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tumors are characterized by KRAS mutations,-catenin and PTEN mutations are common-ly seen with endometrioid borderline ovar-ian tumors [4]. In addition, endometriosis isan important precursor of endometrioid andclear cell borderline ovarian tumors.

Serous borderline ovarian tumors areunique neoplasms that may behave in an ag-gressive fashion with associated peritonealimplants and regional lymphadenopathy.Because women with extraovarian spread ofdisease have a very good prognosis, the peri-toneal lesions are classied as implants in-stead of metastases. Although conservativemanagement sufces in women with early-stage borderline ovarian tumors wanting topreserve fertility, radical surgery is warrant-ed in patients with late-stage disease. In con-tradistinction to high-grade serous carcino-mas (the most common ovarian malignancy),borderline ovarian tumors are notoriously re-sistant to platinum-based chemotherapy [5].Prognosis is generally excellent. Althoughthe imaging features of borderline ovariantumors signicantly overlap with those of in-vasive epithelial cancers, cross-sectional im-

aging studies play a major role in the diagno-sis, management, and surveillance of patientswith borderline ovarian tumors [6].

Epidemiology and TaxonomyBorderline ovarian tumors are relative-

ly uncommon with an incidence of 1.52.5per 100,000 people per year. Approximately,3,000 cases of borderline ovarian tumors areannually diagnosed in the United States [7].Borderline ovarian tumors most commonly

Current Update on BorderlineOvarian Neoplasms

Neeraj Lalwani 1Alampady K. P. Shanbhogue 1Raghunandan Vikram 2Arpit Nagar 3Jaishree Jagirdar 4Srinivasa R. Prasad 1

Lalwani N, Shanbhogue AKP, Vikram R, Nagar A,Jagirdar J, Prasad SR

1Department of Radiology, University of Texas HealthScience Center at San Antonio, 7703 Floyd Curl Dr.,San Antonio, TX 78 229. Address correspondence toS. R. Prasad ([email protected]).

2Department of Diagnostic Radiology, Division ofDiagnostic Imaging, University of Texas M.D. AndersonCancer Center, Houston, T X.

3Department of Radiology, Ohio State University MedicalCenter, Columbus, OH.

4Department of Surgical Pathology, University of TexasHealth Science Center at San Antonio, San Antonio, T X.

Wo m e ns I m ag i ng Rev i ew

AJR 2010; 194:330 336

0361803X/10/1942330

American Roentgen Ray Society

Borderline ovarian tumors com-prise up to 1520% of ovarian ep-ithelial neoplasms [1]. Borderlineovarian tumors a re histologically

characterized as epithelial tumors with a strat-ied growth pattern but without destructivestromal invasion. Serous and mucinous neo-plasms constitute the majority of borderlinetumors and occur mostly in women of repro-ductive age [1]. Howard C. Taylor, Jr., [2] iscredited with the rst use of the term semi-malignant tumors in 1929 for a subset oflarge ovarian tumors that had an indolent clin-ical course with relatively favorable patientoutcome despite the presence of peritonealdisease. However, borderline ovarian tumorswere not considered a distinct entity until 1971when the International Federation of Obstet-ric Gynecology (FIGO) established a separateborderline category of tumors. Since then,considerable controversy has surrounded thedenition and management of borderlineovarian tumors because of their enigmaticpathogenesis and perplexing biologic behav-ior [3]. Synonyms of borderline ovarian tu-mors include tumors of borderline malignan-

cy, tumors of low malignant potential, andatypical proliferative tumors.Several studies have described the char-

acteristic cytogenetics, epidemiology, natu-ral history, and biologic behavior of specicsubtypes of borderline ovarian tumors. Re-searchers have postulated that specic ge-netic changes contribute to their pathogenesisand stepwise progression to low-grade inva-sive ovarian carcinomas. Although the major-ity of serous and mucinous borderline ovarian

Keywords: borderline ovarian tumors, imagingneoplasms, ovarian cancer, ovarian tumors of lowmalignant potential

DOI:10.2214/AJR.09.3936

Received November 9, 2009; accepted after revisionNovember 13, 2009 .

