This document discusses ovarian tumours, including their epidemiology, embryology, risk factors, classification, staging, pathology, screening, management, and various treatment options. It addresses how ovarian cancer accounts for nearly 4% of cancers in women and is a leading cause of death from female genital tract malignancies. Various types of ovarian tumours are described, such as epithelial tumours including serous, mucinous and endometrioid tumours, as well as sex cord-stromal tumours and germ cell tumours. Risk factors, prevention strategies, and challenges with screening for early detection are also summarized.

1. Ovarian TumoursOvarian Tumours
Kapila GunawardanaKapila Gunawardana
M.B.B.S.,M.S.(Obs & Gyn), F.R.C.O.G.,F.C.O.C.(S.L )M.B.B.S.,M.S.(Obs & Gyn), F.R.C.O.G.,F.C.O.C.(S.L )
Consultant Obstetrician and GynaecologistConsultant Obstetrician and Gynaecologist
Teaching Hospital,Teaching Hospital,
Peradeniya.Peradeniya.

2. OvarianOvarian TumoursTumours
 EpidemiologyEpidemiology
 EmbryologyEmbryology
 AetiologyAetiology
 Risk factorsRisk factors
 WHO classificationWHO classification
 StagingStaging
 Pathology of ovarianPathology of ovarian
tumourstumours
 ScreeningScreening
 Natural historyNatural history
 Prognostic factorsPrognostic factors
 Management (diagnosis &Management (diagnosis &
management)management)
 SurgerySurgery
 RadiotherapyRadiotherapy
 ChemotherapyChemotherapy
 HRT for post treatmentHRT for post treatment
 Immune therapyImmune therapy
 Gene therapyGene therapy

3. WhyWhy is it important?is it important?
 Accounts for nearly 4% of all cancers occurring in womenAccounts for nearly 4% of all cancers occurring in women
 Leading cause of death from malignancies arising in theLeading cause of death from malignancies arising in the
female genital tractfemale genital tract
 Life time riskLife time risk
in the general population is 1.5%in the general population is 1.5%
with one affected family member is 4%with one affected family member is 4%
with two affected family members is 7%with two affected family members is 7%
with BRCA-1 & BRCA-2 gene mutation 16-65%with BRCA-1 & BRCA-2 gene mutation 16-65%
 Most fatal and most feared cancerMost fatal and most feared cancer
 The risk could be reducedThe risk could be reduced

4. EmbryologyEmbryology of the ovaryof the ovary
 Primitive gonads appear around the 5Primitive gonads appear around the 5thth
week of IUL as theweek of IUL as the
gonadal ridge from the coelomic epithelium on the medialgonadal ridge from the coelomic epithelium on the medial
aspect of the urogenital ridge.aspect of the urogenital ridge.
 In the xx embryo , the cortex develop as the ovary and theIn the xx embryo , the cortex develop as the ovary and the
medulla regress to a small area.medulla regress to a small area.
 The ovarian serosa is the direct descent of the coelomicThe ovarian serosa is the direct descent of the coelomic
epithelium and it give rises toepithelium and it give rises to
endocervical,endometrial,endosalphinx and theendocervical,endometrial,endosalphinx and the
epithelium of the urogenital system.epithelium of the urogenital system.
 The undifferentiated serosal cells can undergo neoplasticThe undifferentiated serosal cells can undergo neoplastic
changes and lead to tumours of the above tissues.changes and lead to tumours of the above tissues.

