2. MALIGNANT Ovarian Tumor
 Dr Kanupriya
 Dr Rajeev

3.  Epidemiology
 Risk factors
 Pathology and pathogenesis
 Diagnosis
 Screening
 Staging
 Prognosis
 Management
OVERVIEW

4.  Ovarian malignancies represent the greatest challenge of all the
malignancies because of its high mortality.
 Ovarian cancers -6% of all cancers among women
 Approximately 27% of gynecologic cancers are of ovarian origin
 About 53% of all the deaths of gynecological cancers are of ovarian origin
(highest fatality to case ratio)
American cancer society incidence
INTRODUCTION

5.  Incidence of ovarian cancers are highest in Sweden (19.6/100000) united
states (15.4/100,000) and lowest in Japan (10.1/100,000)
 Incidence in India 0.9 to 8.4 per 100,000
EPIDEMIOLOGY

6. The “silent killer”: asymptomatic in early stages
 75% diagnosed with advanced stage disease; 5-year
survival only 10-28%
 Woman’s lifetime risk of
 developing sporadic epithelial ovarian cancer is
1%-1.5% in developed nations and 0.75% in India.
 dying from ovarian cancer is 0.5%

7.  Age
 Rare before 40yrs,
increases steadily
thereafter, peaks at 65-
75yrs.
 Reproductive history
 early menarche,
nulliparity or age >30 at
first child-bearing, and
late menopause
Nulliparity is the most
important non genetic
factor.
 Fertility drugs
 prolonged use
especially without
achieving pregnancy
 Personal history of breast
cancer
 Hormone replacement
therapy > 10 years
 May be associated with
30% increased risk
 Talcum powder
 Some studies have
shown slightly increased
risk in women who use
talc powder on genital
area
American Cancer Society 2001

8. - Hereditary breast-ovarian cancer syndrome (HBOC)
- Hereditary site – specific ovarian cancer syndrome
(HSSOC)
- Hereditary nonpolyposis colon cancer syndrome
(HNPCC)
* Inherited - 10% of ovarian cancers while 90% sporadic
* Mode of inheritance is autosomal dominant
*Occurs 10 years younger than sporadic
FAMILIAL OVARIAN CANCERS

9. Lifetime risk of ovarian cancer is estimated
- 39 % of BRCA 1 mutations
- 11% with BRCA2 mutations
Life time probability of ovarian cancer
1.6 % without family history
5% if one relative is affected
7% if two relatives affected

10.  ~7% of hereditary ovarian cancer cases
 Responsible genes: mutation in mismatch repair genes
(MMR) including MLH1, MSH2, and MSH6
 Predominance of early onset proximal colon cancer, ca
ovary and endometrium.
 Estimated lifetime risk of ovarian cancer 10-12%.
HNPCC OR LYNCH SYNDROME

11.  Multiparity: First pregnancy before age 30
• Oral contraceptives: decreases approx 11% per year of use.
Max of 46% after 5 years of use .
• Tubal ligation
• Hysterectomy (Salpingectomy/ Fimbriectomy)
• Bilateral oopherectomy -↓ risk by 80% to 95%
• Lactation
PROTECTIVE FACTOR

12.  Role of ovulation in the pathogenesis of the malignancy.
 Risk is related directly to the number of uninterrupted
ovulatory cycles.
 As repair follows multiple ovulations, the surface
epithelium of the ovary often extends into the ovarian
stroma to form inclusion glands and cysts.
PATHOGENESIS

13.  Incessant ovulation
 Retrograde menstruation hypothesis.
 Retrograde transportation of carcinogens from lower
genital tract.
 Exposure of ovarian epithelium to persistently high levels
of pituitary gonadotropins.
THEORIES ……..
Te Linde's

14.  Very recently, Lee et al. have proposed
 many high-grade serous carcinomas actually arise in the
mucosa of the fimbriated end of the fallopian tube.

15. THEORY TO IMPLICATE FT
 Ovary has no cells of Mullerian origin.
 FT has cells of mullerian origin i.e. tall mucuos
secreting ciliated columnar cells.
 SOC are cells of mullerian origin i.e. columnar
epithelium.
 HGSOC express mullerian marker PAX8.

