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Ovarian cancers essay synopsis

Of all gynecologic malignancies, ovarian malignancy continues to have

highest fatality and is the most difficult to detect. In the United States

woman population, ovarian cancer rates high fifth in absolute mortality among

cancer related deaths (13, 000/yr). In most reported circumstances, ovarian malignancy

once first diagnosed is in periods III or perhaps IV in about 70 to 70% of patients

which usually further complicates treatment of the disease (Barber, 3).

Early detection in ovarian cancer can be hampered by the lack of suitable

growth markers and clinically, most patients fail to develop significant

symptoms right up until they reach advanced level disease. The functions

of ovarian malignancy have been researched in principal tumors in addition to established

ovarian tumor cell lines which provide a reproducible source of tumor materials.

Among the major clinical problems of ovarian cancers, malignant development

rapid introduction of medicine resistance, and associated cross-resistance remain

unresolved. Ovarian cancer contains a high frequency of metastasis but generally

remains local within the peritoneal cavity. Tumor development has been

associated with saugrenu, dysfunctional expression and/or changement of

numerous genes. This could include oncogene overexpression, extreme or

mutation, aberrant tumor suppressor expression or perhaps mutation. As well, subversion

of web host antitumor defense responses may possibly play a role in the pathogenesis of

malignancy (Sharp, 77).

Ovarian clear cellular adenocarcinoma was first described simply by Peham in 1899 while

hypernephroma of the ovary due to the resemblance to renal cellular carcinoma.

By 1939, Schiller known a histologic similarity to mesonephric tubules and

grouped these tumors as mesonephromas. In 1944, Saphir and Lackner explained

two cases of hypernephroid carcinoma of the ovary and proposed clear cell

adenocarcinoma as an alternative term. Crystal clear cell tumors of the ovary are now

generally regarded as being of mullerian and in the genital tract of mullerian origin.

A number of types of clear cell adenocarcinoma have already been reported to arise

from the epithelium of an endometriotic cyst (Yoonessi, 289). At times, a reniforme

cell carcinoma metastasizes to the ovary and may end up being confused with , the burkha clear

cell adenocarcinoma.

Ovarian obvious cell adenocarcinoma (OCCA) have been recognized as a distinct

histologic business in the World Overall health Organization (WHO) classification of ovarian

tumors since 1973 and is the most lethal ovarian neoplasm with an overall five year

survival of just 34% (Kennedy, 342). Crystal clear cell adenocarcinoma, like most ovarian

cancers, originates from the ovarian epithelium which is a single level of cellular material found on

the top of ovary. Individuals with ovarian clear cellular adenocarcinoma are normally

above the regarding 30 using a median of 54 which can be similar to those of ovarian epithelial

cancer in general. OCCA symbolizes approximately 6% of ovarian cancers and bilateral

ovarian involvement happens in fewer that 50 percent of sufferers even in advanced cases.

The connection of OCCA and endometriosis is very well documented (De La Rampa

243). It was confirmed by simply Kennedy ou al whom encountered histologic or intraoperative

proof of endometriosis in 45% with their study individuals. Transformation

coming from endometriosis to clear cell adenocarcinoma has been previously demonstrated in

sporadic circumstances but was not really observed by simply Kennedy et al. Hypercalcemia occurs in a

significant percentage of people with OCCA. Patients with advanced disease are more

typically affected than patients with nonmetastatic disease. Patients with OCCA are usually

more likely to include Stage My spouse and i disease than are people with ovarian epithelial cancer in

general (Kennedy, 348).

Histologic grade has been beneficial as a primary prognostic determinant in some studies

of epithelial cancers with the ovary. The grading of ovarian obvious cell adenocarcinoma has

been problematic and is also complicated by multiplicity of histologic patterns found in

precisely the same tumor. Similar problems have been found in attempted grading of crystal clear cell

adenocarcinoma of the endometrium (Disaia, 176). Despite these types of problems, tumour

grading continues to be attempted although has failed to demonstrate prognostic value.