5. Development of the ovaryDevelopment of the ovary
1. Cortical cords
2. Degenerating mesonephric tubule
3. Mesonephric duct
4. Paramesonephric duct
5. Degenerating medullary cords
6. Surface epithelium

6. WHO Classification of ovarian tumoursWHO Classification of ovarian tumours
1.Epithelial tumours1.Epithelial tumours
Benign,Boarderline tumours andBenign,Boarderline tumours and
CarcinomasCarcinomas
2.Sex cord and Mesenchymal tumours2.Sex cord and Mesenchymal tumours
Benign,Boarderline tumours andBenign,Boarderline tumours and
carcinomascarcinomas
3.Germ cell tumours3.Germ cell tumours
Benign,Boarderline tumours andBenign,Boarderline tumours and
carcinomascarcinomas

7. WHO Classification,contWHO Classification,cont
1.EPITHELIAL TUMOURS1.EPITHELIAL TUMOURS
 Serous tumoursSerous tumours
 Mucinous tumoursMucinous tumours
 Endometroid tumoursEndometroid tumours
 Clear cell tumoursClear cell tumours
 Brenner tumoursBrenner tumours
 Mixed tumoursMixed tumours
 Undifferentiated tumoursUndifferentiated tumours
 Unclassified epithelial tumoursUnclassified epithelial tumours
 Metastatic tumoursMetastatic tumours

8. 1.Epithelial tumours1.Epithelial tumours
ClassificationClassification
 Pathway of differentiationPathway of differentiation
 Potential biologic behaviourPotential biologic behaviour
 Epithelium of fallopian tube(serous tumours)
 Endocervix (mucinous tumours)
 Endometrium (endometroid tumours)
 Urinary bladder (Brenner tumours)

9. Serous tumours – Serous cystadenomaSerous tumours – Serous cystadenoma
 Reproductive yearsReproductive years
 10% bilateral10% bilateral
 Cystic and unilocularCystic and unilocular
 No solid areasNo solid areas
 Smooth inner and outerSmooth inner and outer
cystic linings and clearcystic linings and clear
serous contentsserous contents

10. Serous cystadenofibromaSerous cystadenofibroma
 Size 1 - 20 cmSize 1 - 20 cm
 Similar appearance toSimilar appearance to
serous cystadenoma withserous cystadenoma with
clusters of small firmclusters of small firm
whitish noduleswhitish nodules

11. Serous tumour of low malignant potentialSerous tumour of low malignant potential
(LMP, borderline tumours)(LMP, borderline tumours)
 Mostly cysticMostly cystic
 Exuberant papillaryExuberant papillary
projections on inner/outerprojections on inner/outer
surfacessurfaces
 Usually no necrosis orUsually no necrosis or
haemorrhagehaemorrhage
 20-40% of cases have20-40% of cases have
omental implantsomental implants
 Also pelvic, peritoneum,Also pelvic, peritoneum,
mesosalpinxmesosalpinx

12. Serous carcinomaSerous carcinoma
 Commonest primaryCommonest primary
malignant ovarianmalignant ovarian
neoplasmneoplasm
 40-60 years40-60 years
 50% bilateral50% bilateral
 Serosanguinous fluid,Serosanguinous fluid,
friable haemorrhagicfriable haemorrhagic
cyst contentscyst contents

13. Mucinous tumours – MucinousMucinous tumours – Mucinous
cystadenomacystadenoma
 Reproductive age
 5% bilateral
 Cystic and
multilocular, smooth
lining, thick mucinous
contents
 Large in size : 1 - 50 cm

14. WHO Classification - contWHO Classification - cont
2 .2 .SEX CORD STROMAL(GONADAL) TUMOURSSEX CORD STROMAL(GONADAL) TUMOURS
 Granulose theca cell tumoursGranulose theca cell tumours
 Sertoli-Leydig cell tumourSertoli-Leydig cell tumour
 Malignant thecomas(Gynandroblastomas)Malignant thecomas(Gynandroblastomas)

15. SCST with ovarian differentiationSCST with ovarian differentiation
Adult granulosa cell tumoursAdult granulosa cell tumours
 95% post pubertal95% post pubertal
 50% post menopausal50% post menopausal
 5% bilateral5% bilateral
 Frequently associated withFrequently associated with
hyperoestrogenismhyperoestrogenism
(DUB, endometrial(DUB, endometrial
hyperplasia and evenhyperplasia and even
carcinoma)carcinoma)
 Prognostic factors-Prognostic factors-
size(<5cm-100%, 6-size(<5cm-100%, 6-
15cm- 60%,>15cm-15cm- 60%,>15cm-
50%)50%)
mitotic activitymitotic activity
stage- best prognosticstage- best prognostic
indicatorindicator
tumour rupturetumour rupture