16.  The epithelium, via neoplastic transformation, may exhibit
differentiation toward a variety of müllerian-type cells
 Serous  fallopian tubal lining
 Mucinous
 Intestinal  gastrointestinal mucosa
 Müllerian  endocervix
 Endometrioid  endometrial glands
 Brenner/transitional  bladder
 Clear cell  mesonephric (renal cell)

17.  PRIMARY(80%)
1)Surface epithelial – 80-90%
2)Non-epithelial
Germ cell tumors – 15-20%
Sex cord stromal– 5-8%
 SECONDARY(20%)
1) Typical
2) Atypical (Krukenberg)
PATHOLOGIC CLASSIFICATION
Dutta Gynae

18.  Serous (tubal) ----75-80%
 Mucinous (endocx & intestinal)-----8-10%
 Endometrioid-----10%
 Transitional cell – Brenner-------<1%
 Clear cell-----<1%
SURFACE EPITHELIAL TUMORS
Novak's Gynecology

19. All types can be benign, borderline , or malignant,
depending upon;
 Benign
 Gross: mostly cystic
 Microscopic; fine papillae, single layer covering (no
stratification), no nuclear atypia, no stromal
invasion)
 Borderline
 Gross; cystic / solid foci
 Microscopic; papillary complexity, stratification,
nuclear atypia, no stromal invasion
 Malignant
 Gross; mostly solid & hemorrhage / necrosis
 Microscopic; papillary complexity, stratification,
nuclear atypia, stromal invasion
SURFACE EPITHELIAL TUMORS

20. • Formed by cells that resemble
internal lining of fallopian tube.
o Most common. 75% of
epithelial ovarian tumor.
o Most common in 4th & 5th
decades of life
o Bilateral in 50% of cases.
SEROUS TUMORS

21. Malignant (low grade serous and high grade serous
carcinomas)
 Stromal invasion . Abundant
delicate to coarse papillae
Psammoma bodies in 80%
per-se do not denote
malignancy .
Novak's
PSAMMOMA BODIES

22.  These are extracellular round laminar dark
eosinophilic collections of calcium.

23. Low grade: papillary and
glandular structures
predominate
High grade: solid sheets of
cells , high mitotic activity ,
nuclear pleomophism

24. • 8-10% of epithelial ovarian tumors.
• Largest ovarian tumors; may fill entire abdominal cavity.
• 5% are malignant.
• Bilateral in 8-10% cases.
•Cystic tumor; have loculi lined with mucin secreting
epithelium. Cut surface shows honey-comb appearance. If it
ruptures, may lead to formation of pseudomyxoma
peritonei & adhesion formation
MUCINOUS TUMOURS

25. • Resemble either those of
the endocervical
epithelium (endocervical
or mullerian type) or,
more frequently, those of
the intestinal epithelium
(intestinal type)
• Histologically, distinction
may be impossible
without clinical
correlation.
Irregular glandular spaces lined with a
layer of tall columnar cells

26.  6-8% of epithelial tumors.
 Most are unilateral (40% are
bilateral)
 Almost all are malignant
 Associated with endometrial
cancer (15-20%)
 Patient may have concurrent
endometriosis (10-20%)
 May be cystic or solid
 Content tends to be hemorrhagic
rather than serous or mucinous
ENDOMETRIOID TUMORS
Resembling proliferative
endometrial glands

27. • Clear, peglike or hobnail-like cells.
• Most clear cell ovarian tumors are
malignant.
• 50–70% have endometriosis
• One-fourth of all clear cell tumors
arise in the lining of benign
endometrioid cyst.
• These tumours are almost
invariably high grade (grade 3) ,
hence not graded.
CLEAR CELL TUMORS

