ovarian cancer

1. Ovarian Cancer

2. Background
 Malignant lesions of the ovaries include primary lesions arising
from normal structures within the ovary and secondary lesions
from cancers arising elsewhere in the body. Primary lesions
include epithelial ovarian carcinoma (70% of all ovarian
malignancies), germ-cell tumors, sex-cord stromal tumors, and
other more rare types. Metastases to the ovaries are relatively
frequent, with the most common being from the endometrium,
breast, colon, stomach, and cervix. Although many histologic
types of ovarian tumors have been described, more than 90% of
ovarian malignancies are epithelial tumors. (See
Pathophysiology.)
 The precise cause of ovarian cancer is unknown, but several risk
and contributing factors (including both reproductive and genetic
factors) have been identified. (See Etiology.)
 Ovarian cancer is the most common cause of cancer death from
gynecologic tumors in the United States. Around the world, more
than 200,000 women are estimated to develop ovarian cancer
every year and about 100,000 die from the disease. The lifetime
risk of a woman developing epithelial ovarian cancer is 1 in 70.
(See Epidemiology.)
 Early disease causes minimal, nonspecific, or no symptoms.
Therefore, most cases are diagnosed in an advanced stage. The
prognosis of ovarian cancer is closely related to the stage at
diagnosis; thus, overall, prognosis for these patients remains

3. Pathophysiology
 Most theories of the pathophysiology of ovarian
cancer include the concept that it begins with the
dedifferentiation of the cells overlying the ovary.
During ovulation, these cells can be incorporated into
the ovary, where they then proliferate. Ovarian cancer
typically spreads to the peritoneal surfaces and
omentum.
 Ovarian carcinoma can spread by local extension,
lymphatic invasion, intraperitoneal implantation,
hematogenous dissemination, and
transdiaphragmatic passage. Intraperitoneal
dissemination is the most common and recognized
characteristic of ovarian cancer. Malignant cells can
implant anywhere in the peritoneal cavity but are
more likely to implant in sites of stasis along the
peritoneal fluid circulation. As discussed later, these
mechanisms of dissemination represent the rationale
to conduct surgical staging, debulking surgery, and

4. Epithelial ovarian cancer
 Epithelial tumors represent the most common
histology (90%) of ovarian tumors. Other
histologies include the following:
 Sex-cord stromal tumors
 Germ cell tumors
 Primary peritoneal carcinoma
 Metastatic tumors of the ovary
 Epithelial ovarian cancer is thought to arise
from epithelium covering the ovaries, which is
derived from the coelomic epithelium in fetal
development. This coelomic epithelium is also
involved in formation of the Müllerian ducts,
from which the Fallopian tubes, uterus, cervix, and
upper vagina develop.

5. Five main histologic subtypes, which are
similar to carcinoma, arise in the epithelial
lining of the cervix, uterus, and fallopian tube,
as follows:
 Serous (from fallopian tube)
 Endometrioid (endometrium)
 Mucinous (cervix)
 Clear cell (mesonephros)
 Brenner

6. Some variation is observed in the patterns of spread and
disease distribution within the various histologic subtypes
 Epithelial tumors are found as partially cystic
lesions with solid components. The surface may
be smooth or covered in papillary projections
(see the image below), and the cysts contain
fluid ranging from straw-colored to opaque brown
or hemorrhagic.
An enlarged ovary with a papillary serous carcinoma on the surface.

7.  Epithelial ovarian cancer most often spreads initially
within the peritoneal cavity (see the images below).
Metastatic disease often is found on the peritoneal
surfaces, particularly on the undersurface of the
diaphragms, the paracolic gutters, the bladder, and the
cul-de-sac. Other common sites are the surface of the
liver, the mesentery and serosa of the large and small
bowel, in the omentum, the uterus, and para-aortic and
pelvic lymph nodes.
Laparotomy on a patient with intermittent small bowel obstruction. A loop of
small bowel (bottom of frame) is adherent to a poorly differentiated primary
epithelial ovarian carcinoma (left of frame) that has spread to involve the
pelvic sidewall, the bladder peritoneum, the serosa of the uterus, and the
fallopian tube.