16. SCST with testicular differentiationSCST with testicular differentiation
Sertoli leydig cell tumourSertoli leydig cell tumour
 Mixed cell typesMixed cell types
 0.2% of ovarian tumours0.2% of ovarian tumours
 Reproductive ageReproductive age
 50% androgenized, rare50% androgenized, rare
estrogenic effectsestrogenic effects
 1.5% bilateral1.5% bilateral
 Well differentiated tumoursWell differentiated tumours
– good prognosis– good prognosis

17. FibromaFibroma

18. WHO Classification - ctdWHO Classification - ctd
3.3.GERM CELL TUMOURSGERM CELL TUMOURS
 DysgerminomasDysgerminomas
 Embroyonal (tumours of totipotential cells) carcinomasEmbroyonal (tumours of totipotential cells) carcinomas
-Embroyonic-Teratomas(mature/immature)-Embroyonic-Teratomas(mature/immature)
-Extra embryonic –Endodermal sinus tumours-Extra embryonic –Endodermal sinus tumours
.Yolk sac and non-gestational choriocarcinomas.Yolk sac and non-gestational choriocarcinomas
.Mixed germ cell tumours.Mixed germ cell tumours

19.  2nd most common germ cell tumour2nd most common germ cell tumour
 Elevated AFP (alpha feto protein)Elevated AFP (alpha feto protein)
 MalignantMalignant
 RadioresistantRadioresistant
 UnilateralUnilateral
Endodermal sinus tumour
(yolk sac tumours)

20.  Large, solid and lobulatedLarge, solid and lobulated
 Grey white with necrosisGrey white with necrosis
 Schiller-Duvall bodiesSchiller-Duvall bodies
(glomeruloid tufts)(glomeruloid tufts)
 Microscopic patterns-Microscopic patterns-
papillary, alveolar,papillary, alveolar,
microcystic, cystic, solidmicrocystic, cystic, solid
 Myxomatous, polyvesicularMyxomatous, polyvesicular
 PAS positive hyalinePAS positive hyaline
globulesglobules
Endodermal sinus
tumour
(yolk sac tumours)
cont.

21. TeratomaTeratoma
 Derived from all threeDerived from all three
germ layers; ectoderm,germ layers; ectoderm,
mesoderm andmesoderm and
endodermendoderm
 Variable according toVariable according to
the degree ofthe degree of
“maturity”“maturity”
 Immature elementsImmature elements
show features ofshow features of
primitive embryonicprimitive embryonic
tissuestissues

22. Metastatic carcinoma of the ovary

23. AetiologyAetiology
 Hereditary cancersHereditary cancers
10% occurs in women who carry mutations in cancer10% occurs in women who carry mutations in cancer
susceptibility genes BRCA-1,BRCA-2(these aresusceptibility genes BRCA-1,BRCA-2(these are
tumour suppressor genes)tumour suppressor genes)

24. AetiologyAetiology - ctd- ctd
 Sporadic cancersSporadic cancers
-90% of the cases-90% of the cases
-alteration of the p53 tumour suppressor is the most-alteration of the p53 tumour suppressor is the most
frequent genetic eventfrequent genetic event
(amplification,overexpression,mutation and deletion)(amplification,overexpression,mutation and deletion)

25. AetiologyAetiology
 Incessant ovulationIncessant ovulation
 Gonadotrophin and sex hormone therapyGonadotrophin and sex hormone therapy
-Inclusion cyst formation-Inclusion cyst formation
-Repair of the germinal epithelium following-Repair of the germinal epithelium following
ovulationovulation
-Persistent stimulation and exposure to-Persistent stimulation and exposure to
gonadotrophinsgonadotrophins
and sex hormones(proliferation and mitotic activity)and sex hormones(proliferation and mitotic activity)
-Theoretical risk of artificial ovulation induction-Theoretical risk of artificial ovulation induction

