ovarian tumours

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1 RESTRICTED INTRODUCTION 1. Ovarian tumour is one of the major gynaecological disease and is a frequent site for primary and metastatic tumours. Due to its complex structure, primary ovarian neoplasm are of diverse histological types. Ovarian cancer accounts for 25% of all gynaecologic malignancies and 3rd commonest cause of death due to malignancies of female genital tract in western world 1 . Ovaries are subjected to monthly endocrine and traumatic insult during ovulatory cycle and prime site for tumour genesis. The primary and secondary carcinoma of ovary are frequent with variety of pathologic pattern, which is seen in all ages 2 . Histological classification of ovarian tumours along with clinical stage forms an integral part of evaluation of optimum mode of therapy. RESTRICTED

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INTRODUCTION

1. Ovarian tumour is one of the major gynaecological disease and is a

frequent site for primary and metastatic tumours. Due to its complex

structure, primary ovarian neoplasm are of diverse histological

types. Ovarian cancer accounts for 25% of all gynaecologic

malignancies and 3rd commonest cause of death due to

malignancies of female genital tract in western world1. Ovaries are

subjected to monthly endocrine and traumatic insult during ovulatory

cycle and prime site for tumour genesis. The primary and secondary

carcinoma of ovary are frequent with variety of pathologic pattern,

which is seen in all ages2. Histological classification of ovarian

tumours along with clinical stage forms an integral part of evaluation

of optimum mode of therapy.

AIM

2. To present a case of Ovarian Carcinoma, study the various

histomorphological features of the ovarian tumours and their pattern

of occurrence in relation to age and type diagnosed at in last one

year.

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3 months

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CASE STUDY

3. Bio Data of Patient

a.

Name XYZ

b.

Age 55 years

c. Sex Female

d.

Residence Chakwal

e.

Marital Status Married

f. Education Illiterate

g.

Menopause 8 yrs

h.

Date of Admission 18th March, 2011

4. Presenting Complaints

a. She presented as a known case of moderately differentiated

Adenocarcinoma.

b. Pain lower abdomen

c. Dyspepsia

d. Weakness

5. History of Presenting Illness. The patient had consistent pain

lower abdomen for 3 months, which was dull in nature and

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associated with weakness, nausea and weight loss. There were no

aggravating or relieving factors. No history of urinary or bowel

complaints. Consulted a civil hospital. Laparotomy was done,

bilateral ovarian cysts were found. Cystectomy was done.

Histopathology report revealed moderately differentiated

adenocarcinoma. After this procedure the patient reported to MH

along with histopathology report for consultation. Her staging

laparotomy was planned on 29th Mar 2011.

6. Past History. Not Significant

7. Obstetrical History

a. Married for 30 yrs

b. P7 - SVD

c. Menopause for 8 yrs

8. Menstrual History

a. Menarche - 13 yrs of age

b. Menopause – 50 yrs of age

9. Personal History.

a. Huqqa Smoker

b. HTNº,DMº, Asthmaº, IHDº

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10. Family History

a.

No H/O Ca Breast, Ca Ovary, Ca Endometrium

b.

Both parents were Hypertensive

c. her sister having TB

11. Socio Economic History. Belongs to a middle class family.

12. General Physical Examination. Well oriented lady, thin and lean

looking pale and lethargic.

a.

BP 100/70mm of Hg

b.

Pulse 92 b/min

c. Temp 98.6 º F

d.

Pallor Positive

e.

Lymph Nodes Not Palpable

f. Thyroid Not Enlarged

g.

Breasts Normal Bilaterally

h.

Cyanosis

Absenti. Jaundice

j. Edema

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NAD

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k. Weight 50 Kgs

13. Gynaecological Examination

a. Speculum Examination

(1) Vulva Vagina – Hypoestrogenized, Scanty hair distribution

(2) Cervix normal looking

(3) No Vaginal discharge

(4) No local lesion

b.