28. Resemble those of the internal lining of the urinary bladder .
Borderline brenner tumors – surgical removal results in
complete cure .
• Malignant Brenner – benign or borderline when coexisting
with invasive transitional cell carcinoma
• Transitional cell carcinoma- when primary resembles
transitional cell ca of Bladder without a recognisable brenner
tumor -- sensitive to chemotherapy , more favourable
prognosis .
BRENNER TUMORS

29. Germ Cell Tumors
Seminoma,
Dysgerminoma
(primitive germ
cells)
Embryonic, ectoderm,
mesoderm,
endoderm
Teratoma
(hcg- AFP-)
Extra embryonic
structures
(Vitelline)
Endodermal
Sinus tumour
(AFP+ HCG-)
(Yolk Sac Tumour)
(Trophoblastic)
Choriocarcinoma
(AFP- HCG+)
Totipotent
cells
Embryonal
Carcinoma
AFP (+)
hCG (+)
Embryonic
differentation
AFP (-)
hCG (-)
GERM CELL TUMORS
mature immatureNOVAKS

30.  Germ cell tumors -20-25% of all ovarian cancers
 Benign 97% ,malignant 3%
 M.C age – young women. In 1st two decades of life, 70%
are of Germ cell origin.
 Rapidly growing; Palpable abdominal mass and pelvic
pain.
 FIGO staging same as epithelial ovarian tumor

31. • Commonest malignant germ cell tumors (30 to 40% )
• 75 % occur between 10 to 30 years of age. Rare after 50yrs.
• Consists of germ cells that have not differentiated to form
embryonic or extraembryonic structures .
• Tumor marker - Elevated LDH , HCG or AFP
• As they present relatively at early stage - surgery followed
by radiation has excellent cure rate . Loss of fertility is a
problem.
• 85% of all patients with dysgerminoma are younger than 30
yrs , CONSERVATIVE THERAPY & PRESERVATION OF
FERTILITY of major consideration .
DYSGERMINOMA

32.  3rd most frequent malignant GCT of
ovary.
 Median age 16 – 18 yrs
 Unilateral in 100 % hence biopsy from
opposite ovary is not needed
 Highly malignant with rapid growth
 Abdomen or pelvic pain (75 %) ,
Asymptomatic pelvic mass (10%)
 Gross appearance soft grayish brown
with cystic areas
 Histology – SCHILLER DUVAL bodies
 Tumor maker- AFP correlates extent of
disease
& monitoring response to treatment
YOLK SAC TUMOR/ ENDODERMAL SINUS TUMOR
Schillar Duval body with
its central capillary and
mantle of endoderm

33. MATURE CYSTIC TERATOMA
Tissues usually derived from 2 or 3 germ cell layers.
Accounting 95% of all ovarian teratomas
Age < 20 years
Clinical manifestation related to size ; TORSION most common
complication – 16%
Ovarian cystectomy appears to be adequate .
TERATOMA

34. Has age specific incidence – Mc in first 2 decade
According to Norris et al the quantity of immature neural tissue
alone determines the grade .
Grade I – mature teratoma containing only rare immature foci
Grade III- large portion embryonal tissue with atypia and
mitotic activity
Rarely bilateral. So present method of therapy unilateral
SALPINGOOPHERECTOMY with wide sampling of
peritoneal implants .
IMMATURE TERATOMA

35. Most malignant but rare (4%).
Very young (4-28yrs) Median age
is 14yrs.
Manifests as abdominal mass
pelvic mass. Associated with
hormonal abnormalities (may
secrete estrogen).
Tumor makers - AFP, HCG
EMBRYONAL CARCINOMA

36.  Extremely rare
 Composed of numerous
embryoid bodies that resemble
morphological normal embryo.
 Occur in very young,
premenarcheal girls.
 Highly malignant .least sensitive
to chemo & radiotherapy
POLYEMBRYOMA

37. Atleast 2 or more malignant germ cell elements, one of
which is primitive.
Components –dysgerminoma(commonest)
yolk sac tumor, immature teratoma, embryonal ca ,
choriocarcinoma, and polyembryoma.
Most significant component of the MIXED GC tumor
determines therapy and follow-up .
MIXED GERM CELL TUMORS

