than stage IA disease.
Commonly used regimen include BEP or for high-risk
patients POMB/ACE.
MOGCT-Radiotherapy
Dysgerminomas are exquisitely radiosensitive
Widespread use of chemotherapy & the long
term toxicities and effects of radiotherapy
(ovarian failure/infertility and higher risk of
fatal second malignancies) it no longer forms a
part of routine treatment algorithms.
Rarely in a palliative setting or in rare/unusual
circumstances where chemotherapy is
refused/contraindicated.
Standard recommendations
Tumour Stage Treatment
Dysgerminoma Stage IA/IB Surgery + surveillance
Stage IC Surgery + postoperative
chemotherapy
Non-dysgerminoma Stage IA, IB of any type or Stage Surgery +
IC immature GCT grade 1/2 postoperative surveillance

Stage IC, grade 3 immature Surgery + surveillance


or
Surgery + postoperative
adjuvant chemotherapy

Stage IC or unsuspected stage II Surgery + chemotherapy

Stage II or greater Neoadjuvant


chemotherapy followed by
surgery
Primary fallopian tube carcinoma (FTC)
0.14% - 1.8% of female genital malignancies
Only 1200 cases of primary FTC have been reported
in the literature
Aetiology of FTC is unknown but hormonal,
reproductive & possibly genetic factors
BRCA-1 and BRCA-2
90% of FTCs are serous papillary adenocarcinoma,
the other subtypes are clear cell and endometrioid
adenocarcinoma.
Treated -same way.
Rarer subtypes include lymphoma, sarcoma and
germ cell tumours.