Bimanual Vaginal Examination

(1) Uterus Normal in size (postmenopausal), Mobile

(2) Fullness of all fornices

c. Digital Rectum Examination - Normal

14. Systemic Examination

a. Abdomen

(1) Protuberant

(2) Soft, non tender

(3) Liver – lower border Palpable

(4) Spleen – Not Palpable

(5) BS - Positive

(6) No mass Palpable(7) Ascites - Positive

b. Respiratory System

c. CVS

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d. CNS

15. Investigation

a. Blood CP

(1) Hb12.1 g/dl

(2) Plateletes370 x 10^9/L

(3) TLC9.4 x 10^9/L

b.CA-125

24 U/ml

c. BSR4.6 mmol/l

d. Urine for Biochemistry/Microscopy WNL

Negative

e. HBSAg/Anti HCV

f. LFTsWNL

g. RFTsh. Urea/Creatinine/Na+/K+

i. Chest X-RayNormal

j. ECGk. USG Abdomen/Pelvis Bilateral Adnexal

massesl. CT Scan Bilateral Adnexal

masses Pelvic ascites Mild hepatomegaly

16. Diagnosis. Moderately Differentiated Adenocarcinoma

17. Management

a. Counselling

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b. High risk consent taken

c. Cross match sent

d. 03 units RCC arranged

e. Gut preparation done

f. DJ Stenting done on 24th Mar 2011

g. Staging Laparotomy done on 29th Mar 2011

(1) Uterus Atrophic, adherent to large gut & peritoneum on lt side

(2) Rt Adenexal friable mass (3 x 4 cm), bleed to touch & adherent to ureter

(3) Omentum Healthy looking(4) Peritoneum Unhealthy looking(5) Ascitic fluid taken for cytology(6) Omentum and Uterus sent for histopathology

Postoperative Management

18. Immediate Postoperative care

a. Kept under high nursing care

b. Given I/V antibiotics & I/V fluids

c. Postoperative recovery was smooth

19. Histopathological Reports

a. Omentum - no evidence of malignancy seen

b. Ovaries – Papillary Adenocarcinoma

20. Peritoneal washing cytology showed no malignant cells

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21. Chemotherapy was started on 13th April 2011

22. Final Diagnosis. Papillary Adenocarcinoma

CLASSIFICATION & STAGING OF OVARIAN TUMORS

23. The World Health Organization classification (WHO) was introduced

in 1973 based on four major types of tissues. Namely Surface

germinal epithelium, Sex cords, Germ cells and Specialized

ovarian stroma. All these can give rise to a variety of neoplasms. It

relied primarily on the recognition of cell types and pattern of

growth3.

24. Modified WHO scheme of classification in 1995

a. Surface epithelial tumours

(1) Serous tumours

(a) Benign

i. Cystadenoma and papillary cystadenomaii. Surface paillomaiii. Adenofibroma and cystadenofibroma

(b) Borderline malignancy (low malignant potential)

i. Cystic tumor and papillary cystic tumorii. Surface papillary tumoriii. Adenofibroma and cystadenofibroma

(c) Malignant

i. Adenocarcinoma, papillary adenocarcinom and

papillary cystadenoma

ii. Surface papillary adenocarcinoma

iii. Adenocarcinofibroma and cystadenofibroma.

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(2) Mucinuous tumors (endocervical like and intestinal type)

(a) Benign

i. Cystadenoma ii. Adenofibroma and cystadenofibroma

(b) Malignant

i. Adenocarcinoma and cystadenocarcinomaii Adenocarcinofibroma & cystadenocarcinofibroma

(3) Endometrioid tumors

(a) Benign

i. Cystadenoma with squamous differentiation ii. Adenofibroma and cystadenofibroma

iii. Adenofibroma and cystadenofibroma with squamous differentiation

(b) Malignant

i. Adenocarcinoma and cystadenocarcinoma ii. Adenofibroma and cystadenofibroma with squamous differentiation iii. Adenocarcinofibroma & cystadenocarcinofibroma iv. Adenocarcinofibroma & cystadenocarcinofibroma with squamous differentiation

(c) Epithelial (endometrioid) stromal and (endometrioid) stroma

i. Adenosarcoma, homologous and heterologousii. Mesodermal (Mullerian) mixed tumor

(carcinosarcoma) homologous and heterologousiii. Stroma sarcoma.

