PG case presentation on ovarian cancer and discussion on tumor markers

1. CASE PRESENTATION
Dr Gitanjali Kumari
Moderator- Dr Singh sir

2. • 43 year Old, nulligravida, came to Bharati hospital referred from surgery department with complaints of pain
in abdomen 4-5 months ,dull aching ,non radiating
• She was operated for lap cholecystectomy on 27/6/20.She was detected to have bulky ovaries
intraoperatively, her ascitic fluid tap showed cells suspicious of malignancy.
Pain was
• Insidious in onset, gradually progressive
• Localized to lower abdomen
• No relieving and aggravating factors, not association with food intake.
• No history of palpable lump or any obvious swelling .
• She also gives history of weight loss and loss of appetite.
• Hence her staging laparotomy with frozen section with pan hysterectomy was planned

3. • MENSTRUAL HISTORY-
LMP-26/6/2020
PMH- 4-5 DAYS/28-30 DAYS/RMF.
NO H/O HEAVY MENSTURAL BLEEDING
NO H/O PASSAGE OF CLOT
• OBSTRETIC HISTORY- Married since 23 YEARS , NCM.
NULLIGRAVIDA

4. General examination
• No pallor/icterus/edema/lymphadenopathy
• PR- 80 bpm, BP 110/70mmhg
• Systemic check up:
• R.S – clear,bilateral air entry equal
• CVS – NAD
• Breast- normal

5. P/A –
Inspection- Abdomen flat
Umbilicus Inverted.
No Dilated Veins, Visible Peristalsis, Laparoscopy scar+ healthy
Palpation-soft non tender ,no mass palpable, no evidence of free fluid

6. P/s- cervix – cervix and vagina - healthy
P/v- uterus – bulky ,anterior fornix fullness
Right lateral fornix fullness
no forniceal tenderness
no appreciable mass on pv examination
. P/R- rectal mucosa free
DIAGNOSIS -43 YEAR OLD NULLIGRAVIDA WITH b/l OVARIAN MALIGNANT TUMOR

7. Investigation
• HB/TlC/Plt-12.2/10,000/3.35
• S.B-HCG <1.20
• LDH-1104
• CA-125-66
• 27/06/2020 ,CYTOLOGY REPORT
• ASCTIC FLUID – SUSPICIOUS FOR MALIGNANCY
• CXR – NORMAL
• PAP Smear- NILM

8. • CT SCAN (ABDOMEN+ PELVIS)- 24/5/2020
• UTERUS - Appear normal , right ovary enlarged 7.6x6.4 cm shows cystic lesion measuring 4x2.8cm within .
left ovary enlarged 5.2x4.4 cm in size .No abdominal/pelvic lymphadenopathy.
• USG ABDOMEN & PELVIS ON 24/6/2020
• Uterine outlines are poorly visualised due to the pelvic mass. Endometrium measures 6 mm.
• Right ovary measures 8.2 x 6.8 x 4.5 cm.
• Left ovary measures 5.2 x 5.1 x 4.4 cm.
• Both ovaries are enlarged, hypoechoic & heterogonous in echotexture. They show raised vascularity.
• Small amount of free fluid is seen in pod and interbowel Region.
• No significant para aortic lymphadenopathy

10. PROCEDURE :EXPLORATORY LAPROTOMY +TAH+BSO+OMENECTOMY+APPENDICETOMY
• Anaesthesia :general +epidural
• Intraoperative findings-
• Minimal ascites noted – fluid collected for histopathology .
• Omental thickening present
• Appendix thickened
• Liver and undersurface of diaphragm were normal
• Evidence of b/l ovarian masses around 8x9 cm with irregular surfaces
• Pouch of douglas thickening present on both uteroscaral .Right parametrium thickening present
• Bilateral Ovarian masses removed and sent for Frozen section.
• Appenedectomy done ,partial infracolic omenectomy done .
• Frozen section – suggestive of granulosa cell tumour

11. • Hpe was s/o->
• Poorly differentiated malignancy of both ovaries
1.Suggestive of metastatic adenocarcinoma
2. Malignant sex cord stromal tumor