8.  Outside the peritoneal cavity, epithelial ovarian cancer
may spread to the pleural cavity, lungs, and groin lymph
nodes. Presence of pleural effusion does not necessarily
indicate disease in the chest, and malignancy can be
diagnosed only cytologically. Mucinous tumors tend to
form large dominant masses, while papillary serous
tumors have a more diffuse distribution and are more
commonly bilateral. Endometrioid and clear-cell variants
more commonly exhibit local invasion, retroperitoneal
disease, and hepatic metastases.
Metastases from epithelial ovarian carcinoma involving the omentum

9. Etiology
 The precise cause of ovarian cancer is
unknown, but several risk and contributing
factors have been identified.
 Hippisley-Cox and Coupland developed an
algorithm to determine risk of breast cancer in
women with and without symptoms.[2] , In
their cohort study, 10% of women with the
highest-predicted risk had 63% of all ovarian
cancers diagnosed over the next 2 years.

10. Reproductive factors
 Parity is an important risk factor. The risk of epithelial ovarian
cancer is increased in women who have not had children and
possibly those with early menarche or late menopause. Women
who have been pregnant have a 50% decreased risk for
developing ovarian cancer compared with nulliparous women.
Multiple pregnancies offer an increasingly protective effect. Oral
contraceptive use decreases the risk of ovarian cancer.
 These factors support the idea that risk for ovarian cancer is
related to ovulation. Two theories regarding this relationship
have been proposed. The incessant ovulation theory suggests
that repeated ovarian epithelial trauma caused by follicular
rupture and subsequent epithelial repair results in genetic
alterations within the surface epithelium. The gonadotropin
theory proposes that persistent stimulation of the ovaries by
gonadotropins, coupled with local effects of endogenous
hormones, increases surface epithelial proliferation and
subsequent mitotic activity.
 Thus, the probability of ovarian cancer may be related to the
number of ovulatory cycles, and conditions that suppress the
ovulatory cycle may play a protective role. Ovulation suppression
has been shown to decrease cancer incidence. Although
treatment with agents that induce ovulation in women with
infertility has been suggested to increase the incidence of

11. Genetic factors
 Family history plays an important role in the risk of developing ovarian
cancer. The lifetime risk for developing ovarian cancer is 1.6% in the
general population. This compares with a 4-5% risk when 1 first-degree
family member is affected, rising to 7% when 2 relatives are affected.
From 5-10% of cases of ovarian cancer occur in an individual with a
family history of the disease. Only a small percentage of these patients
have an inherited genetic abnormality, and the risk of this occurrence
increases with the strength of the family history. Hereditary epithelial
ovarian cancer occurs at a younger age (approximately 10 years
younger) than nonhereditary epithelial ovarian cancer, but the prognosis
may be somewhat better.
 At least 2 syndromes of hereditary ovarian cancer are clearly identified,
involving either (1) disorders of the genes associated with breast cancer,
BRCA1 and BRCA2, or (2) more rarely, genes within the Lynch II
syndrome complex. Breast/ovarian cancer syndrome is associated with
early onset of breast or ovarian cancer. Inheritance follows an autosomal
dominant transmission. It can be inherited from either parent. Most
cases are related to the BRCA1 gene mutation. BRCA1 is a tumor
suppressor gene that inhibits cell growth when functioning properly; the
inheritance of mutant alleles of BRCA1 leads to a considerable increase
in risk for developing ovarian cancer.
 Women with a history of breast cancer have an increased risk of
epithelial ovarian cancer.