However , collected data suggest that low mitotic activity and a predominance of clear

cells may be good histologic features (Piver, 136).

Risk factors for OCCA and ovarian cancer generally speaking are much much less clear than for

additional genital tumors with standard agreement about two risk factors: nulliparity and friends and family

history. There is a higher frequency of carcinoma in unmarried ladies and in hitched

women with low parity. Gonadal dysgenesis in kids is linked to a higher risk

of developing ovarian cancer when oral contraceptives are associated with a decreased

risk. Hereditary and applicant host family genes may be altered in susceptible families. Amongst

those presently under research is BRCA1 which has been connected with an

elevated susceptibility to breast cancer. About 30% of ovarian adenocarcinomas

communicate high degrees of HER-2/neu oncogene which correlates with a poor prognosis

(Altcheck, 375-376). Mutations in host growth suppresser gene p53 are normally found in fifty percent of

ovarian carcinomas. There as well appears to be a racial predilection, as the greater part

of cases are noticed in Caucasians (Yoonessi, 295).

Significant variation is available in the gross appearance of ovarian crystal clear cell

adenocarcinomas and they are generally indistinguishable from other epithelial ovarian

carcinomas. They could be cystic, solid, very soft, or rubbery, and may also contain

hemorrhagic and mucinous areas (ODonnell, 250). Microscopically, clear cell

carcinomas will be characterized by the existence of variable ratios of obvious and hobnail

cells. The former contain considerable clear cytoplasm with typically centrally located nuclei

while the second option show clear or pink cytoplasm and bizarre principal nuclei with atypical

cytoplasmic intraluminal predictions. The cell phone arrangement can be tubulo acinar

papillary, or solid, with the great majority displaying a mixture of these habits. The

hobnail and clear cells main with tube and stable forms, correspondingly (Barber


Obvious cell adenocarcinoma tissue set with liquor shows an increased cytoplasmic

glycogen content which is often shown by means of special staining techniques.

Abundant extracellular and uncommon intracellular natural mucin combined with sulfate and

carboxyl group is usually present. The crystal clear cells are recognized histochemically and

ultrastructurally (short and blunt microvilli, intercellular limited junctions and desmosomes

cost-free ribosomes, and lamellar endoplasmic reticulum). The ultrastructure of hobnail and

clear cellular material resemble the ones from the comparable cells noticed in clear cell carcinomas of the

remainder with the female penile tract (OBrien, 254). A variation in patterns of histology

is observed among these kinds of tumors and frequently within the same one.

Whether both tube components with hobnail skin cells and the stable part with obvious cells

are required to establish a medical diagnosis or the occurrence of just one of the patterns is definitely

sufficient is actually not clearly established. Fortunately, many tumors demonstrate a mixture of

these kinds of components. Not cancerous and borderline counterparts of clear cellular ovarian

adenocarcinomas are assumptive possibilities. Yoonessi et approach reported that nodal

metastases could be discovered even when the disease appears to be largely limited to the

pelvis (Yoonessi, 296). Study of retroperitoneal nodes is essential to allow for

more factual staging and carefully organized adjuvant therapy.

Surgery remains the spine of treatment and generally contains removal of the

uterus, pontoons and ovaries, possible incomplete omentectomy, and nodal biopsies. The

success and value of curative radiotherapy and chemotherapy is not clearly

demonstrated. Therefore , in patients with unilateral exemplified lesions and

histologically confirmed uninvolvement in the contralateral ovary, omentum, and biopsied

nodes, a case could be made for (a)no adjuvant remedy after total surgical removal

and (b) removal of only the infected ovary within an occasional affected person who may be young

and desirous of preserving her reproductive ability (Altchek, 97). In the even more adv-

anced stages, associated with the womb, ovaries, omentum, and as much tumor as possible

followed by pelvic radiotherapy (if residual disease is limited to the pelvis) or perhaps

chemotherapy must be considered. The chemotherapeutic routines generally entail

adriamycin, alkylating agents, and cisPlatinum that contains combinations (Barber, 442).