13. Thank you

14. OVARIAN MALIGNANCY
• Ovarian cancer is the seventh most common cancer in united states, accounting for 3 % of all malignancies
and 6 % of deaths from cancer in women and almost one-third of invasive malignancies of female genital
organs.
• The Ovarian cancer cases contribute to around 5.9% of the total cancer cases in India
• It is fifth most common cause of death from malignancy in women.
• A woman risk at birth of having ovarian cancer at some point in her lifetime is 1% to 1.5 % and that of dying
from ovarian cancer is almost 0.5 % .
• In first two decades of life almost 70% of ovarian tumors are of germ cell origin, and one-third of these are
malignant.
• The peak incidence of invasive epithelial ovarian cancer is at about 60 years of age. About 30 % of ovarian
neoplasms in postmenopausal women are malignant , whereas only about 7 % ovarian epithelial tumors in
premenopausal women are frankly malignant.
• Most epithelial ovarian cancers are sporadic but at least 5- 10 % result from inherited susceptibility and are
hereditary.

15. Risk factors
• Family history
• Ethnicity
• Reproduction
• Others

16. Family history
• Accounts for 5- 10 % ovarian cancers
• More than 90 % of inherited ovarian cancers result from BRCA 1 AND BRCA2 genes.
Tumor suppressor genes
(interact with recombination / DNA repair proteins to preserve intact chromosomal structure.)
Chromosome breakage
Genome instability
BRCA 1 OR BRCA2
Dysfunction
intact or not?
YES NO
Checkpoint activates genomic errors tolerated
selective growth occurs lead to malignant transformation
Cells with damaged DNA are prohibited from
Entering into mitotic phase
Cell cylce
checkpoint
( p53)

17. - Both are inherited in an autosomal dominant fashion, but with variable penetrance.
- Estimated life time risk of breast cancer with BRCA1 AND BRCA2 IS 65 TO 74 %
- Carrier has 50 :50 chance of passing the gene to a son or daughter , but it is uncertain whether an
individual with the gene mutation will actually develop breast or ovarian cancer. As a result these
mutations can skip generations.
- Hereditary ovarian cancers occur in women approximately 10 years younger than those with non
hereditary tumors.
- Most BRCA1 ovarian cancers are high grade serous carcinomas.
- Women with primary history of breast cancer have twice the expected incidence of subsequent
ovarian cancer.
BRCA 1 BRCA 2
Chromosome 17q21 13q12
High risk for developing ovarian cancer 39
to 46 percent
Relatively less risk 12-20 percent

18. ACOG recommendation for woman at high risk for ovarian cancer
1. Genetic counselling is recommended for all woman with ovarian/fallopian tube/peritoneal epithelial cancer
and for individuals with family history of breast/ovarian cancer
2. Woman who wish to preserve their fertility can undergo screening by TVS every 6 months or CA-125
measurement may be reasonable for short tern surveillance strategy for woman at high risk of ovarian
cancer starting at age of 30-35 yrs until they decide to purse definitive risk reduction Bso
3. Ocps are recommended to young woman before embark on an attempt to have a family
4. Woman who don’t wish to maintain their fertility or have completed her family can undergo Bso after the
age of 35 yrs but before 40
5. Woman with BRCA mutation or who carry deleterious mutations i.e predisposing to breast cancer should
be offered risk reducing Bso b/l
6. For risk reducing BSO all tissues form ovaries & FTs must be removed
7. For woman aged 25-29 yrs with known BRCA mutation ,recommended breast surveillance includes clinical
breast examination every 6-12 months & annual radiographic evaluation (MRI), For woman aged 30yr or
more with known BRCA mutation ->annual mammography & annual MRI with contrast,often alternatin
every 6 monthsS

19. • Woman with family h/o breast/ovarian cancer who don’t have documented mutation in BRCA1 or 2 etc
should be managed based on their family history
• Woman with documented LYNCH syndrome should undergo periodic colonoscopy (1-2yr) starting at the age
of 20-25yrs or 2-5 yrs before the earliest colon cancer diagnosis in the family,whichever is earlier.
Endometrial biopsy is recommended every 1-2 yrs starting at the age of 30-35yrs.