26. Risk factorsRisk factors
 Advanced age(average age is 60 yrs)Advanced age(average age is 60 yrs)
-90%of the tumours occur among post menapausal-90%of the tumours occur among post menapausal
femalesfemales
-<40 yrs infrequent-<40 yrs infrequent
-<30 yrs fewer than 3/100,00-<30 yrs fewer than 3/100,00
 Caucasian 1Caucasian 1stst
degree relative with Ca-3.5 fold riskdegree relative with Ca-3.5 fold risk
 BRCA-1, BRCA-2 mutant genes (17q,13q)BRCA-1, BRCA-2 mutant genes (17q,13q)
 NulliparityNulliparity
 Early age of menarcheEarly age of menarche
 Late age of menopauseLate age of menopause
 Non usage of contraceptivesNon usage of contraceptives
 Personal or family history of breast, ovarian or colonic CaPersonal or family history of breast, ovarian or colonic Ca
(hnpcc)(hnpcc)

27. PREVENTION (FACTORS REDUCING THEPREVENTION (FACTORS REDUCING THE
RISK FOR OVARIAN CANCER)RISK FOR OVARIAN CANCER)
 ““Reduction of ovarian cancer predominantly are associatedReduction of ovarian cancer predominantly are associated
with reduction in the number of ovulatory cycleswith reduction in the number of ovulatory cycles
 Prolong use of OCPProlong use of OCP
 MultiparityMultiparity
 Breast feedingBreast feeding
 Tubal legationsTubal legations
 Place of prophylactic oophorectomy (performed when she isPlace of prophylactic oophorectomy (performed when she is
still in the reproductive age-specially with a family history ofstill in the reproductive age-specially with a family history of
ovarian cancer. There is reduction in the incidence of ovarianovarian cancer. There is reduction in the incidence of ovarian
and breast cancer)and breast cancer)
 Use of vitamin A derivativesUse of vitamin A derivatives
 ScreeningScreening

28. SCREENING FOR OVARIAN TUMOURSSCREENING FOR OVARIAN TUMOURS
WHO CRETERIA FOR A SCREENING PROGRAMMEWHO CRETERIA FOR A SCREENING PROGRAMME
 The condition should an important health problemThe condition should an important health problem
 There should be an accepted treatment for the patients withThere should be an accepted treatment for the patients with
recognized diseaserecognized disease
 Facilities for diagnosis and treatment should be availableFacilities for diagnosis and treatment should be available
 There should be a recognized early stage of the diseaseThere should be a recognized early stage of the disease
 There should be a suitable testThere should be a suitable test
 The test should be acceptable to the populationThe test should be acceptable to the population
 The natural history of the condition should be wellThe natural history of the condition should be well
understoodunderstood
 There should be an agreed policy on whom to screenThere should be an agreed policy on whom to screen
 It should be cost effectiveIt should be cost effective
 Case finding should be a continuning processCase finding should be a continuning process

29. OVARIAN TUMOUR SCREENING MULTIOVARIAN TUMOUR SCREENING MULTI
MODELMODEL
ca 125 and vaginal scanningca 125 and vaginal scanning
Ca 125 >30 uml is abnormalCa 125 >30 uml is abnormal
Ca 125 is an antigen found in the foetal amniotic and coelomic epithelium.inCa 125 is an antigen found in the foetal amniotic and coelomic epithelium.in
adults it is found in mesothelial cells of pleuraadults it is found in mesothelial cells of pleura
Pericardium and tubal, endometrial, endocervical and the ovary.Pericardium and tubal, endometrial, endocervical and the ovary.
The surface epithelium of normal foetal and adult ovaries does not expressThe surface epithelium of normal foetal and adult ovaries does not express
the antigen , except in inclusion cysts, papillae or metaplasiathe antigen , except in inclusion cysts, papillae or metaplasia
An elevated level is found in 50% of stage 1 and >90% in women withAn elevated level is found in 50% of stage 1 and >90% in women with
advanced disease.advanced disease.
Sensitivity is 97%Sensitivity is 97%
Specificity is 96%Specificity is 96%
False positive in ca endometrium ca colon, endometriosis, fibroid, PID,False positive in ca endometrium ca colon, endometriosis, fibroid, PID,
pregnancy and menstruationpregnancy and menstruation