(4) Clear cell tumour

(a) Benign

i. Cyst adenoma ii. Adenofibroma and cystadenofibroma

(b) Malignant

i. Adenocarcinoma ii. Adenocarcinofibroma and cystadenofibroma

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(5) Transitional cell tumours

(a) Brenner tumour(b) Brenner tumor of borderline malignancy/ proliferating(c) Malignant Brenner tumour(e) Transitional cell carcinoma (non-Brenner type)

(6) Squamous cell tumour

(7) Mixed epithelial tumour (specific types)

(a) Benign(b) Of borderline malignancy/ or low malignant potential(c) Malignant

(8) Undifferentiated carcinoma

(9) Unclassified

b. Sex-cord Stromal Tumours

(1) Granulosa cell tumour

(a) Juvenile(b) Adult

c. Germ cell tumours

(1) Dysgerminoma

(a) Variant with syncytiotrophoblast cells

(2) Yolk sac tumour (endodermal sinus tumor)

(a) Variant Polyvesicular vitelline tumor(b) Hepatoid(c) Glandular

(3) Embryonal carcinoma

(4) Polyembryoma

(5) Choriocarcinoma

(6) Teratoma

(a) Premature(b) Mature

i. Solid

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ii. Cystic (dermoid cyst)iii. With secondary tumour formation (specify types)iv. Fetiform (Homunculus)

(c) Monodermal and highly specialized

i. Strauma ovary ii. Ariant with thyroid tumour (specify type) iii. Carcinoid iv. Insular v. Trabecular vi. Strauma carcinoid vii. Mucinous carcicoid viii. Neuroectodermal tumours ix. Sebaceous tumours x. Others

(7) Mixed (specify types)

(a) Gonadoblastoma

i. Variant with dysgerminoma or other germ cell tumor

(b) Tumours of rete ovari

i. Adenoma and cystadenoma

ii. Carcinoma

(c) Mesothelial tumours

i. Adenomatoid tumour

ii. Others

(d) Tumours of uncertain origin

i. Small cell carcinoma ii. Tumour of probable Wolffian origin iii. Hepatoid carcinoma iv. Oncocytoma

(e) Gestational trophoblastic diseases

(f) Soft tissue tumours specific to ovary

(g) Malignant lymphomas

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(h) Unclassified tumours

(i) Secondary (metastatic) tumours

(j) Tumour like lesions

i. Solitary follicle cyst

ii. Multiple follicle cyst (polycystic disease) (sclero cystic ovaries)

d. Large solitary leuteivized follicle cysts of pregnancy and puerperium

e. Hyper-rectio luteinalis (multiple leutinized follicle cysts) – variant with corpora lutea.

(1) Corpus luteum cyst

(2) Pregnancy luteoma

(3) Ectopic pregnancy

(4) Hyperplasia of stroma

(5) Stromal hyperthecosis

(6) Massive edema

(7) Fibromatosis

(8) Fibromatosis

(9) Endometriosis

(10) Cyst, unclassified (simple cyst)

f. Inflammatory lesions

(1) Xanthogranuloma

(2) Malakoplakia

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(3) Other

25. Histologic Staging/Classification (FIGO, 1971)

STAGE  I  - Tumour is confined to the ovary / ovariesIa Only one ovary is affected by the tumour, the ovary

capsule is intact No tumour is detected on the surface of the ovary Malignant cells are not detected in ascites or peritoneal

washings

Ib Both ovaries are affected by the tumour, the ovary capsule is intact

No tumour is detected on the surface of the ovaries Malignant cells are not detected in ascites or peritoneal

washings

Ic The tumour is limited to one or both ovaries, with any of the following:

The ovary capsule is ruptured The tumour is detected on the ovary surface Positive malignant cells are detected in the ascites or

peritoneal washings

STAGE II – Tumour involves one or both ovaries and has extended into the pelvisIIa The tumour has extended and/or implanted into the

uterus and/or the fallopian tubes. Malignant cells are not detected in ascites or peritoneal

washings

IIb The tumour has extended to another organ in the pelvis Malignant cells are not detected in ascites or peritoneal

washingss

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IIc Tumours are as defined in 2A/B, and malignant cells are detected in the ascites or peritoneal washings

STAGE III – The tumour involves one or both ovaries with microscopically confirmed peritoneal metastasis outside the pelvis and/or regional lymph node metastasis.

Includes liver capsule metastasis.IIIa Microscopic peritoneal metastasis beyond the pelvis

IIIb Microscopic peritoneal metastasis beyond the pelvis 2 cm or less in greatest dimension

IIIc Microscopic peritoneal metastasis beyond the pelvis more than 2 cm in greatest dimension and/or regional lymph nodes metastasis

STAGE: IV – Distant metastasis beyond the peritoneal cavity. And, liver parenchymal metastasis.

HISTOGENESIS

26. Epithelial Tumours. Are derived from the surface epithelium of the

ovary and are further classified as benign, borderline or malignant,

according to cell type and behavior4. Epithelial tumours account for

60-65 % of all Ovarian tumours and approximately 90% of those that

are malignant5.

a. Serous Tumours : Serous tumours are the most common

epithelial tumours (40-50%). Serous carcinoma is usually large

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and is often bilateral. It exhibits a mixture of cystic, papillary, and

solid growth patterns. The carcinoma often invades through the

ovarian capsule and grows on the surface of the ovary. Foci of

necrosis and hemorrhage are common in serous carcinoma.

Microscopically it has a papillary pattern and some times shows

areas of calcification, which is called Psammoma bodies.

b. Mucinous Tumours. Mucinous carcinoma is typically large,

unilateral and composed of irregular cysts and glands lined by

atypical mucinous cells, which often are stratified into four or more

cell layers. They contain only endocervical-type cells, only

intestinal-type mucinous cells, or a combination of the two, but are

usually composed of cells that are not specifically suggestive of

either endocervical- or intestinal-type mucinous cells. The main

criterion of invasive mucinous carcinoma is the presence of

obvious stromal invasion. Dissection of mucin into the stroma is

especially common and extensive in cases of pseudomyoma

peritonei and is designated pseudomyxoma ovarii2.

c. Endometrioid Tumours. Endometrioid carcinomas histologically

resemble the usual adenocarcinoma of the endometrium. These

tumours are solid masses with a soft, firm, or fibrous consistency.

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They are often predominantly cystic and contain soft or firm solid

nodular masses. These cysts are usually filled with chocolate-

coloured fluid. 15 % cases of endometrioid carcinoma of ovary

are associated with endometrial carcinoma.

d. Clear Cell Tumours. These are commonly unilateral. The tumor

is predominantly cystic which is unilocular and contains brown

fluid. The inner surface has polypoidal projection. The

characteristic microscopic appearance is called “Hob Nail”

appearance. Clear cell carcinoma frequently co exist with ovarian

endometriosis and endometriod carcinoma of ovary , which

suggests that it may be a variant of endometriod tumor.

e. Transitional Cell Tumours (Brenner Tumours ). Malignant

transitional cell tumours (Brenner tumours) have both solid and

cystic components. The cysts contain papillary or polypoid

masses or solid nodules in their walls. The presence of soft

masses or foci of necrosis may suggest malignancy. Malignant

transitional cell tumors (Brenner tumors) resemble a high-grade

transitional cell carcinoma of the bladder5. The tumor cells have

pleomorphic, atypical nuclei, and the malignant transitional cells

obviously infiltrate the stroma.