38. Classification the sex cord-stromal tumors are divided into :
• Granulosa cell tumor
• Thecoma –fibroma group
 Sertoli-Ledyig cell tumors(Androblastoma)
• Gynandroblastoma
• Sex cord tumor with annular tubules
• Unclassified
• Steroid cell tumors
SEX CORD-STROMAL TUMORS

39. 10% of all solid tumor,
Bilateral in 2%
• Two SUBTYPES : Adult
and Juvenile
• Adult GC – (95%) MC in
postmenopausal . Avg age
is 50years.Associated with
ESTROGEN production.
Endometrial HYPERPLASIA
( 25-50%) and Ca
endometrium (5-10%)
GRANULOSA CELL TUMORS
 Juvenile GC – In children and
young adults ; 90% before
puberty. Mean age at
diagnosis is 13 years.
Menstrual irregularities ,
amenorrhea, precocious
puberty.
True GC tumors are low grade;
confined to one ovary with
EXCELLENT PROGNOSIS :
long term survival 75-90 %

40. M/E- classic adult granulosa cell is round/ovoid with scant
cytoplasm. “COFFEE BEAN” grooved nuclei are characteristic
CALL- EXNER BODIES- adult granulosa cells show a tendency to arrange
themselves in small clusters or rosettes around a central cavity, resembling
primordial follicles.

41. THECOMA-FIBROMA GROUP
THECOMA FIBROMA
 Rarely malignant.
 In postmenopausal women;
typically in 60’s.
 Most hormonally active.
Usually produce excess
estrogen.
 Abnormal bleeding , pelvic
mass.
 Cells resemble theca cells
 B/L involvment rare. Surgical
resection is curative.
 Generally benign.
 Perimenopusal and menopausal
women.
 Hormonally inactive.
 1% women present with MEIG’S
SYNDROME( TRIAD of solid
ovarian mass, ascites and pleural
effusion).
 Arise from spindled stromal cells
that form collagen.
 Malignant transformation in 1%
cases.
WILLIAMS GYNAE

42. SERTOLI-LEYDIG CELL TUMOUR (ARRHENOBLASTOMA)
 Extremely rare(0.2% of ovarian cancers)
 Occur most frequently in 3rd or 4th decade
 75% seen in women <40 yrs
 Produce androgens  clinical virilisation in
70-85%
 Signs of virilisation  oligomenorhoea f/b
amenorrhoea, breast atrophy, acne, hirsuitism,
clitoromegaly, deepening of voice, receding hair
line
 Rarely estrogenisation (iso-sexual precocity,
irregular or postmenopausal bleeding) seen.
NOVAK'S GYNAE

43. Metastatic tumours
 About 5-6% of ovarian tumours are metastatic most frequently
from the female genital tract,breast & GIT (pylorus, colon,
rarely small bowel, pancreas, gall bladder)
 Two forms of secondary ovarian carcinoma
1. Growth corresponds in its histology with its primary
growth
 Dissemination by implantation from metastasis within
peritoneal cavity
 Retrograde lymphatic spread
 Ovarian tumours are much larger than other secondary
deposits
 Solid, irregular surface, nearly always bilateral, ascitis is
common, peritoneal metastasis (omentum)

44. Krukenberg tumour
1. Usually bilateral
2. Most often arise from primary carcinoma of stomach(70%),
large bowel (15%), breast (6%)
3. Smooth surface, slightly bossed, freely movable in pelvis
4. No infiltration through the capsule, no tendency to form
adhesions
5. Tumour retains the shape of normal ovary, solid waxy
consistency
6. Histologically, cellular or myxomatous stroma, scattered signet
ring cells (ovoid cell with granular cytoplasm, nucleus
compressed against one pole of the cell)

46.  ̴̴75% to 85% of patients with epithelial ovarian cancer
are diagnosed at the time when their disease has spread
throughout the peritoneal cavity.
 Our main aim is to identify women at high risk ,offer
management option .. Suspect and establish diagnosis
and treat cancer aggressively
DIAGNOSIS AND CLINICAL EVALUATION