12. Previous hormone therapy
 A nationwide prospective cohort study over 10 years that
included all Danish women aged 50-79 years concluded
that risk for ovarian cancer is increased with hormone
therapy, regardless of duration of use, formulation,
estrogen dose, regimen, progestin type, and
administration route.[6] Nearly 1 million women without
hormone-sensitive cancer or bilateral oophorectomy were
followed. In an average of 8 years of follow-up, 3068
ovarian cancers were detected, of which 2681 were
epithelial cancers.
 Current users of hormones had incidence rate ratios for
all ovarian cancers of 1.38 (95% confidence interval [CI],
11.26-1.51) compared with women who never took
hormone therapy. Risk declined as years since last
hormone use increased. Incidence rates in current and
never users of hormones were 0.52 and 0.40 per 1000
years, respectively. This translates to approximately 1
extra ovarian cancer for approximately 8300 women

13. Other factors
Lactose consumption and the use
of talcum powder on the vulva and
perineum may be associated with
increased risk of epithelial ovarian
cancer.

14. Epidemiology
 In the United States, the incidence of ovarian
cancer is 33 cases per 100,000 women aged 50
years or older. The average patient age at
diagnosis is 57 years. The estimated lifetime risk
is 1 case in 70 women, which is a 1.4% lifetime
incidence.
 International statistics
 Internationally, the incidence is 3.1 cases per
100,000 women in Japan and 21 cases per
100,000 women in Sweden. Around the world,
more than 200,000 women are estimated to
develop ovarian cancer every year and about
100,000 die from the disease. Epithelial ovarian
cancer occurs most commonly in white women in
the industrialized countries of northern and

15. Although the 5-year survival rate for ovarian cancer has improved significantly
in the past 30 years, the prognosis for ovarian cancer remains poor overall,
with a 46% 5-year survival rate. The prognosis of ovarian cancer is closely
related to the stage at diagnosis,[8, 9] as determined according to the staging
system developed by the International Federation of Gynecology and
Obstetrics (FIGO). (See Staging.) Approximately 20%, 5%, 58%, and 17% of
women present with stage I, II, III, and IV, respectively.
The 5-year survival rates (rounded to the nearest whole number) for epithelial
ovarian carcinoma by FIGO stage are as follows:
 Stage IA - 87%
 Stage IB - 71%
 Stage IC - 79%
 Stage IIA - 67%
 Stage IIB - 55%
 Stage IIC - 57%
 Stage IIIA - 41%
 Stage IIIB - 25%
 Stage IIIC - 23%
 Stage IV - 11%
 Overall survival rate
– 46%
Prognosis

16. Tumors of Low Malignant Potential
 Stage IA - 93%
 Stage IB - 90%
 Stage IC - 91%
 Stage IIA - 88%
 Stage IIB - 86%
 Stage IIC - 100%
 Stage IIIA - 29%
 Stage IIIB - 75%
 Stage IIIC - 62%
 Stage IV - 30%
 Overall survival rate
- 86%
Overall survival rate at 5 years according to FIGO is shown below. Others
have reported better survival rates with 5-year, 10-year, 15-year, and 20-year
survival for patients with serous LMP as 97%, 95%, 92%, and 89%,
respectively.
Five-year-survival rate for LMP tumors by FIGO stage (survival percentages
rounded to nearest whole number) are as follows

17. Clinical Presentation
 History
 Assessment of women for their risk of ovarian
cancer necessitates obtaining a careful family
history of both male and female relatives,
including those relatives without cancer.
 Carriers of mutations may be detected
through laboratory analysis of the genetic
structure of white blood cells.
 Epithelial ovarian cancer presents with a wide
variety of vague and nonspecific symptoms,
including bloating, abdominal distension or
discomfort, pressure effects on the bladder
and rectum, constipation, vaginal bleeding,
indigestion and acid reflux, shortness of
breath, tiredness, weight loss, and early
satiety. The patient may feel an abdominal