W O M E N S

I M A G I N G F O C U S O N :

OBJECTIVE. Borderline ovarian tumors comprise a unique group of noninvasive ovarianneoplasms with characteristic histology and variable tumor biology that typically manifest aslow-stage disease in younger women with resultant excellent prognosis.

CONCLUSION. Borderline tumors are considered to be precursors of low-grade ovar-ian cancers. Accurate diagnosis and staging facilitate optimal patient management particu-larly in patients desiring to preserve fertility.

Lalwani et al.Borderline Ovarian Neoplasms

Womens ImagingReview


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Borderline Ovarian Neoplasms

affect white women of reproductive age typi-cally during the fourth decade. Up to 27% ofpatients with borderline ovarian tumors areyounger than 40 years [8]. The mean age ofpresentation of borderline ovarian tumors isapproximately 20 years earlier than that of in-vasive ovarian carcinomas [9]. Most patientswith borderline tumors present with nonspe-cic symptoms such as abdominopelvic painor mass. Approximately 16% of patients areasymptomatic at the time of diagnosis [10].According to the 2003 World Health Orga-nization classication schemata [11], border-line ovarian tumors are classied on the ba-sis of histopathology and histogenesis intoserous, mucinous, endometrioid, clear cell , and transitional (Brenner) subtypes. Salientfeatures, including precursor lesions and cy-togenetics, of borderline ovarian tumors aresummarized in Table 1.

Serous Borderline Ovarian TumorsSerous borderline ovarian tumors com-

prise the most common histologic subtypeof borderline ovarian tumors, accounting forapproximately 65% of all borderline ovari-an tumors [12]. The mean age range of pre-sentation is 3440 years. Serous borderlineovarian tumors are slow-growing neoplasmsthat may be associated with aggressive bio-logic behavior in the form of peritoneal im-plants and regional lymphadenopathy inapproximately 35% and 27% of patients, re-spectively. Histologically, serous borderlineovarian tumors are divided into typical, 90%of serous borderline ovarian tumors, and mi-cropapillary, 10% of serous borderline ovari-an tumors, types [11]. Most low-grade serouscarcinomas are thought to arise from micro-papillary borderline ovarian tumors. Seroussurface borderline tumor is another variant

that shows polypoid excrescences that occu-py the outer surface of the ovary.

Recent advances in cytogenetics haveyielded unique insights into the pathogen-esis and biologic behavior of serous border-line ovarian tumors. In several studies, inves-tigators have found that only a small subset ofserous cystadenomas progress to serous bor-derline ovarian tumors and that activatingmutations of BRAF and KRAS genes are ear-ly events in tumorigenesis of borderline ovar-ian tumors. In contradistinction to high-gradeserous carcinomas, the most common sub-type of ovarian cancer, that are characterizedby p53 mutations in more than 50% tumors,serous borderline ovarian tumors are charac-terized by KRAS and BRAF mutations in twothirds of tumors (Fig. 1). Up to 50% of serousborderline ovarian tumors are characterizedby BRAF mutations, and KRAS mutations are

TABLE 1: Summary of Borderline Ovarian Tumors

Type of BorderlineOvarian Tumor Precursor Progression to Cytogenetics Characteristic Features Prognosis

Serous Serous cystadenoma oradenobroma

Invasive low-gradeserous carcinoma

Mutations in KRAS orBRAF genes 67%

May follow dualistic oncogenicpathway; invasive or noninvasiveimplants may occur; presence ofinvasive implants is a poorprognostic factor; associatedwith regional lymphadenopathy

Typical subtype (90%)

Micropapillary subtype (10%) isclosely associated with invasiveimplants

70% of cases are stage I;survival is almost 100%

30% of cases are advancedstages; survival is 95.3% ifimplants are noninvasiveand 66% if implants areinvasive

Mucinous Intestinal subt ype (9 0%):mucinous cystadenoma

Mllerian subtype (10%):endometriotic cysts?