47. Symptoms are Non specific amd vague.
-Bloating ,abdominal distension
-Pelvic or abdominal pain
-Difficulty eating or feeling full quickly
-Urinary symptoms ( frequency and urgency)
Symptoms present for less than one year and occur on
more than 12 days per month .
SYMPTOMS IN OVARIAN CANCER

48. Signs
 Anaemia
 Left Supraclavicular (Virchow’s) & inguinal
lymphadenopathy
 Unilateral non-pitting oedema of legs
 Tumours are often bilateral & fixed
 Ascitis, abdominal lump, enlarged liver
 Vaginal examination: fixed nodules in POD, adnexal
massess felt separate from uterus
 Pleural effusion

49. TRANSVAGINAL SONOGRAM
SERIAL CA125 Testing
OVARIAN CANCER SCREENING

50.  Initial imaging modality of choice for benign vs malignant
 Results of screening trials have consistently demonstrated
that US detects more stage I ovarian carcinomas than
CA125 levels and physical examination
 TVS showed very high sensitivity (>95%) for detection of
early stage carcinoma.
 Each ovary is measured in three dimensions.
 Ovarian volume is calculated using the prolate
ellipsoid formula (L x H x W x 0.523).
Premenopausal women vol >20cm3
postmenopausal women vol>10cm3
Any solid or papillary projection from tumor wall
ULTRASOUND
ABNORMAL

51.  Most valuable clinical tool by combining serum CA125
values with ultrasound findings and menopausal status to
calculate a Risk of Malignancy Index (RMI).
 RMI = U x M x CA125
 U is ultrasound score. 1 point each for :
multilocular cysts, solid areas, metastasis, ascites
and bilateral lesions.
 M is menopausal status ; scored as 1 = pre-
menopausal and 3 = post-menopausal
 Serum CA125 in IU/ml and can vary between 0 and
hundreds or even thousands of units.
RISK OF MALIGNANCY INDEX (RMI)

52.  It yielded a sensitivity of 85% and a specificity of 97%.
 LOW RISK: RMI <25
 MODERATE RISK: RMI 25-250
 HIGH RISK: RMI >250
 Risk of cancer is 75% when RMI value is >250
DUTTA GYNAE

53. Serum CA125 has been widely used as marker for possible
epithelial ovarian ca in assessment of pelvic mass.
 Poor sensitivity (elevated in only 25-50% of women with Stage
I disease)
 Poor specificity (elevated in many gynecologic and non-
gynecologic malignancies and benign conditions).False positive
results common.
- Postmenopausal women = > 35 U/ml
- Premenopausal women = > 200 U/ml
- CA125 is important tumor marker for diagnosis , treatment
and follow up care of patients with epithelial ovarian ca , can
be used to determine response to t/t , relapse and survival.
TUMOR MARKERS( CA-125)

54. Benign conditions
Endometriosis
Uterine fibroids
PID
Pregnancy
Menstruation
Diverticulitis
Pancreatitis,liver
disease
Renal failure
Appendicitis, IBD
Malignant conditions
 Cervical CA
 Fallopian tube CA
 Endometrial CA
 Pancreatic CA
 Colon CA
 Breast CA
 Lymphoma
 Mesothelioma

55.  Several other markers studied
 Human epididymis protein 4
 Mesothelin
 B7-H4
 Decoy receptor 3
 Spondin 2
OVA1 is an FDA-cleared blood test that uses results of 5
biomarkers (transthyretin, apolipoprotien A1, transferrin,
beta-2 microglobin and CA-125), with an algorithm to indicate
the probability of malignancy of an ovarian mass. Sensitivity
: 93%, specificity: 43%
OvaSure screening test- 6 biomarkers
Leptin, prolactin, osteopontin, IGFII, MIF and CA-125. Not
recommended. WILLIAMS GYNAE