30. OVARIAN TUMOUR SCREENINGOVARIAN TUMOUR SCREENING-ctd-ctd
 Ovarian volume >20ml in reproductive age, andOvarian volume >20ml in reproductive age, and
>8-10ml in post menopausal are abnormal.>8-10ml in post menopausal are abnormal.
 Ultrasound findings (scoring system)Ultrasound findings (scoring system)
 VolumeVolume
 Thick wallThick wall
 SeptaeSeptae
 Solid areaSolid area
 Cystic areas with solid areasCystic areas with solid areas
 PapillaePapillae
 AscitisAscitis
 SecondarySecondary

31. Microscopic features suggestive ofMicroscopic features suggestive of
MalignancyMalignancy
 HyperchromaciaHyperchromacia
 PolychromasiaPolychromasia
 Nuclear atypiaNuclear atypia
 Increased nuclearIncreased nuclear
cytoplasmic ratiocytoplasmic ratio
 Invasion of basementInvasion of basement
membranemembrane

32. Macroscopic features suggestiveMacroscopic features suggestive
of malignancyof malignancy
 Cystic and solid areasCystic and solid areas
 Hemorrhagic areasHemorrhagic areas
 Necrotic areasNecrotic areas
 Increased vascularityIncreased vascularity
 Bilateral tumoursBilateral tumours
 Associated ascitisAssociated ascitis

33. SURGICAL STAGINGSURGICAL STAGING
Stage 1-growth limited to ovariesStage 1-growth limited to ovaries
1a growth limited to one ovary1a growth limited to one ovary
1b growth limited to both ovaries1b growth limited to both ovaries
1c tumour either 1a or 1b with any of the1c tumour either 1a or 1b with any of the
followingfollowing
- tumuor on the surface- tumuor on the surface
- capsular rupture- capsular rupture
- Ascitis containing malignant cells- Ascitis containing malignant cells
- Positive peritoneal washings- Positive peritoneal washings

34. SURGICAL STAGING-ctdSURGICAL STAGING-ctd
Stage ii growth involving one or both ovaries withStage ii growth involving one or both ovaries with
pelvic extensionspelvic extensions
ii a extension or metastasis to the uterus or tubesii a extension or metastasis to the uterus or tubes
ii b extension to other pelvic tissuesii b extension to other pelvic tissues
ii c tumour either 1a or 1b with any of the followingii c tumour either 1a or 1b with any of the following
-tumour on the surface-tumour on the surface
-capsular rupture-capsular rupture
-ascitis containing malignant cells-ascitis containing malignant cells
-positive peritoneal washings-positive peritoneal washings

35. SURGICAL STAGING- ContSURGICAL STAGING- Cont
Stage iii growth involving one or both ovaries withStage iii growth involving one or both ovaries with
peritoneal implants out side the pelvis or positiveperitoneal implants out side the pelvis or positive
inguinal or retro-peritoneal nodes (superficial liveringuinal or retro-peritoneal nodes (superficial liver
metastasis or histologically proven omental or bowelmetastasis or histologically proven omental or bowel
metastasis)metastasis)
iii a limited to true pelvis with negative nodes butiii a limited to true pelvis with negative nodes but
with microscopically positive seedingswith microscopically positive seedings
iii b tumour implants in the abdominal cavity<2cmiii b tumour implants in the abdominal cavity<2cm
iii c tumour implants in the abdominal cavity >2cmiii c tumour implants in the abdominal cavity >2cm
with positive nodeswith positive nodes