20. Ethnicity
• White race
• Residence in north america and northern europe
• Ethinic background(european jewish,icelandic hungarian)

21. Reproduction
• Uninterrupted ovulatory cycles during reproductive years. Repeated stimulation of the ovarian surface
epithelium is hypothesized to lead to malignant transformation.
• Theoretically the surface epithelium undergoes repetitive disruption and repair.it is thought that this process
might lead to higher probability of spontaneous mutations that can unmask germline mutations or
otherwise lead to oncogenic phenotype.
• Nulliparity
• infertility
• Early menarche
• Late menopause
• Postmenopausal hormone therapy

22. Protective factors
• Multi parity ( having at least 1 child is protective for the disease with risk reduction of 0.3 to 0.4).
• Oral contraceptive pills ( if consumed for 5 or more years reduce their relative risk to 0.5)
• Prophylactic oophorectomy
• Tubal ligation and hysterectomy are protective as it prevents irritants from reaching the ovaries from lower
genital tract.
• Lactation
• Vitamin d , retinoids, NSAIDS
• Consumption of foods low in fat but high in fiber, carotene and vitamins

24. Classification
• Epithelial
1. Serous (75-80%) resemble glandular epithelial lining of fallopian tube
2. Mucinous (5%) resemble GI epithelium, endocervical gland cells
3. Endometroid (10%) resemble proliferative endometrium
4. Clear cell (5%) resemble secretory or gestational endometrium
5. Brenner(<1%) resemble bladder urothelium
6. Mixed epithelial tumors(<1%)
• Sex cord stromal tumors( 5-8 % of all ovarian malignancy)
(derived from sex cord ,ovarian stroma and mesenchyme)
1. Granulosa cell tumors
2. Tumors in thecoma-fibroma group
3. Androblastomas- sertoli-leydig cell tumors
4. Gynandroblastoma
5. Unclassified
• Lipoid cell tumors

25. • Germ cell tumors
1. Dysgerminoma
2. Endodermal sinus tumors
3. Embryonal carcinoma
4. Polyembryoma
5. Choriocarcinoma
6. Teratomas
7. mixed
• Gondoblastoma
1. Pure
2. Mixed with dysgerminoma or other forms of germ cell tumors
• Soft tissue tumors not specific to ovary
• Secondary( metastatic tumors) 5-6 %
 From breast and gastro intestinal tracts
 Direct extension 1) tubal carcinoma ( 13%) cases
2) Cervix (<1%)

26. - Krukenberg tumors-
 Account for 30- 40 % of metastatic cancers
 Arise in ovarian stroma
 metastatic mucinous/signet ring cell adenocarcinoma of ovaries that typically originates from primary tumors of intestinal
tract, characteristically the stomach.
 Bilateral

27. BENIGN MALIGNANT
Slow growing, usually unilateral ,well
defined
Rapidly growing, usually bilateral
Thin walled cyst Thick walled cyst
Simple cyst Solid tumor
No loculations Mixed cystic and solid mass
Absent Internal papillary excrescences
Shrinking in size Large amount of free fluid in pelvis or
abdomen
Mobile Fixed

28. • Tumor markers
• Tumor markers are glycoprotein that can be detected in higher than normal amount in blood,urine,body
tissues of some patients of certain type of cancer
• It is classified into 2 groups: Cancer specific & Tissue specific
• Cancer specific-related to presence of certain cancerous tissues, eg- CEA , CA 19-9, CA 125
• Tissue specific-related to specific tissue which had developed cancer, Eg- B-hcg, PSA,AFP

29. What is a tumor marker?
• A tumor marker is a substance present in or produced by a tumor (benign or malignant)
• or by the tumor’s host in response to the tumor’s presence that can be used to differentiate a tumor from normal
tissue
• or to determine the presence of a tumor based on measurement in the blood or secretions and that can be detected
in various body fluids and on the surface of cancer cells.