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f. Mixed epithelial tumors. Admixtures of the various subtypes of

the surface epithelial- stromal category often occur. Almost all

combinations of mixed epithelial tumors have been encountered.

The WHO limits their identification to those neoplasms in which

one or more components other than the predominant component

account for at least 10% of the tumor on microscopic examination.

g. Undifferentiated Tumour. Undifferentiated carcinoma is one that

shows no differentiation or contains only rare, minor areas of

differentiation according to the WHO. Marked cellular atypia,

bizarre giant cells, and atypical mitoses are frequent.

Undifferentiated carcinoma grows rapidly, usually exhibits extra

ovarian spread, and has the poorest prognosis of any epithelial

carcinoma adenocarcinoma.

AETIOLOGY OF OVARIAN CANCER

27. The cause of Ovarian Cancer is unknown but some of the

aetiological factors of ovarian cancer are

a. Tubal ligation and hysterectomy (with ovarian conservation) is

associated with a decrease risk of ovarian cancer [C]

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b. the use of combined oral contraceptive pills appears protective,

with increasing duration of use increasing the level of

protection afforded [C]

c. Women from families with hereditary ovarian cancer syndromes

may reduce their risk of developing ovarian cancer by ever use

of the combined oral contraceptive pills[C]

d. Factors which reduce ovulation are associated with a reduced

risk of ovarian cancer.

e. Evidence of causal association between the use of ovulatory

stimulants and the subsequent development of epithelial

ovarian tumours is inconclusive.

f. Hereditary ovarian cancers represent fewer than 10% of all

ovarian cancers.

g. Bilateral salpingo-oopherectomy is protective in BRCA mutation

carriers [B]

h. HNPCC has an association with cancers of the ovary and

endometrium4

i. Infertility Treatment. Drugs used for ovulation induction

suggested being associated with subsequent increase risk of

ovarian carcinoma.

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j. Pelvic Irradiation. Pelvic irradiation increases the risk of pelvic

cancers including ovarian cancers.

SYMPTOMS

28. Symptoms of ovarian cysts and tumours include

a. Indigestion, gas or bloating

b. difficulty urinating, or frequent need to urinate

c. dull ache in the lower back

d. pain during sexual intercourse

e. painful menstruation and abnormal bleeding

f. swelling and/or pain in the abdomen

g. Pelvic pain radiating down the inner aspect of the leg is a

common presenting symptom, and torsion classically presents

as severe pain associated with vomiting

h. Rupture of a large cyst may produce signs of peritonitis,

particularly if the cyst contents are irritant (e.g. endometriotic

cyst or dermoid cyst), and the patient may be shocked in cases

of extensive rupture or continuing haemorrhage.

DIAGNOSIS

29. Tests that look for ovarian cysts or tumours include

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a. Ultrasound . To determine the size and location of the cyst or

tumour.

b. Imaging tests. Computed tomography (CT), magnetic

resonance imaging (MRI), and positron emission tomography

(PET) are highly detailed imaging scans to find ovarian tumours

and see whether and how far they have spread.

c. Laparoscopy. used for the treatment of ovarian cysts.

d. CA-125. to look for a protein called CA-125, tend to be higher

in some -- but not all -- women with ovarian cancer. This test is

mainly used in women over age 35, who are at slightly higher

risk for ovarian cancer.

TREATMENT

30. In general, the course of treatment is determined by the stage of the

cancer. Stages range from I to IV based on the cancer's specific

characteristics, such as whether it has spread beyond the ovaries.

Surgery is the main treatment for ovarian cancer. Following surgery,

women with higher-stage tumours may receive chemotherapy.