Intraepithelialcarcinoma then toinvasive mucinouscarcinoma

Mutations in KRAS (> 60%) Intestinal subtype (90%) isunilateral; is multicystic withsmooth capsule; is associatedwith pseudomyxoma peritonei;has larger multilocular cysticlesions; shows uids of differentsignal intensities on T1- orT2-weighted MR images

Mllerian subtype (10%) isbilateral in 2030%; is exophyticand paucilocular; mimics serous tumors hence termed seromuci-nous; implants may present

82% of cases are stage I;5-year survival is up to99100%

18% of cases are advancedstages; mortality mayreach up to 50% dependingon stage

Endometrioid Endometriosis, endo-

metrioid adenobroma

Intraepithelial

carcinoma then tolow-grade invasiveendometrioidcarcinoma

Gene mutations in

-catenin (> 50%); loss ofheterozygosity or PTEN mutations (20%);microsatellite instability(1350%)

None Benign course with high

survival rates

Clear cell Endometriosis, clear celladenobroma

Intraepithelialcarcinoma then toinvasive clear cellcarcinoma

KRAS mutations (516%);microsatellite instability( 13%)

None Benign course with highsurvival rates

Brenner Benign Brenner Malignant Brenner? Not yet identied None Benign course with highsurvival rates


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Lalwani et al.

seen in more than a third of serous borderlineovarian tumors.

A dual oncogenic pathway has been de-scribed in which serous borderline ovariantumors undergo stepwise transformation tolow-grade serous carcinomas and high-gradeserous carcinomas possibly arise de novofrom surface epithelia due to p53 and BRCA mutations [1315]. Serous borderline ovari-an tumors are characterized by activation ofspecic tumor suppressor genes ( SERPINA5 and dual specicity phosphatase 4 [ DUSP4 ])that inhibit degradation of the extracellu-lar matrix, a key event in the pathogenesisof invasive growth [16]. Thus, serous bor-derline ovarian tumors charter an indolentcourse due to genetic events that promote tu-mor proliferation but not metastases. In addi-tion, pharmacologic inhibitors of the KRAS

BRAF pathway are being considered to treatpatients with advanced serous borderlineovarian tumors to improve patient survival.

The serous borderline ovarian tumors areunique among the borderline ovarian tumorsin that invasive or noninvasive peritoneal im-plants may occur in 35% of cases. The no-menclature is dependent on whether theimplants are simply stuck on the perito-neal surfaces (noninvasive) or have invadedthe underlying tissue such as omentum andbowel wall [3]. Although noninvasive im-plants are associated with benign behavior,the presence of invasive implants portendsa poor prognosis [11, 17]. A small subset of

implants also may originate de novo fromnodal endosalpingiosis (spectrum of second-ary mllerian system involvement in the pel-vis) [3]. Psammoma bodies may be associ-ated with noninvasive implants.

Lymph node involvement may be seen inabout 27% of serous borderline ovarian tu-mors [18]. Although lymph node involvementhas no prognostic value, lymph nodes mayserve as sites of recurrence and progressionto carcinoma [18, 19]. It is hypothesized thatthese nodal metastases most likely exit theovary through the peritoneal lymphatics rath-er than through the ovarian lymphatics. Com-monly involved lymph nodes in advanced se-rous borderline ovarian tumors include thefollowing in descending order of frequency:pelvic, omental and mesenteric, and paraaor-tic and supradiaphragmatic regions [19].