18.  A case-control study showed that symptoms
independently associated with the presence of
ovarian cancer were pelvic and abdominal pain,
increased abdominal size and bloating and
difficulty eating or feeling full.[13] Another study
reported that gastrointestinal (GI) symptoms
such as nausea and vomiting, constipation, and
diarrhea, or other digestive disorders were
associated with later-stage disease.[14]
Presentation with swelling of a leg due to venous
thrombosis is not uncommon. Paraneoplastic
syndromes due to tumor-mediated factors lead to
various presentations.
 A prospective case-control study of 1,709 women
visiting primary care clinics found that the
combination of bloating, increased abdominal
size, and urinary symptoms was found in 43% of
those with ovarian cancer but in only 8% of those

19. Physical Examination
 Physical findings are uncommon in
patients with early disease. Patients with
more advanced disease may present
with ovarian or pelvic mass, ascites,
pleural effusion, or abdominal mass or
bowel obstruction.

20. Diagnostic Considerations
 The normal functioning ovary produces a follicular cyst 6-7 times
each year. In most cases, these functional masses are self-limiting
and resolve within the duration of a normal menstrual cycle. In rare
situations, they persist longer or become enlarged. At this point, they
represent a pathological condition.
 Evaluation of adnexal masses
 Adnexal masses present a diagnostic dilemma; the differential
diagnosis is extensive, with most masses representing benign
processes.[18, 19, 20] However, without histopathologic tissue
diagnosis, a definitive diagnosis is generally precluded. Physicians
must evaluate the likelihood of a pathologic process using clinical
and radiologic information and balance the risk of surgical
intervention for a benign versus malignant process.
 Since ovaries produce physiologic cysts in menstruating women, the
likelihood of a benign process is higher. In contrast, the presence of
an adnexal mass in prepubertal girls and postmenopausal women
heightens the risk of a pathologic etiology.
Adnexal tumors

21.  Presence of advanced ovarian cancer is
often suspected on clinical grounds but
can be confirmed only pathologically by
removal of the ovaries or, when disease
is advanced, by sampling tissue or
ascitic fluid.
 Routine imaging is not required in all
patients in whom ovarian cancer is
highly suggested. If diagnostic
uncertainty is present, a pelvic
ultrasound or CT scan of the abdomen
and pelvis is warranted.
 MRI can increase the specificity of
imaging evaluation in cases where the

22.  When imaging studies demonstrate an adnexal
mass, the decision whether to observe the patient
with repeat imaging or to proceed to surgical
evaluation must take into account not only the
imaging characteristics but also the patient's
medical history, physical examination results, and
cancer antigen 125 (CA125) level.[25] Tumor
markers such as CA125 are not good
discriminators of benign lesions from malignant
lesions in premenopausal women but have better
accuracy in postmenopausal women
 Fine-needle aspiration (FNA) or percutaneous
biopsy of an adnexal mass is not routinely
recommended. In most cases, this approach may
only serve to delay diagnosis and treatment of
ovarian cancer. Instead, if a clinical suggestion of
ovarian cancer is present, the patient should
undergo a laparotomy for diagnosis and staging.
An FNA or diagnostic paracentesis should be

23. Screening
 Ovarian cancer does not lend itself to screening because it
has a relatively low prevalence within the general
population and no proven precursor lesion exists that can
be detected and treated to prevent the cancer from
occurring. No approved screening method is available for
ovarian cancer.
 The U.S. Preventive Services Task Force (USPSTF)
recommends against screening for ovarian cancer in the
general population. The USPSTF found fair evidence that
although screening with serum CA125 level or
transvaginal ultrasonography can detect ovarian cancer at
an earlier stage, earlier detection is likely to have a small
effect, at best, on mortality from ovarian cancer. In
addition, because of the low prevalence of ovarian cancer
and the invasive nature of diagnostic testing, the USPSTF
concluded that the potential harms outweigh the potential
benefits.[26] A randomized trial in a US population found
that simultaneous screening with ultrasonography and
CA125 did not reduce ovarian cancer mortality, and