30. A good tumor marker should…
1. It should be highly sensitive
2. It should be highly specific
3. 100% accuracy in differentiating between healthy individuals and tumor patients.
4. should be able to differentiate between neoplastic and non-neoplastic disease and show positive correlation with tumor
volume and extent.
5. It should predict early recurrence and have prognostic value.
6. It should be clinically sensitive i.e. detectable at early stage of tumor.
7. Its levels should be preceding the neoplastic process, so that it should be useful for screening early cancer.
8. It should be easily assayable and be able to indicate all changes in cancer patients receiving treatment.

31. uses
Screening in general population
Differential diagnosis of symptomatic patients
Clinical staging of cancer
Estimating tumor volume
As a prognostic indicator for disease progression
Evaluating the success of treatment
Detecting the recurrence of cancer
Monitoring reponse to therapy
In order to use a tumor marker for screeningin the presence of cancer in asymptomatic individuals in general
population, the marker should be produced by tumor cells and not be present in healthy people.
However, most tumor markers are present in normal, benign and cancer tissues and are not specific enough
to be used for screening cancer.

32. 1. Enzymes –ALP,PSA
2. HORMONES- HCG,AFP,CEA
3. CARBOHYDREATE ANTIGEN-CA-125, CA-19,CA-19-3
4. REECPTOR Marker –Estrogen Progesterone
5. Protein marker – thyroglobulin,Ferrtin,Immunoglobulin

33. COMMONLY USED GYNECOLOGIC
TUMOR MARKERS

34. Screening
• CA 125
- Also known as MUC 16, it is a cell surface glycoprotein normally expressed in tissues derived from coelomic epithelia such as
ovary ,fallopian tube , peritoneum , pleura , pericardium , colon , kidney , and stomach.
- Useful for monitoring epithelial ovarian cancer patients during their chemotherapy.
- Sensitivity of test, elevated CA 125 levels seen in 50 % of patients with stage 1 disease.
- Specificity of test is improved when it is combined with transvaginal ultrasonography or when CA 125 levels are followed over
time.
- For postmenopausal patient with an adnexal mass and very high serum CA 125 level ( >200U/ml) there is a 96 % positive
predictive value for malignancy.
- For premenopausal specificity of test is very low because the CA 125 levels are elevated in other benign conditions also.
- Raised in-Fibroids
Endometriosis
Adenomyosis
Pid, Benign ovarian cyst
Physiological states like pregnancy and menstruation.

35. CA-125
• Approx 90% of ovarian cancers are epithelial carcinomas and contain a epithelium–related glycoprotein, cancer
antigen 125.
• The major forms in serum have molecular weights of 200 kDa to 400 kDa.
• CA-125 can be localized in most serous, endometrioid, and clear cell ovarian carcinomas; less frequently in
mucinous tumours.
• proven to be a useful first-generation marker for monitoring ovarian cancer and triaging patients with pelvic
masses, despite limitations in sensitivity and specificity.
• False-positive results in peritoneal inflammation, such as endometriosis, adenomyosis, pelvic inflammatory disease,
menstruation, uterine fibroids, or benign cysts.

36. • CA-125 values elevated in a number of gynecologic (eg, endometrium, fallopian tube) and nongynecologic (eg,
pancreas, breast, colon, lung) cancers.
• Marked elevations (>1500 U/mL) are generally seen with ovarian cancer.
• The ACOG and Society of Gynecologic Oncologists- recommend gyne-onco referral for women with a pelvic
mass suggestive of ovarian cancer and a serum CA-125 value >35 U/mL in postmenopausal women or >200
U/mL in premenopausal women.