OCCA is of epithelial origin and quite often contains blends of different epithelial tumors

such as serous, mucinous, and endometrioid. Obvious cell adenocarcinoma is characterized

by large epithelial cellular material with abounding cytoplasm. Since these tumors sometimes

result from association with endometriosis or endometrioid carcinoma of the ovary and

appear like clear cellular carcinoma in the endometrium, vehicle thought to be of

mullerian duct origin and variants of endometrioid adenocarcinoma. Clear cellular tumors of

the ovary can be mostly solid or perhaps cystic. In the solid neoplasm, the very clear cells happen to be

arranged in sheets or perhaps tubules. Inside the cystic kind, the neoplastic cells series the spots.

Five-year survival is approximately 50% when these tumors are confined to the ovaries

but these tumors tend to end up being aggressive and spread over and above the ovary which helps make

5-year survival highly unlikely (Altchek, 416).

A few debate goes on as to whether clear cell or perhaps mesonephroid carcinoma is a

independent clinicopathological entity with its personal distinctive biologic behavior and natural

background or a histologic variant of endometrioid carcinoma. In an effort to characterize

clear cellular adenocarcinoma, Jenison et approach compared these tumors towards the most common of

the epithelial malignancies, the serous adenocarcinoma (SA). Histologically determined

endometriosis was strikingly more common between patients with OCCA than with SA.

Other findings by Jenison et approach suggest that the biologic patterns of obvious cell

adenocarcinoma differs as a result of SA. They identified Stage I tumors in 50% of the

observed individual population and a lower incidence of bilaterality in OCCA

(Jenison, 67-69). Additionally , it seems that OCCA is definitely characteristically larger than

SA, probably explaining the more frequency of symptoms and signs by presentation.

Risk Factors

There is controversy regarding talcum powder use leading to ovarian cancers. Until recently, most

talc powders had been contaminated with asbestos. Conceptually, talcum natural powder on the

perineum could reach the ovaries by consumption through the cervix or vagina. Since

talcum powders are no longer contaminated with asbestos, raise the risk is probably will no longer

important (Barber, 200). The high excess fat content of whole milk, rechausser, and meats products

has been implicated with an increased risk for ovarian tumor in general.

The Centers for Disease Control as opposed 546 women with ovarian cancer to 4, 228

controls and reported that for women 20 to fifty four years of age, the use of oral

preventive medicines reduced the chance of ovarian cancer by forty percent and the likelihood of ovarian cancer

decreased because the life long oral birth control method use increased. Even the utilization of oral

contraceptives for three weeks decreased the risk. The safety effect of oral

contraceptives is to reduce the family member risk to 0. 6th or to cure the incidence of disease

by simply 40%. We have a decreased risk as high as 40% for women that have had 4 or

even more children as compared with nulliparous girls. There is a rise in the chance

of ovarian cancer amongst nulliparous ladies and a reduce with elevating parity. The

incessant after ovulating theory proposes that continuous ovulation triggers repeated shock

to the ovary leading to the introduction of ovarian tumor. Incidentally, having two or

more abortions compared to by no means having had a great abortion lessens ones likelihood of

developing ovarian cancer by 30% (Coppleson, 25-28).


It is frequently accepted that cancer results from a series of innate alterations that

disrupt typical cellular progress and differentiation. It has been recommended that hereditary

changes creating cancer take place in two kinds of normal cell phone genes, proto-

oncogenes and tumor suppressor genes. Genetic changes in proto-oncogenes facilitate

the transformation of your normal cellular to a cancerous cell simply by production of the altered or perhaps

overexpressed gene product. This kind of genetic adjustments include changement, translocation, or perhaps

amplification of proto-oncogenes Tumour suppressor family genes are recommended to prevent

tumor. Inactivation or loss of these types of genes leads to development of cancer by the

not enough a functional gene product. This could require mutations in both equally alleles of the tumor

suppressor gene. These genes work as regulatory inhibitors of cellular proliferation, these kinds of

as a DNA transcription aspect, or a cellular adhesion molecule. Loss of these kinds of functions

could cause abnormal cell division or perhaps gene appearance, or elevated ability of cells in

tissues to detach. Tumor such as OCCA most likely comes from the dynamic interaction

of several genetically altered proto-oncogenes and tumour suppressor family genes (Piver, 64-