About 10 - 15% of epithelial ovarian tumours are referred to as

"borderline” because their appearance and behaviour under the

microscope is between benign and malignant. These tumours are

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often referred to as carcinomas of low malignant potential because

they rarely metastasize or cause death. Borderline ovarian tumours

are most often seen in younger women with epithelial ovarian

cancer. Surgery is usually recommended to remove these tumours.

Chemotherapy may also be used to treat borderline tumours that

appear to have more aggressive features (such as recurring after

surgery).

31. Treatment Options for Stage I and Stage II Ovarian Cancer.

Treatment options for stage I and stage II ovarian cancer may

include:

a. Surgery. Removal of the uterus (total hysterectomy), removal

of both ovaries and fallopian tubes (bilateral salpingo-

oophorectomy), partial removal of the omentum, the fatty layer

that covers and pads organs in the abdomen(omentectomy),

and surgical staging of the lymph nodes and other tissues in the

pelvis and abdomen. (Carefully selected premenopausal

women in Stage I with the lowest-grade tumors in one ovary

may sometimes be treated only with the removal of the

diseased ovary and tube in order to preserve fertility.)

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b. Chemotherapy . Patients with stage IA or B disease, grade 1

(or sometimes grade 2), usually do not need further therapy

after surgery. However, higher risk patients (stage IC, stage

I/grade 3) are usually treated with platinum-based

chemotherapy to reduce their risk of subsequent relapse.

32. Treatment Options for Stage III and Stage IV Ovarian Cancer.

Treatment options for stage III and stage IV ovarian cancer may

include

a. Surgery. Removal of the tumour (debulking), total abdominal

hysterectomy, bilateral salpingo-oopherectomy, and

omentectomy

b. Chemotherapy . Combination chemotherapy with a platinum-

based drug and a taxane drug delivered intraperitoneally

(through the abdominal cavity)

33. Treatment Options for Recurrent Ovarian Cancer . If ovarian

cancer returns or persists after treatment, chemotherapy is the

mainstay of treatment, although it is not generally curative in the

setting of relapsed disease. Clinical trial options include additional

surgical debulking, and biologic therapy combined with

chemotherapy5.

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34. Chemotherapy. Single chemotherapeutic agents active in epithelial

ovarian cancer include6

a. Alkylaking agents (eg, cyclopthosphamide)

b. Platinum Compounds (cisplatin and carboplatin)

c. Anthracyclenes (eg, epirubicin)

d. Taxanes (eg, paclitaxel and docetaxel)

35. Combination chemotherapy. The chemotherapeutic agents have

been used in a number of combinations but the combinations

containing cisplatin or carboplatin have shown higher response rate

than others but without improving the survival rate.

36. Radiotherapy. It is not needed in stage Ia disease and is not

effective in patients with stage IV carcinoma of the ovary. It can be

used as an alternative to chemotherapy in patients with stage Ib-IIIa.

FOLLOW UP

37. CA-125. The patients receiving chemotherapy are followed with

regular estimation of CA-125. A rapid fall in its level indicates

chemosensitivity of the tumour. Persistent or rising levels of CA-125

indicate drug resistance or recurrence.

PROGNOSIS

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38. The prognosis of epithelial ovarian tumours is determined by the

following factors

a. Extent of disease at diagnosis

b. Size of residual tumour bulk

c. Positive retroperitoneal nodes

d. Histological subtype and grading of tumour

39. The overall 5 year survival is approximately 35% in all epithelial

ovarian tumours. The stage wise survival is as under

Stage 5 yrs survival

I 60-70%

II 43-51%

III 17.5%

IV 4.7%

CLINICOPATHOLOGICAL REVIEW OF OVARIAN TUMOURS IN RAWALPINDI

40. Ovarian tumours pertaining to the cases diagnosed,

histopathologically at ______________ Laboratory, for the period

from January 2010 to December 2010. During this period, total 264

cases of ovarian tumours were diagnosed. Out of these

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histopathologically about 67 cases were malignant and 197 were

benign cases. The result pattern in relation to age and type

diagnosed is summarized as under.