24.  Currently, the National Cancer Institute
(NCI) recommends that high-risk women
should seek advice from their physician
and consider having annual
ultrasonographic examination, annual
CA125 testing, and be considered for
oophorectomy or participation in a clinical
trial. The NCI recommends no screening
methodology for women at normal risk for
epithelial ovarian cancer, but these women
should also be considered for research
protocols seeking improved detection
methods.
 Urinalysis
 Urinalysis should be obtained to rule out
other possible causes of abdominal or

25. Imaging in Ovarian Cancer
 Imaging studies used in ovarian cancer include
ultrasonography, chest radiography, and magnetic
resonance imaging (MRI). Positron emission tomography
(PET) scanning does not have an established role in the
diagnosis of primary ovarian malignancy.
 Ultrasonography is the most useful initial investigation in a
patient found to have a pelvic mass. This may define the
morphology of the pelvic tumor. In addition, it can
determine whether large masses are present in other parts
of the abdomen, including in the liver. Chest radiography is
useful in helping exclude pulmonary spread of malignant
diseases of the ovary. The primary advantage of using MRI
in the evaluation of ovarian masses is the ability to employ
this modality in the characterization of tissue. The
presence of fat, hemorrhage, mucin, fluid, and solid tissue
within an ovarian mass can be determined with the aid of
MRI. The ability to characterize tissue in this way is most
useful in determining whether a mass is definitely benign.

26. Mammography
 The preoperative workup also should
include mammography for women older
than 40 years who have not had one in
the preceding 6-12 months. This is
especially important in women with
estrogen-producing tumors because
these may increase the risk of breast
malignancies.
 Additionally, breast cancers can
metastasize to the ovaries and are often
bilateral. Mammography can help rule

27. Treatment & Management
 In women who present with GI carcinomatosis but
without an obvious pelvic mass, an extensive
search often fails to identify a primary tumor.
These patients can be presumed to have ovarian
carcinoma or primary peritoneal carcinoma and
treated with cytoreductive surgery followed by
platinum-based chemotherapy.
 Surgery is the initial treatment of choice, provided
patients are medically fit. Patients who are not fit
for surgery may be given chemotherapy and
considered for surgery later. The aim of surgery is
to confirm the diagnosis, define the extent of
disease, and resect all visible tumor. The role of
cytoreduction was demonstrated by Griffiths in
1975 and has been confirmed by many others.
 A retrospective analysis from Lin et al found that
epidural anaesthesia and analgesia for ovarian

28. Choosing Appropriate Surgery
 Appropriate surgery depends on whether or not disease is visible
outside the ovaries. It is essential that where no disease is visible
outside the ovaries, the patient be adequately surgically staged
because the incidence of microscopic metastases is significant.
Surgery for patients with stage IV disease should be individualized,
particularly when disease is in the liver and above the diaphragm.
Patients who are in stage IV because of small-volume disease in the
liver, abdominal wall, or lung should undergo cytoreductive surgery if
medically fit.
 If there is no visible disease outside an ovary, aspirate ascitic fluid for
cytology studies. Perform peritoneal washings for cytology if ascites is
not present. Remove the ovary and ovarian tumor intact. Perform
diaphragmatic scraping or biopsy for cytology studies. Obtain
peritoneal biopsy specimens. Perform a subcolic omentectomy. Obtain
bilateral para-aortic and pelvic node samples. Obtain biopsy samples
of adhesions or other suspicious areas.
 If the patient does not desire future fertility, perform a total abdominal
hysterectomy and excise the opposite ovary. Remove the appendix if
mucinous tumor is present.
 If macroscopic disease is visible outside of the ovary, all visible tumor
should be removed. This may require extensive surgery, including
bowel resection, excision of peritoneal implants, liver resection,
omentectomy, and splenectomy.