Until recently, there was clearly little data that the origins of ovarian was genetic. Before

1970, familial ovarian cancer had been reported in just five people. A familial cancer

registry was established by Roswell Recreation area Cancer Start in 1981 to record the

number of cases occurring in the usa and to study the setting of inheritance. If

a genetic autosomal dominant transmission of the disease can be founded, counseling

for prophylactic oophorectomy at an ideal age may lead to a reduction in the death

rate from ovarian cancer in this sort of families.

The registry at Roswell Park reported 201 situations of ovarian cancer in 94 people in

1984. From 1981 through 1991, 820 households and 2946 cases have been observed.

Familial ovarian cancer is not a uncommon occurrence and might account for 2 to 5% of all situations

of ovarian cancer. 3 conditions which might be associated with family ovarian malignancy are

(1) site certain, the most common contact form, which is restricted to ovarian malignancy, and (2)

breast/ovarian cancers with clustering of ovarian and breasts cases in extended pedigrees

(Altchek, 229-230). One characteristic of inherited ovarian cancers is that that occurs for a

substantially younger era than the non-inherited form.

Cytogenetic investigations of intermittent (non-inherited) ovarian tumors include revealed

recurrent alterations of chromosomes 1, 3, 6, and 10. Many proto-oncogenes have been

planned to these chromosomes, and deletions of sectors of chromosomes (particularly

3p and 6q) in some tumors is according to a role for loss of tumour suppressor family genes.

Just lately, a hereditary linkage research of familial breast/ovary malignancy suggested linkage of

disease susceptibility together with the RH blood group positionnement on chromosome 1p.

Allele reduction involving chromosomes 3p and 6q as well as chromosomes 11p, 13q, and

18 have been usually observed in ovarian cancers. Besides allele reduction, point variations

have been identified in the tumor suppressor gene p53 situated on chromosome17p13.

Deletions of chromosome 17q have been reported in sporadic ovarian tumors suggesting

an over-all involvement of the region in ovarian tumour biology. Allelic loss of MYB and

ESR genes map on chromosome 6q nearby the provisional positionnement for FUCA2, the positionnement for

a-L-fucosidase in serum. Low activity of a-L-fucosidase in serum much more prevalent in

ovarian cancers patients. This suggests that lack of a-L-fucosidase activity in serum

may be a hereditary condition connected with increased exposure to possible developing ovarian

cancer. This kind of together with cytogenetic data of losses of 6q plus the allelic failures at 6q

point to the actual importance of chromosome 6q in hereditary ovarian cancer

(Altchek, 208-212).

Account activation of regular proto-oncogenes by either mutation, translocation, or gene

hyperbole to produce changed or overexpressed products can be believed to perform an

natural part in the progress ovarian tumors. Activation of several proto-

oncogenes (particularly K-RAS, H-RAS, c-MYC, and HER-2/neu) occurs in ovarian

tumors. Yet , the significance remains to be determined. It is questionable as to

whether overexpression in the HER-2/neu gene in ovarian cancer can be associated with poor

prognosis. Additionally to studying proto-oncogenes in tumors, it can be beneficial to

check out proto-oncogenes in germ-line DNA from associates of families with histories

of ovarian cancer (Barber, 323-324). It truly is questionable if inheritance or rare

alleles of the H-RAS proto-oncogene may be linked to susceptibility to ovarian cancer.