Serous borderline ovarian tumors manifestas complex cystic adnexal masses with thinseptations and endocystic or exocystic veg-etations [20] (Fig. 2). The solid componentscommonly show moderate enhancement dur-

ing contrast-enhanced CT or dynamic MRI(Fig. 3). Approximately one third of serousborderline ovarian tumors are bilateral. Non-invasive peritoneal implants occur more fre-quently than invasive implants (78% vs 22%,respectively) [12]. A serous tumor with in-vasive implants macroscopically may haveprofuse papillary projections that actual-ly consists of many vesicles perforating andextending beyond the ovarian capsule with-out a solid component. The lesion may havehigh signal intensity on contrast-enhanced T1-weighted imaging and water signal intensityon the T2-weighted imaging, suggesting the

absence of solid elements [21]. Barring thepresence of extraovarian disease (Fig. 4), theimaging ndings of serous borderline ovariantumors are indistinguishable from other bor-derline ovarian tumors and advanced border-line ovarian tumors masquerade as invasiveovarian carcinomas.

At the time of presentation, 70% of serousborderline ovarian tumors a re conned to theovary (stage I). Survival for women with stageI tumors is vir tually 100%. The overall prog-nosis is dependent on the presence of perito-neal implants. After 7.4 years (mean) of fol-low-up, the survival for advanced stage serous

Fig. 352-year-old woman

with serous carcinomawith background serousborderline tumor. Axialcontrast-enhanced CTscan through pelvis showsleft ovarian cystic lesion(arrowheads ) with multipleenhancing intracystic solidpapillary excrescences.Surgical excision conrmeddiagnosis of serouscarcinoma with backgroundserous borderline tumor.

Serous cystadenoma

Serous borderline tumor

Low-grade serous carcinoma

Mutations in BRAF or KRAS

Fig. 1Schematic representation shows progressionof serous borderline tumor to low-grade serouscarcinoma.

AFig. 2Benign serous cystadenoma versus serous borderline tumor: imaging ndings.A, 46-year-old woman with benign serous cystadenoma. Axial T2-weighted MR image shows well-denedhyperintense cystic lesion ( arrowheads ) in pelvis without mural nodules or solid components. Surgical excisionconrmed diagnosis of left ovarian serous cystadenoma.B, 45-year-old woman with serous borderline tumor. Axial contrast-enhanced CT image through pelvis showswell-dened cystic lesion with thin internal septations ( arrowhead ) and eccentric wall thickening along rightanterolateral wall ( arrow ).

B


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stage in the orderly, stepwise progression toinvasive carcinoma akin to the adenomacar-cinoma sequence in colorectal carcinomas.Mucinous borderline ovarian tumors are as-sociated with KRAS mutations in more than60% of cases. The increasing frequency ofKRAS mutations (3386%) has been de-scribed in mucinous cystadenomas, border-line ovarian tumors, and carcinomas [4, 13].

On imaging, mucinous borderline ovariantumors may be twice the size of serous bor-derline ovarian tumors and may manifest asmultilocular or unilocular cystic masses (Figs.5 and 6). Mucinous borderline ovarian tu-mors commonly appear as multilocular cys-tic masses with numerous septa and containuids of different signal intensities on T1- orT2-weighted MR images [20]. The endocysticvegetations of mucinous borderline ovarian tu-

mors show delayed uptake of contrast medium.On T1-weighted images, the mucinous compo-nent may impart a high signal intensity.

The imaging features of mllerian muci-nous borderline ovarian tumors arising fromendometriotic cysts are distinctive. The ml-

borderline ovarian tumors with noninvasiveimplants is 95.3%, whereas survival for pa-tients with tumors with invasive implants is66% [19]. Micropapillary architecture in theprimary ovarian tumor is closely associatedwith the presence of invasive implants [10].Serous borderline ovarian tumors with inva-sive and noninvasive implants may have 45%and 11% recurrence rates, respectively, over aperiod of 15 years [20]. The tumors usuallyrecur as invasive carcinomas in up to 77% ofpatients, with a high rate of resultant mortal ity(up to 74%) [22].