56.  Several publications have demonstrated HE4 ‘s
superiority over CA125 . Specifically , HE4 ‘s ability to
distinguish benign diseases with malignancies(ie its
sensitivity )
 As a single marker, HE4 had the highest sensitivity at
72.9% (specificity 95%)
 Combined, CA125™ and HE4 yielded the highest
sensitivity at 76.4% (specificity 95%)
 The combination of CA125 and HE4 added 33.1% to the
sensitivity of CA125 alone and 4.5% to the sensitivity of
HE4 alone.
HE-4 A NOVEL TUMOR MARKER

57.  Recently, a more sensitive risk of ovarian cancer
algorithm (ROCA) has been developed. This algorithm
is based on the slope of serial CA125 measurements
drawn at regular intervals.
 It has been proposed to increase the performance of
single-threshold measurements of CA-125 concentrations.
 ROCA method is being evaluated in conjunction with TVS
as a two-stage screening process, and results from trials
are pending.
ROCA

58. Patterns Of Spread
1. Transcoelomic
Most common & earliest mode by exfoliation of cells which
implant along surfaces of peritoneal cavity
Follows circulatory path of peritoneal fluid
Metastasis typically seen on POD, paracolic gutters, right
hemidiaphragm, liver capsule, peritoneal surface of intestine
& mesenteries, omentum
It seldom invades intestinal lumen, but progressively
agglutinates loops of bowel  functional intestinal
obstruction  carcinomatous ileus

59. 2.Lymphatic
First involves pelvic lymph nodes through broad ligament
Advanced stage disease  retrograde dissemination via
lymphatics to round ligament to inguinal lymph nodes
follows ovarian vein to precaval & paraaortic lymph nodes
3.Hematogenous
Hematogenous dissemination at the time of diagnosis is
uncommon
Spread to vital organs parenchyma (lungs & liver) occur
only in 2-3% patients

60. FIGO staging of Ca Ovary

61. STAGE I: TUMOR CONFINED TO OVARIES

62. STAGE II: TUMOR INVOLVE 1 OR BOTH OVRIES WITH PELVIC EXTENSION OR
PRIMARY PERITONEAL CANCER

63. STAGE III: TUMOR INVOLVE 1 OR BOTH OVRIES WITH CYTOLOGICALLY
OR HISTOLOGICALLY CONFIRMED SPREAD TO PERITONEUM OUTSIDE
THE PELVIS AND /OR METASTASIS TO THE REPTROPERITONEAL NODES

64. STAGE IV: DISTANT METASTASIS EXCLUDING PERITONEAL
METASTASIS

65. MANAGEMENT OF OVARIAN
TUMORS

66. a) PATHOLOGICAL FACTORS:
a) Histologic type: Clear cell & Mucinous histologies – poorer survival
low malignant potential – better survival
b) Grade of tumor: poorly differentiated – poorer survival
c)Stage of disease: According to FIGO
b) BIOLOGICAL FACTORS:
a) Aneuploidy poorer prognosis compared to diploidy
c) CLINICAL FACTORS:
a) Extent of residual disease post primary surgery,
b) Volume of disease: small volume disease have better prognosis despite the
stage
c) Age: Older age poorer prognosis

67. Management:
 Preoperative evaluation
 Surgical management
 Chemotherapy
 NACT
 Follow up
 Management of commonly encountered tumors
67

68. PREOPERATIVE EVALUATION
 CBC, Coagulogram, LFT, RFT
 ECG/ CXR
 Urine R/E & C/S
 F/PP Sugars
 IMAGING:TAS/ TVS
CECT abdomen & pelvis / MRI/ PET Scan
 Paracentesis
Rule out other primary sites :
 Mammography
 GI Endoscopies
Tumor markers
68

69. ROLE OF FNAC
Diagnostic cytology has poor sensitivity to detect malignancy
 Aspiration of a malignant mass may induce spillage and seeding of
cancer cells into the peritoneal cavity, thereby changing the stage and
prognosis.
INDICATION : Advanced ovarian cancer patients who are
medically unfit to undergo surgery permitting initiation of
neoadjuvant chemotherapy(NACT)
69