37. Detection of recurrence and progression of
ovarian cancer
• Increase in the serum CA-125 value during or after treatment is a strong predictor of future disease progression.
• A rapid decrease in the CA-125 value during initial treatment correlates with longer progression-free intervals and
survival.
• value < 15 U/mL after a standard 6-course treatment generally correlates with longer progression-free intervals,
although it does not predict whether microscopic disease is present.
• value >35 U/mL after a standard 6-course chemotherapy treatment predicts the presence of disease.
• Disease may also progress when CA-125 values are stable.
• Rising CA-125 values may precede clinical detection of recurrent disease by at least 3 months.

38. Human epididymal protein 4 (HE4)
• Detects ovarian cancer with 67 % sensitivity , at a specificity level of 96 %.
• Elevated HE 4 levels are expressed in early stage ovarian cancer and hence HE4 can detect
stage I disease.
• Differentiates between ovarian cancer and benign ovarian conditions.
• Its levels elevate at least 5-8 months prior to relapse of ovarian cancer.
• Over expressed in 93 % of serous, 100 % of endometroid and 50 % of clear cell tumors, but
not in mucinous ovarian carcinomas.
The diagnostic accuracy and sensitivity of the combination of HE 4 and Ca125 is significantly
higher than either of the biomarkers used alone.

39. B-hcg
• hCG is a heterodimer composed of 2 glycosolated sub- units (alpha and beta chains) non-covalently bonded
• distinctive 24 amino acid carboxy-terminal extension.
• hCG can exist in multiple forms including the intact 2- chain peptide, free alpha and beta chains, as well as various
degradation products (e.g., beta core fragment).
• Produced by syncytiotrophoblast of placenta
• To maintain progesterone production by the corpus luteum during early pregnancy. hCG can be detected as early as
one week after conception.
• Type of sample for assay- Serum or urine. Reference range- Serum: 0 - 5IU/L.
• Done in patients <40yrs with T-O mass

40. Malignancies with elevated levels
a. Virtually all patients with gestational trophoblastic disease (GTD) (i.e., complete and partial molar pregnancy,
choriocarcinoma and placental site trophoblastic tumours).
b. Non-seminomatous germ cell tumours (NSGCT) (e.g., of testis and ovary).
c. Seminomatous germ cell tumours of testis (approx. 20%).
• Benign Diseases With elevated levels- e.g., ectopic pregnancy
• Physiological conditions with elevated levels--Pregnancy, after termination of pregnancy
• Main clinical applications
• a. For monitoring patients with GTD.
• b. In conjunction with AFP, for determining prognosis and monitoring patients with NSGCT of ovary.

41. Alpha-Fetoprotein (AFP)
• AFP is a 70 kDa glycoprotein homologous to albumin.
• fetal serum protein synthesized by the liver, yolk sac, and gastrointestinal tract.
• AFP is a major component of fetal plasma, reaching a peak concentration of 3 mg/mL at 12 weeks of gestation.
• Following birth, AFP rapidly clears from the circulation, because its half-life is 3.5 days.
• AFP concentration in adult serum is less than 20 ng/mL.
• Physiological function- Appears to perform some of the functions of albumin in the foetal circulation.
• Malignancies with elevated levels-
a. Non-seminomatous germ cell tumours (NSGCT) of testis, ovary and other sites.
b. Hepatocellular carcinoma (HCC).
c. Hepatoblastoma (in children, extremely rare in adults).
d. AFP may be occasionally elevated in patients with other types of advanced adenocarcinoma.
• Benign conditions which may have elevated levels- Hepatitis, cirrhosis, biliary tract obstruction, alcoholic liver disease,
ataxia telangiectasia and hereditary tyrosinaemia.
• Reference range- 0 - 10 kU/L or 0-12 mg/L Half life in serum Approx. 5 days.

42. Main clinical applications
• AFP and beta-hCG play crucial role in the management of patients with nonseminomatous germ cell tumors.
• AFP or beta-hCG is elevated in 85% of patients with these tumors but in only 20% of patients with stage I disease.
Hence, these markers have no role in screening.
• .In patients with extragonadal disease or metastasis at the time of diagnosis, highly elevated AFP or
beta-hCG values can be used in place of biopsy to establish a diagnosis of nonseminomatous germ cell tumor.
• AFP >10,000 ng/mL or beta-hCG >50,000 mIU/mL at initial diagnosis portend a poor prognosis, with a 5-year
survival rate of 50%.
• Similarly staged patients with lower AFP and beta-hCG levels have a cure rate of greater than 90%.
• Patients with AFP and beta-hCG levels that do not decline as expected after treatment have a significantly worse
prognosis, and changes in therapy should be considered.