Diagnosis and Treatment

The early diagnosis of ovarian cancer is actually a matter of opportunity and not a triumph of

scientific procedure. In most cases, the finding of any pelvic mass is the only available

method of diagnosis, with the exception of operating tumors that might manifest

endocrine even with nominal ovarian enhancement. Symptomatology comes with vague

stomach discomfort, dyspepsia, increased unwanted gas, sense of bloating, particularly

after consuming food, gentle digestive disruptions, and pelvic unrest which might be present

for a few months before diagnosis (Sharp, 161-163).

There is a great number of imaging methods that are available. Ultrasounds

particularly penile ultrasound, has grown the rate of pick-up of early lesions

particularly when colour Doppler method is used. Regrettably, vaginal sonography

and LOS ANGELES 125 have had an increasing number of phony positive tests. Pelvic

findings are often nominal and not helpful in making an analysis. However , mixed

with a high index of suspicion, this may alert the physician for the diagnosis.

These types of pelvic indicators include:

Mass in the ovarian area

Comparative immobility due to fixation of adhesions

Anomaly of the tumor

Shotty consistency with increased stiffness

Tumors in the cul-de-sac referred to as a handful of knuckles

Relative insensitivity of the mass

Increasing size under remark

Bilaterality (70% for ovarian carcinoma vs 5% for benign cases) (Barber, 136)

Tumor indicators have been specifically useful in monitoring treatment, yet , the

markers have and will probably always have a drawback in determining an early

growth. To date, only two, man gonadotropin (HCG) and alpha fetoprotein, happen to be

known to be hypersensitive and certain. The problem with tumor indicators as a means of

making an analysis is that a tumor marker is produced from a particular volume of tumour.

By simply that time it is no longer a beginning but rather a biologically past due tumor (Altchek, 292).

Many studies have defined murine monoclonal antibodies (MAbs) as potential tools

pertaining to diagnosing cancerous ovarian tumors. Yamada ainsi que al attemptedto develop a MAb

that can identify cells with early cancerous change from adjacent benign tumor cells

in cases of borderline malignancy. They designed MAb 12C3 by immunizing mice with

a cell line based on a human ovarian tumor. The antibody reacted with human

ovarian carcinomas rather than with germ cellular tumors. MAb 12C3 discolored 67. seven percent of

ovarian epithelial malignancies, but exhibited an extremely low reactivity to

malignancies. MAb 12C3 diagnosed a new antigen in whose distribution in normal tissues is

restricted. According to Yamada ainsi que al, MAb 12C3 can serve as an excellent new application for

the histologic detection of early malignant within borderline epithelial neoplasms.

MAb 12C3 may also be valuable as a concentrating on agent to get cancer chemotherapy (Yamada


Currently there are several serum markers that are available to help make a diagnosis.

These include LOS ANGELES 125, CEA, DNB/70K, LASA-P, and serum inhibin. Recently the

urinary gonadotropin peptide (UCP) plus the collagen-stimulating component have been

added. Although the growth markers have a low specificity and level of sensitivity, they are often

utilized in screening for ovarian malignancy. A new tumour marker CA125-2 has higher

specificity than CA125. Generally speaking, tumor markers have a very limited role in screening

intended for ovarian cancers.

The normal epithelial tumor of the ovary is unique in killing the sufferer while getting

in the great majority of the instances, enclosed inside the anatomical region where it initially

created: the peritoneal cavity. Despite having early local cancer, lymph node

metastases are not rare in the pelvic or aortic areas. In most of the circumstances, death is a result of

intraperitoneal growth, ascites, proteins loss and cachexia. The concept of

debulking or perhaps cytoreductive medical procedures is currently the dominant strategy in treatment.

The initial goal in debulking surgical treatment is inhibited of debulking surgery is usually inhibition of

the vicious cycle of malnutrition, nausea, vomiting, and dyspepsia commonly found in

individuals with core to advanced stage disease. Cytoreductive surgical procedure enhances the

efficiency of chemotherapy as the survival shape of the people whose largest residual

mass size was, after surgical treatment, below the 1 ) 5 centimeter limit is the same as the competition of the

individuals whose largest metastatic lesions were below the 1 . a few cm limit at the outset

(Altchek, 422-424).