29. Cytoreductive Surgery
 This should be performed by a gynecologic oncologist at
the time of initial laparotomy. The volume of residual
disease at the completion of surgery represents one of the
most powerful prognostic factors. According to the 2011
National Comprehensive Cancer Network (NCCN) ovarian
cancer guidelines, residual disease of less than 1 cm is
evidence of optimal cytoreduction, although the greatest
possible effort should be made to remove all obvious
disease. As of this guideline, distal pancreatectomy may be
considered in all stages for optimal surgical
cytoreduction.[36]
 Patients with advanced ovarian cancer are classified in 3
groups as follows, based on the postoperative residual
tumor:
 Good risk - Microscopic disease outside the pelvis (stage
IIIa) or macroscopic disease less than 2 cm outside the
pelvis (stage IIIb)
 Intermediate risk - Macroscopic disease less than 2 cm

30. Laparoscopic Surgery
 According to guidelines developed by the American College of Obstetricians
and Gynecologists, laparoscopy may be used for diagnostic purposes in a
patient with low risk for ovarian cancer and to remove cystic masses. The
mass must be 10 cm or smaller as viewed by a sonogram, must have a distinct
border and no solid parts, and must not be associated with ascites. The serum
CA125 level must be normal (< 35 U/mL), and the patient must have no family
history of ovarian cancer. If a chance exists that ovarian cancer may be
present, surgery is best arranged in conjunction with a specialist in gynecologic
cancer surgery. The patient can then undergo all necessary surgery for her
cancer under a single anesthetic, without delay.
 As part of initial treatment of epithelial ovarian cancer, laparoscopic surgery
may be performed for early stage disease when no disease is visible outside of
the ovaries. Its use in more advanced disease, when spread is visible outside
the ovaries, is more limited due to the scope of cytoreductive surgery
necessary and the risk of port-site recurrence. Laparoscopy also has a role in
second-look inspection and in the staging of apparently early-stage disease
found by chance during another surgery.
 The 2011 NCCN ovarian cancer guidelines state that minimally invasive
surgery may be considered in selected patients with Stage 1 disease. This is
particularly true where an incidental finding of ovarian cancer was made during
prophylactic oophorectomy.[36]
 Secondary Surgery
 An assessment by Park et al found that secondary cytoreductive surgery is
safe and effective in patients with platinum-sensitive recurrent ovarian cancer.

31. Chemotherapy Regimens
 Only a small percentage of women with epithelial ovarian cancer can
be treated with surgery alone. These include patients with stage IA
grade 1 and stage IB grade 1 serous, mucinous, endometrioid, and
Brenner tumors. Clear-cell carcinomas are associated with a
significantly worse prognosis in stage I, and patients with this histologic
subtype should be considered for chemotherapy at all stages.
 Patients not treated with chemotherapy should be monitored closely at
regular intervals with clinical examination, serum CA125 estimation,
and ultrasonography if an ovary is still present. Surgery to remove the
uterus and residual ovary should be considered when the patient no
longer desires to remain fertile.
 The 2011 NCCN ovarian cancer guidelines recommend pelvic
examinations at least every 2-3 cycles in women receiving primary
chemotherapy.[36]
 Higher-risk early-stage disease includes all histologic subtypes with
stage IA and stage IB grade 2 and all stage I grade 3. These patients
should be treated with front-line chemotherapy with a taxane/platinum
combination for a minimum of 3 courses. They should consider
participating in clinical trials.
 All patients with stage II cancer and greater should receive front-line

32. Radiation Therapy
 Radiation has not been widely accepted as a
routine treatment modality in the initial
treatment of patients with epithelial ovarian
cancer, despite reports of efficacy for higher-
risk stage I and II disease and in stage III
disease where small-volume residual disease
is present after surgery. In selected cases,
pelvic diseases may respond to palliative
dosing regimens with minimal toxicity.