Mucinous Borderline Ovarian TumorsMucinous borderline ovarian tumors com-

prise about 32% of all borderline ovarian tu-mors [12]. The mean age of presentation is 45years. Mucinous borderline ovarian tumors

consist of two distinct histologic subtypes: theintestinal (90%) and the mllerian (endocer-vicallike, 10%) histotypes [11]. The intestinalsubtype is usually unilateral and may coexistwith pseudomyxoma peritonei in up to 17% ofcases [1]. The mllerian subtype is bilateral in

up to 40% cases and coexists with ipsilateralovarian or pelvic endometriosis in 2030% ofcases [1, 11]. The mllerian mucinous border-line ovarian tumors mimic serous borderlineovarian tumors to an extent and hence are alsotermed seromucinous borderline ovarian tu-mors. Like serous borderline ovarian tumors,these tumors may be associated with abdomi-nal or pelvic implants, which may be invasivein some cases.

Before the diagnosis of mucinous border-line ovarian tumor is made, it is important toexclude a metastatic adenocarcinoma, mostcommonly from the gastrointestinal tract,usually an appendiceal or colonic primary.Immunohistochemistry using a cytokeratinpanel is useful in differentiating metastaticversus primary ovarian tumors [3].

There is strong evidence that the muci nous

borderline ovarian tumors associated withpseudomyxoma peritonei (i.e., ascites withabundant mucoid or gelatinous material) areactually metastatic rather than an ovarian pri-mary [3, 11]. Mucinous borderline ovarian tu-mors are thought to represent an intermediate

A

Fig. 4Serous implants.A, 48-year-old woman with noninvasive implantsshowing psammomatous calcications. Axial CTimage through pelvis shows midline paraumbilicalcalcied implant ( arrow ) in anterior abdominal wall.B, 37-year-old woman with right paracolic invasiveimplants (arrow ).

B

A

Fig. 544-year-old woman with mucinous borderline tumor.A and B, Transvaginal ultrasound images show large multiloculated cystic mass with thick internal septations and small solid components ( arrowhead , B). Largerloculation (star , A) on left anterolateral aspect shows ne internal echoes.C, Axial contrast-enhanced CT image through pelvis shows large cystic mass ( arrowhead ) with thick septations and mural nodules along periphery.

CB


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Lalwani et al.

lerian mucinous borderline ovarian tumorsare typically uni- or paucilocular cystic mass-es with mural nodules (Figs. 7 and 8). The u-id component shows high intensity on bothT1- and T2-weighted images. The mural nod-ule shows high intensity on T2-weighted im-ages as well as contrast enhancement [23].

At the time of diagnosis, approximately82% mucinous borderline ovarian tumorsare conned to the ovary and clinically be-have similarly to serous borderline ovariantumors with 5-year survival rates of up to99100% [24]. Patients with these tumorsrarely have a recurrence or die of the disease.

Advanced-stage (18%) mucinous borderlineovarian tumors, however, may have a mortal-ity up to 50% that is stage dependent [13].

Miscellaneous Borderline TumorsUncommon subtypes of borderline ovar-

ian tumors encompass 34% all borderlineovarian tumors and include endometrioid,clear cell, and transitional cell (Brenner va-riety) tumors. Endometrioid borderline ovar-ian tumors resemble analogous endometrioidtumors arising from the uterine corpus andarise either from the surface ovarian epitheli-um or from endometriosis. Clear cell border-line ovarian tumors are ovarian tumors of lowmalignant potential characterized by the pres-ence of clear or hobnail cells set in a densebrous stroma with absence of stromal inva-sion. Borderline Brenner tumors are ovariantransitional cell tumors with atypical or ma-lignant features of the epithelium but lackingstromal invasion. The mean age for miscella-neous borderline ovarian tumors ranges be-tween 45 and 65 years.