36. SURGICAL STAGING- ContSURGICAL STAGING- Cont
 Stage iv growth involving one or both ovariesStage iv growth involving one or both ovaries
with distant metastasiswith distant metastasis
 If pleural effusion is present there must beIf pleural effusion is present there must be
positive cytologypositive cytology

37. PROGNOSTIC FACTORSPROGNOSTIC FACTORS
 Pathological factorsPathological factors
-architecture and grade of lesion-architecture and grade of lesion
-differentiation and anaplasia-differentiation and anaplasia
 Biological factorsBiological factors
- flow cytometry- flow cytometry
- diploidy/anaploidy- diploidy/anaploidy
 Clinical factorsClinical factors

38. NATURAL HISORYNATURAL HISORY
 2/3 of the patients present with advanced disease2/3 of the patients present with advanced disease
 Pattern of spread-trans-coelomicPattern of spread-trans-coelomic
-lymphatic-lymphatic
-haematogenic-haematogenic
 stage i-5 years survival 90%stage i-5 years survival 90%
 stage ii-5 year survival 70%stage ii-5 year survival 70%
 stage iii& iv – 5 year survival 30%stage iii& iv – 5 year survival 30%
 Most of them succumb following anorexia, vomitingMost of them succumb following anorexia, vomiting
and catchexiaand catchexia

39. MANAGEMENTMANAGEMENT
DIADNOSIS, PRE-OPERATIVEDIADNOSIS, PRE-OPERATIVE
ASSESMENT &TREATMENTASSESMENT &TREATMENT
 DiagnosisDiagnosis
-History-History
-Examination-Examination
-Investigation-Investigation
 Treatment optionTreatment option
-Surgery-Surgery
-Chemotherapy-Chemotherapy
-Radiotherapy-Radiotherapy
-Immunotherapy-Immunotherapy
-Gene- therapy-Gene- therapy

40. DIAGNOSISDIAGNOSIS
 HISTORYHISTORY
-most women with epithelial tumours are-most women with epithelial tumours are
asymptomatic for a long durationasymptomatic for a long duration
-often the symptoms are vague-often the symptoms are vague
-irregular menstruation-irregular menstruation
-bowel and urinary symptoms-bowel and urinary symptoms
-distention, bloating,constipation,nausea,vomiting-distention, bloating,constipation,nausea,vomiting
and anorexia in advanced stagesand anorexia in advanced stages

41. DIAGNOSISDIAGNOSIS
 EXAMINATIONEXAMINATION
- information about the tumour and the- information about the tumour and the
fitness for surgeryfitness for surgery
- post-menopausal palpable ovary- post-menopausal palpable ovary
syndromesyndrome
- the presence of a pelvic mass (fixed,- the presence of a pelvic mass (fixed,
irregular, solid ,cystic and solid, bilateralirregular, solid ,cystic and solid, bilateral
- if in additional, an upper abdominal mass- if in additional, an upper abdominal mass
or ascitis is present, the diagnosis ofor ascitis is present, the diagnosis of
ovarian malignancy is certain.ovarian malignancy is certain.

42. INVESTIGATIONSINVESTIGATIONS
 Routine investigationRoutine investigation
- Hb- Hb
- UFR- UFR
- FBS- FBS
- BUSE- BUSE
- LFT- LFT
- ECG- ECG
- CXR- CXR

43. INVESTIGATIONSINVESTIGATIONS
 Special investigationSpecial investigation
- Ca 125- Ca 125
- Alpha feto protein- Alpha feto protein
- Ultrasound scan- Ultrasound scan
- CT scan- CT scan
- MRI scan- MRI scan

44. PRE-OPERATIVE ASSESMENTPRE-OPERATIVE ASSESMENT
 Optimize the healthOptimize the health
- Correction- Correction
- Medical fitness- Medical fitness
- Anti-coagulation- Anti-coagulation

45. SURGICALSURGICAL MANAGEMENTMANAGEMENT
 THE CORNER STONE OF THEREPY FOR OVARIANTHE CORNER STONE OF THEREPY FOR OVARIAN
MALINANCY IS SURGERYMALINANCY IS SURGERY