70. • PRIMARY SURGERY
1. EARLY STAGE OVARIAN CA( stage 1 and stage 2)
• COMPREHENSIVE SURGICAL STAGING
• FERTILITY SPARING SURGERY
2. ADVANCED STAGE OVARIAN CA
1. PRIMARY CYTOREDUCTIVE SURGERY
• NEOADJUVANT CHEMOTHERAPY AND INTERVAL
CYTOREDUCTIVE SURGERY
• LAPAROSCOPY SURGERY
• SECONDARY SURGERY
• SECOND LOOK LAPAROTOMY

71. COMPREHENSIVE SURGICAL STAGING
 Vertical midline abdominal incision
 Peritoneal cytology. Minimum of 25cc should be sent.
 In the absence of ascites, separate saline washings should be
obtained from
(a) pelvic cul-de-sac,
(b) right paracolic space,
(c) left paracolic space, and
(d) undersurface of each hemidiaphragm.
 The ovarian tumor should be inspected for presence of papillary
excrescences or rupture of the capsule.
 Abdominal inspection and palpation in a systematic fashion.
71TE LIINDE’S

72.  What is the sequence of systemic exploration of
abdominal organs???

73.  Beginning with– peritoneum of cul-de-sac and small
bowel mesentry.
 Ascending colon
 Liver
 Omentum
 Undersurface of right and left hemidiaphragm
 Stomach
 And Finally----
 Tranverse colon, spleen, descending colon and bladder
peritoneum.

74.  TAH + BSO
 Infracolic omentectomy in patients with epithelial ovarian cancer
and an omental wedge biopsy taken in patients with germ-cell or
stromal tumors.
 Suspicious areas to be biopsied
 Retroperitoneal lymph node sampling
 Appendectomy should be performed in all patients with mucinous
epithelial cancers involving the ovary.
 Operative findings present at staging laparotomy must be carefully
documented.
74TE LINDE’S

75. SURGICAL THERAPY
BORDERLINE TUMOUR
Primary resection- Unilateral oophorectomy
no subsequent chemo or RT required.
 Stage I epithelial ovarian cancer :
 TAH + BSO with omentectomy and lymph node sampling
ovarian cancer 75

76. STAGE II
 TAH + BSO with careful surgical staging
 Followed by chemotherapy usually platinum based .
76ovarian cancer

77.  Indications for fertility sparing surgery ?

78. Fertility sparing surgery:
 Desirous of preserving fertility
 Pt & family agrees for close follow up
 No e/o dysgenetic gonads
 Unilateral GCT, Sex cord stromal tumor, borderline tumor.
 Early stage ovarian carcinoma (IA)
Follow up :
 Routine periodic pelvic examinations and determinations of serum CA125
levels.
 Endometrial biopsy / curettage as 5% to 15% of patients with granulosa cell
tumor develop endometrial cancer or hyperplasia.
 Generally, the other ovary and the uterus are removed at the completion of
childbearing.

79. ADJUVANT THERAPY ??----- RISK
ASSESSMENT
 Benefit of post-op or adjuvant therapy depends
on risk of relapse.
 EARLY STAGE OVARIAN CANCER classified
into
LOW RISK HIGH RISK
Stage IA or IB, grade 1 and 2 Stage IA or IB, grade 3 Stage IC
Standard treatment is SURGERY ALL Stage 2
ALONE. 5year survival is atleast
95%.
[ No role of adjuvant therapy] Platinum based chemotherapy.
Optimal regimen & duration of therapy
ELUSIVE

80. ADVANCED OVARIAN CA
Stage III/ STAGE IV
MAXIMUM CYTOREDUCTIVE SURGERY F/B
COMBINATION CHEMOTHERAPY

81. Stage III/ IV:
 PRIMARY CYTOREDUCTIVE SURGERY :
 Goal is to reduce the amount of tumor as much as possible in a patient
with metastatic ovarian cancer.
 It is considered in context of responsiveness of residual tumor to post-
operative therapies.
 Lesser the residual tumor volume, better is the survival.
 OPTIMAL DEBULKING- Minimal residual disease ≤ 1-2 cm in greatest
dia.
 SUBOPTIMAL DEBULKING- Bulky residual disease > 1-2 cm in dia.
Complications:
Infection,
hemorrhage
prolonged ileus
cardiopulmonary problems
81TE LINDE'S

82. PRINCIPLES:
 Close observation & treatment of any
complications during chemotherapy
 Assessment for response & monitoring for any
long term complications.
 Chemosensitivity/ resistance assay.