Endometriosis and endometrioid adeno-bromas serve as precursors of endometri-oid borderline ovarian tumors. In contrast toserous and mucinous borderline ovarian tu-mors, endometrioid borderline ovarian tu-mors are characterized by mutations involv-ing the -catenin gene (50%), PTEN gene(20%), and microsatellite instability (up to50%) [11]. Endometrioid borderline ovariantumors have the potential to progress to low-grade invasive carcinoma. Although clear cellborderline ovarian tumors have been associ-ated with endometriosis and adenobromas, a

stepwise molecular pathway for the progres-sion of endometriosis or adenobroma to clearcarcinoma has not yet been elucidated. Clearcell borderline ovarian tumors are character-ized by KRAS mutations (516%) and micro-satellite instability (13%) [15]. Molecular andgenetic changes in Brenner tumors have notyet been described [4, 13].

Nonserous, nonmucinous borderline ovar-ian tumors do not show characteristic imag-ing features and may resemble other border-line ovarian tumors as well as early-stageovarian carcinomas (Fig. 9). The miscella-

Fig. 7Mllerian borderline tumors.A, 46-year-old woman with mllerian borderline tumor. Axial fat-suppressed T2-weighted image through pelvisshows unilocular cystic lesion with small eccentric hyperintense mural nodule ( arrow ).B, 52-year-old woman with mucinous (mllerian subtype) borderline tumor with background endometrioticcyst. Axial CT image through pelvis shows small unilocular lesion with enhancing mural nodules ( arrow ).

Fig. 648- year-old woman with unilocularmucinous borderline tumor. Sagittal T2-weightedMR image through pelvis shows large unilocularcystic mass ( arrowheads ) without internalseptations or mural nodules.

BA

Fig. 849-year-old woman with mucinousadenocarcinoma in background of mucinousborderline tumor. Axial contrast-enhanced CT image through pelvis shows large multiloculated cysticlesion with irregular and thick internal septations(white arrow ). There is noticeable variation indensities of various loculi; some loculi ( stars ) appearhyperdense in comparison with others. Intracysticenhancing mural nodules and solid components(black arrows ) are visualized along left anterior wall.

Fig. 941-year-old woman with endometrioidborderline ovarian tumor. Axial contrast-enhancedCT image through pelvis shows unilocular cysticlesion with mural nodule along left posterolateral wall(arrowhead ) mimicking low-grade carcinoma.


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neous borderline ovarian tumors chart a be-nign course after tumor removal with excep-tionally rare recurrences or metastasis. Thesurvival rate is up to 100%.

Imaging Algorithm for the Diagnosisof Borderline Ovarian Tumors

Borderline ovarian tumors commonlypresent as adnexal masses. Accurate diag-nosis and distinction from advanced ovarianmalignancy facilitate management includingfertility-preserving surgery. Transvaginalsonography is the primary screening imag-ing technique in the evaluation of any sus-pected adnexal mass [25, 26]. Borderlineovarian tumors manifest usually as complexcystic masses with septations and occasion-ally as mural nodules.

The use of color and spectral Doppler ul-trasound may provide additional informationabout tumoral angioarchitecture. However,gray-scale and color Doppler sonograms havebeen shown to be of limited value in charac-terizing borderline ovarian tumors. Adnex-al lesions may, at best, be categorized as be-nign or aggressive on sonography. MRI andMDCT can characterize adnexal masses intobenign and malignant in up to 93% [27, 28]and 89% [29] of the cases, respectively. Sono-graphically indeterminate lesions thus requireMRI for fur ther characterization (Fig. 10).

MRI, on account of its superior soft-tissuedistinction and multiplanar capabilities, al-lows better characterization of complex cystic

masses particularly with regard to the depic-tion of septations and mural nodules. Dynam-ic MRI characteristics of ovarian tumors haverecently been studied [3032], rst during thearterial phase (30-second delay) and on de-layed contrast-enhanced MR images (> 4 min-utes). The timeintensity curves of borderlineovarian tumors were compared with those ofnormal outer myometrium. Although the tu-mors that showed a gradual increase in en-hancement without a well-dened peak werecorrelated to benign ovarian tumors, border-line ovarian tumors showed moderate initialenhancement followed by a plateau.