The aggressiveness of the debulking surgical treatment is a crucial question surgeons must face

when treating ovarian cancers. The debulking of substantial metastatic masses makes simply no

sense through the oncologic perspective. As for extrapelvic masses the debulking, regardless if

more appropriate, remains packed with danger and exposes the person to a weighty handicap.

For these reasons the extra-genital resections have to be restricted to lymphadenectomy

omentectomy, pelvic abs peritoneal resections and rectosigmoid junction

resection. That means that stages IIB and IIC and stages IIIA and IIB will be the only the case

indications intended for extrapelvic cytoreductive surgery. Colectomy, ileectomy, splenectomy

segmental hepatectomy are only exceedingly indicated if they let one to perform a

real optimum resection. The conventional cytoreductive medical procedures is the total hysterectomy with

bilateral salpingoophorectomy. This surgery may be carried out with aortic and pelvic lymph

node testing, omentectomy, and, if necessary, resection of the rectosigmoidal junction

(Barber. 182-183).

The idea of administering drugs directly into the peritoneal tooth cavity as therapy of

ovarian cancer was attempted more than three decades ago. However , it has simply been

in the last ten years which a firm basis for this way of drug delivery has become

founded. The essential target is to show the growth to higher concentrations of medicine

for longer periods of time than may be possible with systemic drug delivery. Several providers

have been reviewed for their efficiency, safety and pharmacokinetic benefit when

given via the peritoneal route.

Cisplatin offers undergone one of the most extensive analysis for local delivery. Cisplatin

reaches the systemic area in significant concentrations when it is administered

intraperitoneally. The dosage limiting toxicity of intraperitoneally administered cisplatin is

nephrotoxicity, neurotoxicity and emesis. The depth of penetration of cisplatin in the

peritoneal coating and tumor following local delivery is merely 1 to 2 millimeter from the

surface area which limitations its effectiveness. Thus, the only patients with ovarian tumor who would

most likely benefit would be those with tiny residual growth volumes. Overall

approximately 35 to forty percent of individuals with small volume left over ovarian tumor have

been shown to demonstrate an objective clinical respond to cisplatin-based nearby

administered remedy with twenty to 30% of patients achieving a surgically recorded

complete response. As a general rule, sufferers whose tumors have demonstrated an

inherent resistance to cisplatin following systemic therapy are not regarded as for

treatment with platinum-based intraperitoneal remedy (Altchek, 444-446).

In people with little volume residual disease during the time of second seem laparotomy

who may have demonstrated natural resistance to platinum-based regimens, substitute

intraperitoneal treatment programs can be viewed as. Other real estate agents include

mitoxantrone, and recombinant alpha-interpheron. Intraperitoneal mitoxanthone features

been shown to acquire definite activity in little volume residual platinum-refractory ovarian

cancer. Unfortunately, the dose limiting degree of toxicity of the agent is stomach pain and

adhesion development, possibly bringing about bowel obstruction. Recent data suggests the

local degree of toxicity of mitoxanthone can be lowered considerably simply by delivering the agent in


Ovarian tumors may possess either intrinsic or obtained drug level of resistance. Many

mechanisms of medicine resistance have been described. Appearance of the MDR1 gene that

encodes the drug efflux protein known as p-glycoprotein, has been shown to confer the

feature multi-drug resistance from clones of some cancer. The most generally

considered definition of platinum response is response to first-line american platinum eagle treatment

and disease cost-free interval. Primary platinum level of resistance may be understood to be any progression

on treatment. Secondary platinum resistance is the absence of progression on main

platinum-based remedy but development at the time of platinum retreatment pertaining to relapse

(Sharp, 205-207).