83.  Number of cycles of treatment??

84.  NUMBER OF CYCLES OF TREATMENT
 6-8 cycles: advanced-stage disease
 3 to 6 cycles: earlier-stage disease

85. CHEMOTHERAPY
 Platinum-based combination chemotherapy is generally
recommended. They can be used singly or in combination
with Paclitaxel.
Currently, Paclitaxel and Carboplatin combination found to
have better survival rate.
85

86.  Regime followed-----
 Before starting chemotherapy, Hydrate the patient.
 Inj. Palonosetron, Inj avil, inj dexameethasone, inj
rantac given ½ hr before starting chemotherapy.
 Inj PACLITAXEL 175mg/m2 IV infusion in D5% glass
bottle through CODON SET.
 Inj. CARBOPLATIN 450mg(5-6 AUC) IV infusion
Every 3 weekly with Monitoring of CHG, RFT,LFT &
Serum electrolytes.
D
A
Y
1

87. INTRAPERITONEAL CHEMOTHERAPY
 Patients with low volume residual disease after
surgical cytoreduction are potential candidates for
intraperitoneal (IP) therapy.
 Not been accepted universally as a result of issues
with catheter placement and therapy associated
toxicities
87

88. FOLLOW UP
Complete clinical remission is defined as no objective evidence of
disease
Recommendations : After the completion of primary surgery and
chemotherapy ; Visits : every 2-4 mo for 2 y, then twice yearly for 3 y,
then annually after 5 y
 CA-125/ other tumor markers every visit if initially elevated
CBC / LFT/RFT as indicated
Complete physical & Pelvic examination
Chest/ abdominal/ pelvic USG/ CT/ MRI
PET-CT, or PET as clinically indicated 88

89. ROLE OF NACT
 INDICATIONS: Poor surgical candidates
Possibility of suboptimal resection
Stage IIIC/IV
 Giving 3-6 cycles of CT upfront will reduce tumor burden, makes
subsequent surgery more feasible ( Allow maximal cytoreduction of
residual tumor)
 surgery post NACT c/as: INTERVAL DEBULKING SURGERY
 Prior to giving NACT, the pathologic diagnosis should be confirmed by
either fine needle aspiration, CT-guided biopsy or paracentesis.
89

90. SECOND LOOK SURGERY
 performed on a patient with no clinical evidence of
persistent tumor for the purpose of determining disease
status after a planned interval of treatment with
chemotherapy
 Primary purpose not debulking 0r treating complication
Classification of findings
 Negative - 30% to 50%( seen with Early-stage disease )
 Microscopically positive -20%
 Macroscopically positive- 30% to 50%
NOT RECOMMENDED due to increased surgical morbidity 90

91. ROLE OF LAPAROSCOPY
 Primary surgery for early-stage ovarian cancer
 Restaging of unstaged ovarian cancer
 Assessment of resectability
 Intraperitoneal catheter placement
 Second-look surgery
 Secondary cytoreductive surgery.
Port site metastasis 1% to 2%
91ovarian cancer

92. DYSGERMINOMA
TREATMENT:
SURGERY:TAH &BSO, if fertility not required.
Unilateral oophorectomy- minimum surgery
CHEMOTHERAPY
Advantage : fertility preservation
RADIOTHERAPY Very Radiosensitive
problem :Loss of fertility

93. GRANULOSA CELL TUMOR
 Unilateral salpingo-oophorectomy
 Ovarian biopsy if enlarged
 Endometrial biopsy if uterus left
 Palliative RT for pelvic recurrences (otherwise not
useful).
EMBRYONAL CARCINOMA
Rx-: Unilateral oophorectomy followed by
CT with BEP