33. Estrogen Replacement Therapy
 The safety of estrogen replacement therapy
(ERT) after treatment for epithelial ovarian
cancer has not been tested in a randomized trial,
but current evidence suggests that the benefits
of ERT outweigh the risks.
 Younger women with endometrioid subtypes are
of concern because these tumors theoretically
are estrogen-sensitive. If estrogen is used in
such patients, a progestogen probably should be
given with it.

34. Management of Recurrent
Disease
 In most patients presenting with
advanced epithelial ovarian cancer, the
disease recurs, and the prognosis for
these patients is poor. The goal of
further therapy is to achieve a response
to treatment and to prolong meaningful
quality survival.
 Treatment of recurrent disease may
involve surgery, chemotherapy, and
radiation. Participation in clinical trials
should be considered

35. Experimental Medications
 The OCEANS phase III study reported that when
bevacizumab (Avastin) was combined with chemotherapy,
a 52% risk reduction for recurrence in disease progression
was observed (HR=0.48, P < .0001) compared with women
who received chemotherapy alone. The study included
women with recurrent, platinum-sensitive ovarian,
peritoneal, or fallopian tube carcinoma, who received
bevacizumab in combination with carboplatin and
gemcitabine followed by continued use of bevacizumab
alone until disease progression. Other results of the trial
include a median progression-free survival of 12.4 months,
compared with 8.4 months in women who received
chemotherapy alone. Additionally, the overall response rate
of tumor shrinkage was 79% in women receiving the
bevacizumab-based regimen, compared with 57% in those
who received chemotherapy alone.[64]
 A study by Stone et al concluded the presence of a
paracrine circuit, wherein increased production of
thrombopoietic cytokines in tumor and host tissues leads to

36. Deterrence and Prevention
 The risk of developing epithelial ovarian cancer is significantly reduced by bearing
children, using the combined oral contraceptive pill, undergoing tubal ligation, and
undergoing bilateral oophorectomy.
 Evidence suggests that taking the oral contraceptive pill for at least 5 years reduces
the relative risk of developing EOC to 50% of the risk for a woman who has never
taken it.
 Prophylactic bilateral salpingo-oophorectomy is indicated in high-risk women. The
American College of Obstetricians and Gynecologists recommends offering salpingo-
oophorectomy to women with BRCA1 or BRCA2 mutations by age 40 years or when
childbearing is complete (level A recommendation).[70] Surgical prophylaxis
decreases the risk by at least 90%. Not all cases of ovarian cancer are prevented, as
women are still at risk for developing primary peritoneal carcinomas.
 The epithelial lining of the ovaries is embryologically identical with the lining of the
peritoneal cavity, and similar cancers can develop from the peritoneum. Thus, while
oophorectomy prevents a pure epithelial ovarian cancer from developing, a small risk
still exists for developing carcinoma of the peritoneum, a disease that behaves
similarly to epithelial ovarian cancer.
 BRAC1 and BRAC2 mutations are common among women with invasive ovarian
cancer; thus, women diagnosed with invasive, nonmucinous ovarian cancer are
candidates for genetic testing.
 For patients who are known carriers of BRCA1 or BRCA2 mutations, bilateral
oophorectomy may be performed as soon as childbearing is complete, and probably
before the patient is aged 35 years. This reduces the chance of developing EOC, but
it does not prevent carcinoma of the peritoneum.
 For women with BRCA1 and BRCA2 mutations who opt to not undergo early

37. References
 http://emedicine.medscape.com/article/255771-
medication
 www.cancer.org/downloads/STT/500809web.pdf.
Accessed January 25, 2010.
 http://www.ahrq.gov/clinic/3rduspstf/ovariancan/ovcan
rs.htm. Accessed January 25, 2010.
 http://www.merckmanuals.com/professional/resources
/selected_links/selected_links.html?WT.z_resource=S
elected%20Links- by David M. Gershenson, MD;
Pedro T. Ramirez, MD, November 2008
 American Cancer Society.: Cancer Facts and Figures
2012. Atlanta, Ga: American Cancer Society, 2012.