46. SURGICALSURGICAL MANAGEMENTMANAGEMENT
 Conservative surgeryConservative surgery
-stage 1a-stage 1a
-if the patient has not completed her family-if the patient has not completed her family
 Radical surgeryRadical surgery
-stage 1b-c-stage 1b-c
 Cytoreductive surgeryCytoreductive surgery
-advanced stage-advanced stage
 Second look laparotomy/laparoscopySecond look laparotomy/laparoscopy
 Second cytoreductivesurgerySecond cytoreductivesurgery
 Salvage therapySalvage therapy

47. SURGICALSURGICAL MANAGEMENTMANAGEMENT
 ProcedureProcedure
- vertical abdominal incision- vertical abdominal incision
- collect peritoneal fluid- collect peritoneal fluid
- systematic exploration- systematic exploration
- biopsies- biopsies
- TAH+BSO- TAH+BSO
- omentectomy- omentectomy
- appendicetomy- appendicetomy
- pelvic and para-aortic lymph node sampling- pelvic and para-aortic lymph node sampling

48. CHEMOTHERAPYCHEMOTHERAPY
 Alkylating agentsAlkylating agents
-interfere with base pairing leading to inhibition of-interfere with base pairing leading to inhibition of
DNA,RNA and protein synthesis (Cyclophoshamide,DNA,RNA and protein synthesis (Cyclophoshamide,
melphalan, chlorambucil)melphalan, chlorambucil)
 Anti-tumour antibioticsAnti-tumour antibiotics
-Inserted between DNA base pairs-Inserted between DNA base pairs
(Bleomycin,Mitomycin)(Bleomycin,Mitomycin)
 Ante-metabolites(Methotrexate,5FU)Ante-metabolites(Methotrexate,5FU)
 Plant alkaloidPlant alkaloid
-bind to vital intra-cellular micro-tubular proteins-bind to vital intra-cellular micro-tubular proteins
(Vincristine , vinblastine , paclitaxel)(Vincristine , vinblastine , paclitaxel)

49. CHEMOTHERAPYCHEMOTHERAPY
Early stageEarly stage
-stage 1a,1b,grade 1&2-stage 1a,1b,grade 1&2
-no further adjuvant therapy is needed-no further adjuvant therapy is needed
Early stageEarly stage
-1c or poorly differentiated-1c or poorly differentiated
-low risk-low risk
-alkylating agents and plant alkaloids-alkylating agents and plant alkaloids
Advanced ovarian caAdvanced ovarian ca
-carboplatin and paclitaxel – 3H every 3 weeks for 6 cycles-carboplatin and paclitaxel – 3H every 3 weeks for 6 cycles
-single agent carboplatin-single agent carboplatin

50. RADIORADIO THERAPYTHERAPY
 Intra peritoneal radio-colloids (p53)Intra peritoneal radio-colloids (p53)
 Whole abdominal radiationWhole abdominal radiation

51. IMMUNOTHERAPYIMMUNOTHERAPY
 Biological response modifier therapyBiological response modifier therapy
(corynebacterium parvum,BCD)(corynebacterium parvum,BCD)
-enhancement of host immune response & tumour rejection-enhancement of host immune response & tumour rejection
 Cytokines therapyCytokines therapy
-interferons,tumour necrosis factor-alpha, interleukin-2.-interferons,tumour necrosis factor-alpha, interleukin-2.
 Adaptive immunotherapyAdaptive immunotherapy
-infusion of LAK cells-infusion of LAK cells
 Intra-peritoneal gene therapyIntra-peritoneal gene therapy
-expression of cytokine genes or genetic-expression of cytokine genes or genetic
immunopotentiation (enhancement of anti-tumour immuneimmunopotentiation (enhancement of anti-tumour immune
response)response)

52. GENEGENE THERAPYTHERAPY
 Potential intervention at the molecular levelPotential intervention at the molecular level
 Genetic immuno–potentiationGenetic immuno–potentiation