43. Carcinoembryonic antigen
• Most vulvar tumors of sweat gland origin, including malignant tumors, stain positively for
carcinoembryonic antigen (CEA).
• In patients with vaginal adenosis, surface columnar epithelium and glands may show focal
cytoplasmic membrane staining for CEA.
• In situ and invasive adenocarcinomas underlying extramammary Paget disease of the anogenital
area express CEA.
• CEA is also demonstrable in Paget cells at metastatic sites, such as lymph nodes. CEA is present in most
urothelial adenocarcinomas of the female urethra.

44. .
• CEA levels are elevated in up to 35% of patients with endometrial cancer
• CEA immunohistochemistry cannot distinguish between benign and malignant glandular proliferations of the uterine
cervix; therefore, CEA staining is of no value in the differential diagnosis of endocervical and endometrial
adenocarcinomas.
• Most epithelial neoplasms of the ovary also express CEA. Such as Brenner, endometrioid, clear cell, and serous tumors.
• CEA is frequently present in patients with cancer that has metastasized to the ovary; that is because the primary cancer
is generally mammary or gastrointestinal in origin, and such tumors frequently contain CEA
.

45. Lactate Dehydrogenase
• LDH is involved in tumor initiation and metabolism. Cancer cells rely on increased glycolysis resulting in increased lactate
production in addition to aerobic respiration in the mitochondria, even under oxygen- sufficient conditions
• Elevated levels found in Dysgerminoma

46. Inhibin
• Inhibin is a peptide hormone normally produced by ovarian granulosa cells.
• It inhibits the secretion of FSH by the anterior pituitary gland. It reaches a peak of 772 ± 38 U/L in the follicular
phase of the menstrual cycle and usually becomes nondetectable after menopause.
• Certain ovarian tumors, mostly mucinous epithelial ovarian carcinomas and granulosa cell tumors, also produce
inhibin, and its serum levels reflect the tumor burden.
• An elevated inhibin level in a postmenopausal woman or a premenopausal woman presenting with amenorrhea and
infertility is suggestive of, but not specific for, the presence of a granulosa cell tumor.
• Inhibin levels can also be used for tumor surveillance after treatment to assess for residual or recurrent disease.

47. Other Tumor Markers
• Estradiol
• Estradiol was one of the first markers identified in the serum of patients with granulosa cell tumors.
• In general, it is not a sensitive marker for granulosa cell tumors.
• Approx 30% of tumors do not produce estradiol, because they lack theca cells, which produce
androstenedione, a necessary precursor for estradiol synthesis. However, monitoring serum estradiol
postoperatively may be useful for detecting recurrence of an estradiol-secreting tumor.

48. Squamous cell carcinoma antigen
• Squamous cell carcinoma (SCC) antigen may be increased in patients with epidermoid carcinoma of the cervix,
benign tumors of epithelial origin, and benign skin disorders.
• SCC antigen may be helpful in assessing response to chemotherapy and in determining relapse when monitoring
patients with complete remission.

49. Müllerian inhibiting substance
o• Müllerian inhibiting substance (MIS) is produced by granulosa cells in developing follicles.
• It has emerged as a potential tumor marker for granulosa cell tumors. As with inhibin, MIS is typically undetectable in
postmenopausal women.
• An elevated MIS value is highly specific for ovarian granulosa cell tumors; however, this test is not commercially
available for clinical use.

50. Topoisomerase II
Topoisomerase II has emerged as a promising, clinically relevant biomarker for survival in patients with advanced epithelial
ovarian cancer. Its expression is detected in tumor samples by immunohistochemistry.