Second-line chemotherapy to get recurrent ovarian cancer relies on tastes of

both the patient and physician. Retreatment with american platinum eagle therapy appears to offer

significant opportunity for specialized medical response and palliation yet relatively tiny hope for

long term cure. Paclitaxel (trade term: Taxol), a prototype with the taxanes, is cytotoxic

to ovarian cancer. Approximately twenty percent of american platinum eagle failures interact to standard amounts of

paclitaxel. Studies are in progress of dose rise and intraperitoneal

administration (Barber, 227-228). This class of drugs is now thought to represent an

active addition to the platinum eagle analogs, both as major therapy, along with

platinum, or perhaps as repair therapy after failure of platinum.

In advanced stages, there exists suggestive evidence of partial responsiveness of OCCA to

the radiation as well as cchemotherapy, adriamycin, cytoxan, and cisPlatinum-containing

combinations (Yoonessi, 295). Light techniques contain intraperitoneal radioactive

gold or chromium phosphate and exterior beam therapy to the stomach and pelvis. The

function of radiation therapy in remedying of ovarian canver has diminished in dominance as

the spread routine of ovarian cancer as well as the normal muscle bed involved in the treatment

with this neoplasm produce effective radiotherapy difficult. When the residual disease

after laparotomy is heavy, radiation therapy is specially ineffective. If perhaps postoperative

light is approved for a affected person, it is important that theentire abdomen and pelvis happen to be

optimally remedied to elicit a response through the tumor (Sharp, 278-280).

In the last few decades, the aggressive try to optimize the treatment of

ovarian clear cell adenocarcinoma and ovarian cancer generally has viewed remarkable

improvements in the response rates of patients with advanced level cancer with out

dramatically improving long-term survival. The promises of new medications with activity

when platinum agents fail is stimulating and fosters hope that, in the years to arrive

the undertakings of surgical and pharmacoogical research is likely to make ovarian cancers an

very easily treatable disease.


Altchek, A., Deligdisch, L. (1996). Diagnosis and Management of Ovarian Disorders.

New york city: Igaku Shoin.

Barber, H. (1993). Ovarian Carcinoma: Charge, Diagnosis, and Treatment. New York:

Springer Verlag.

Coppleson, M. (Ed. ). (1981). Gynecologic Oncology (vol. 2). New York: Churchill


Current Clinical Trials Oncology. (1996). Green Brook, NJ: Pyros Education.

De La Cuesta, R., Eichorn, J. (1996). Histologic modification of benign

endometriosis to early epithelial ovarian cancers. Gynecologic Oncology, 60, 238-


Disaia, P, Creasman, W. (1989). Clinical Gynecologic Oncology (3rd ed. ). St . Paillette:


Jenison, E., Montag, A., Griffiths, T. (1989). clear cell adenocarcinoma from the ovary:

a specialized medical analysis and comparison with serous cáncer. Gynecologic Oncology

32, 65-71.

Kennedy, A., Biscotti, C. (1993). Histologic correlates of progression-free period and

endurance in ovarian clear cell adenocarcinoma. Gynecologic Oncology, 40, 334-338.

Kennedy, A., Biscotti, C. (1989). Ovarian clear cell adenocarcinoma. Gynecologic

Oncology, 32, 342-349.

OBrien, Meters., Schofield, L., & Color, S. (1993). Clear cell epithelial ovarian cancer: Poor

prognosis only in early periods. Gynecologic Oncology, 49, 250-254.

ODonnell, Meters, Al-Nafussi, A. (1995). Intracytoplasmic lumina and mucinous blemishes

in ovarian carcinoma. Histopathology, 26, 181-184.

Piver, H. (Ed. ). (1987). Ovarian Malignancies. New York: Churchill Livingstone.

Sharp, N., Mason, G., Blackett, T., Berek, M. (1995). Ovarian Cancer several. New York:

Chapman, Lounge Medical.

Yamada, K., Kiyoshi, O. (1995). Monoclonal antibody, Mab 12C3, is a very sensitive

immunohistochemical gun of early malignant change in epithelial ovarian tumors.

Anatomic Pathology, 103, 288-294.

Yoonessi, M., Weldon, D., Sateesh, S. (1984). Clear cellular ovarian cáncer. Journal

of Surgical Oncology, 27, 289-297.

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