a. Age

Table-1: Age Distribution in 67 Malignant Cases

Age (years) No. of Cases Percentage

11 – 20 08 11.91

21 – 30 08 11.91

31 – 40 09 13.43

41 – 50 19 28.35

51 – 60 15 22.38

61 – 70 06 8.95

> 70 years 02 2.98

Total 67 100.00

Table-2: Age Distribution in 197 Benign Cases

Age (years) No. of Cases Percentage

11 – 20 13 6.59

21 – 30 78 39.59

31 – 40 73 37.05

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41 – 50 25 12.69

51 – 60 04 2.03

61 – 70 04 2.03

> 70 years - -

Total 197 100.00

b. Histological Diagnosis

Table-3: Histological typing of 67 ovarian cancers

Cancers No of Cases

Percentage

Serous Cyst Adenocarcinoma 12 17.91

Mucinous Adenocarcinoma 09 13.43

Granulosa Cell Tumour 07 10.44

Endometriod Adenocarcinoma 06 8.95

Adenocarcinoma (moderately

differentiated)

05 7.46

Mucinous Borderline Tumour 04 5.97

Yolk Sac Tumour 04 5.97

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Serous Borderline Tumour 03 4.47

Clear Cell Carcinoma 03 4.47

Immature Teratoma 03 4.47

Poorly Differentiated Carcinoma 02 2.98

Dysgerminoma 02 2.98

Metastatic Signet Ring Cell

Adenocarcinoma

02 2.98

Carcinoid Tumor 02 2.98

Transitional Cell Carcinoma 01 1.49

Mixed Sex Cord Stromal Tumour 01 1.49

Diffused Large B-Cell Lymphoma 01 1.49

Total 67 100

Table-4:Histological typing of 197 Benign Tumours

Tumours No of Cases

Percentage

Luteal cyst 122 61.92

Follicular cyst 32 16.24

Mucinous cyst adenoma 15 7.61

Serous cyst adenoma 15 7.61

Endometriod cyst 07 3.55

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Dermoid Cyst 06 3.04

Total 197 100

c. Unilateral/Bilateral ovarian tumours

Table-5: ovarian cancer

Unilateral Bilateral Total

No of cases 57 10 67Percentage 85.07 14.93 100

Table-6: Benign ovarian tumours

Unilateral Bilateral Total

No of cases 162 35 197Percentage 82.23 17.77 100

CONCLUSION

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41. Ovarian tumours occurred in all age group. But majority of

malignant cases were in the age group of 41-50 and 51-60 years. In

Benign tumours most of the tumours were in the age group of 21-30

and 31-40. Most of the tumours were unilateral. Amongst the

malignant tumours the highest number of cases seen were of

Serous Cyst Adenocarcinoma (17.91%) followed by Mucinous

Adenocarcinoma (13.43%).

REFERANCES

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1 Novak ER, Jones GS, Jones HW. Ovarian tumours. In: Gynaecological and Obstetrical Pathology. 6th Edition. Philadelphia; Saunders: 1997. P. 365-413.

2 Robert E Scully, Philips B Clement, Robert H Young. Ovarian surface epithelial-stromal tumours. In: Sternberg Diagnostic Surgical Pathology. 4th edn. Vol. 3. Philadelphia; Lippincott Williams & Wilkins: Mills SE, Cartes D, Greenson JK, Obserman HA, Reuter VE, Stoler MH

3

43 Obstetrics & Gynecology by David M Luesely and Phillip N Baker, second edition, page 814.

54 Ibid

5 Harter P, du Bois A, Hahman M et al. Surgery in recurrent ovarian cancer: the Arbeitsgemeinschaft Gynaekologische Onkologie 2006; 13: 1702-10

6 Silva EG, Robey-Cafferty SS, Smith TL, Gershenson DM (1999) Ovarian carcinomas with transitional cell carcinoma pattern. Am J Clin Pathol 93:457–465