Both MRI and MDCT can be used to mapperitoneal disease and provide informationfor preoperative planning and staging. Bor-derline ovarian tumors are not PET-avid andhence are interpreted as benign tumorson FDG PET [33, 34]. Ovarian masses thatshow complex features on MRI that are con-cerning for malignancy but appear as be-nign on PET are said to be characteristic ofborderline ovarian tumors [33]. However, -

nal diagnosis and staging of borderline ovar-ian tumors require pathologic evaluation af-ter surgical excision [5].

Staging, Management, andSurveillance Algorithm

Borderline ovarian tumors follow a stag-ing system similar to that used for stagingovarian epithelial carcinomas. The staging issurgical and the suggested guidelines includetaking specimens from the omentum; intesti-nal serosa and mesentery; pelvic peritoneumincluding the cul-de-sac, bladder peritone-um, and pelvic wall; and abdominal perito-neum including paracolic gutters, diaphrag-matic surface, and retroperitoneal nodes [1,

5]. The FIGO staging for borderline ovariantumors is summarized in Table 2.

When postoperative surgical staging as-certains borderline ovarian tumors withoutinvasion, peritoneal seeding, or distant me-tastasis, no further treatment is required.However, advanced-stage disease requirescytoreduction surgery with or without plat-inum-based chemotherapy. Patients with asuspected borderline ovarian tumor and de-siring fertility preservation may opt for aconservative approach such as cystectomyor salpingo-oophorectomy instead of radi-cal surgery. An outline of optimized patientmanagement is depicted in Figure 11.

Follow-up is usually a combination of clin-ical examination, transvaginal ultrasound,and CA-125 levels. During the initial 2 years,

follow-up evaluation is performed every 3months. Patients are then evaluated biannual-

Adnexal lesion

Transvaginal ultrasound

Staging (borderline tumors may be diagnosed as benign on MRI)

Conservative surger y Radical surgery

Benign Non-benign

Benign or borderlineovarian tumor

Malignant

MRI

Fig. 10Imaging algorithmfor diagnosis of borderline tumors.

No invasive implants

Borderline ovarian tumors

Surgical staging

Follow-up

Salpingo-oophorectomy Cystectomy

Invasive implants present

Both ovaries involvedor one ovary present

One ovary involved

Want fertility conservationRadical surgery

Transvaginal ultrasound, clinical examination, and CA-125 levels

Fig. 11Schematicrepresentation ofmanagement andsurveillance algorithmfor borderline ovarianneoplasms. Information from[5] was incorporated in thisalgorithm.


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ly for 35 years after surgery and then annual-ly thereafter [5]. Transvaginal sonography orpelvic MRI may be performed for the detec-tion of local recurrence. MDCT is better suit-ed for the detection of peritoneal disease orextrapelvic spread of disease.

ConclusionBorderline ovarian tumors are an interest-

ing subset of epithelial neoplasms that affectyounger women in the reproductive age group,chart an indolent course, and show excellentprognosis. Borderline tumors typically mani-fest as complex cystic masses with mural nod-ularity and septations. The imaging ndingsmay be indistinguishable from those of inva-sive ovarian carcinomas. Fertility-sparing sur-gery may sufce in patients with tumors thatare conned to the ovary. Radical surgery isrecommended in patients with advanced dis-ease. Long-term surveillance is recommendedto document and treat late recurrences.

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TABLE 2: Summary of International Federation of Obstetric Gynecology(FIGO) Staging

FIGO Stage Denition

I Tumor conned to ovary

II Peritoneal implants within the pelvis

III Peritoneal implants beyond the pelvis, posit ive lymph nodes, or both

IV Liver parenchyma involvement or tumor beyond the peritoneal cavity

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