51. Carbohydrate antigen 19-9
• Serum carbohydrate antigen 19-9 is elevated in up to 35% of patients with endometrial cancer and can
be used in the follow-up evaluation of patients with mucinous borderline ovarian tumors.
• Measurement of serum tumor markers in the follow-up care of these patients may lead to earlier
detection of recurrence in only a very small proportion of patients; the clinical value of earlier detection
of recurrence remains to be established. Carbohydrate antigen is not specific for ovarian cancer.

52. Human telomerase reverse transcriptase
• Human telomerase reverse transcriptase (hTERT) is a novel biomarker for patients with ovarian and uterine cancers.
• The hTERT mRNA level has a significant correlation with CA-125 and with histologic findings in ovarian cancer.
• Serum hTERT mRNA is useful for diagnosing gynecologic cancer and is superior to conventional tumor markers.
• Up-regulation of hTERT may play an important role in the development of cervical intraepithelial neoplasia (CIN) and
cervical cancer; hTERT could be used as an early diagnostic biomarker for cervical cancer in the future.

53. Lysophosphatidic acid
Lysophosphatidic acid stimulates cancer cell proliferation, intracellular calcium release, and tyrosine
phosphorylation, including mitogen- activated protein kinase activation.
Lysophosphatidic acid has been shown to be a multifunctional signaling molecule in fibroblasts and other cells.
It has been found in the ascitic fluid of patients with ovarian cancer and is associated with ovarian cancer cell
proliferation.
Further studies are needed to determine the role of this marker.

54. Some recommendations
• A serum CA-125 assay does not need to be undertaken in all premenopausal women when an
ultrasonographic diagnosis of a simple ovarian cyst has been made.
• Ovarian cysts in postmenopausal women should be initially assessed by measuring serum CA125 level and
transvaginal ultrasound scan
• Lactate dehydrogenase (LDH), α-FP and hCG should be measured in all women under age 40 with a complex
ovarian mass because of the possibility of germ cell tumour.
-RCOG
• Gyne-onco referral for women with a pelvic mass suggestive of ovarian cancer and a serum CA-125
value>35 U/mL in postmenopausal women or >200 U/mL in premenopausal women should be done.
- ACOG, ASCO

55. • Carbohydrate antigen 19-9
• Serum carbohydrate antigen 19-9 is elevated in up to 35% of patients with endometrial cancer
and can be used in the follow-up evaluation of patients with mucinous borderline ovarian tumors.
• Measurement of serum tumor markers in the follow-up care of these patients may lead to earlier
detection of recurrence in only a very small proportion of patients; the clinical value of earlier
detection of recurrence remains to be established. Carbohydrate antigen is not specific for ovarian
cancer.

57. KEY POINTS
• A large number of tumour markers have been found to be associated with gynecological malignancies.
• However most of them have low & variable specificity.
• The methods of their detection and estimation are difficult, costly and not widely available.
• Careful selection of tumor marker to be investigated should be done

58. • THANK YOU

59. • Borderline serous tumors (10%)
Criteria for diagnosis
1. Epithelial hyperplasia in the form of pseudostratification , tufting , cribriform and micropapillary architecture.
2. Mild nuclear atypia and mild increased mitotic activity
3. Detached cell clusters
4. Absence of destructive stromal invasion
Mucinous tumors
These are the cystic ovarian tumors have loculi lined with mucin secreting epithelium
Mucinous carcinomas are bilateral in 8- 10 % of cases
They may reach enormous size filling the entire abdominal cavity.
Peudomyxoma peritonnei- used to describe abundant mucoid or gelatinous material in the pelvis and abdominal
cavity surrounded by fibrous tissue
Most commonly secondary to well differentiated appendiceal mucinous neoplasm
Rare in ovarian tumors
Endometroid tumors
- 2nd most common histologic type
Clear cell carcinoma
-Histological patterns- tubulocystic, papillary, reticular and solid
-made up of clear and hobnail cells that projects their nuclei into the apical cytoplasm.
-focal areas of endometriosis are common and mixed clear cell and endometroid carcinoma may occur

60. • Thank you