INTRODUCTION — Ovarian germ cell tumors (OGCTs) are derived from primordial germ cells of the ovary (figure 1). They may be benign or malignant. These neoplasms comprise approximately 20 to 25 percent of ovarian neoplasms overall, but account for only an approximate 5 percent of all malignant ovarian neoplasms [1-3]. OGCTs arise primarily in young women between 10 and 30 years of age and represent 70 percent of ovarian neoplasms in this age group [4].

The pathology, epidemiology, clinical manifestations, and diagnosis of OGCTs are reviewed here. Treatment of malignant germ cell tumors of the ovary as well epithelial ovarian carcinoma is discussed separately. (See "Treatment of malignant germ cell tumors of the ovary" and "Epithelial carcinoma of the ovary, fallopian tube, and peritoneum: Clinical features and diagnosis".)

OVERVIEW OF OVARIAN GERM CELL TUMORS

Histopathology overview — The histologic types of OGCTs that arise from the ovary are similar to those developing in the testes of men (table 1) [2,5]. (See "Anatomy and pathology of testicular tumors".)

OGCTs can be broadly divided into those that differentiate toward embryo-like neoplasms (teratomas and their subtypes and dysgerminomas) and those that differentiate primarily toward extraembryonic fetal-derived (placenta-like) cell populations or a mixture of both. Categories include:

●Teratomas

•Benign cystic mature teratomas (dermoid cysts) are the most common OGCTs. Some malignant OGCTs develop when components of dermoid cysts develop into a somatic malignant neoplasm (termed mature cystic teratoma with malignant degeneration).

•Immature teratomas.

●Dysgerminomas – These are the female version of the male seminoma and are essentially comprised of immature germ cells. (See "Anatomy and pathology of testicular tumors".)

●Yolk sac tumors – These are carcinomas (epithelial neoplasms) that differentiate toward yolk sac/primitive placenta forms.

●Mixed germ cell tumors – These are tumors with two or more types of malignant OGCTs. The most common combination is a dysgerminoma and yolk sac tumor.

●Rare OGCTs – Pure embryonal carcinomas, nongestational choriocarcinomas, and pure polyembryoma.

Among malignant OGCTs, dysgerminoma, immature teratoma, yolk sac tumors, and mixed germ cell tumors account for 90 percent of cases [2,3]. Pure embryonal carcinomas and nongestational choriocarcinomas are rare, and pure polyembryomas are very rare.

A study of findings from a United States national cancer database from 1973 to 2002 reported 1262 malignant OGCTs [6]. The distribution by histology was: pure dysgerminomas (33 percent); teratomas, immature plus mature with malignant transformation (39 percent); and nondysgerminoma or mixed cell types (29 percent) (table 2).

OGCTs grow rapidly, unlike the more common epithelial ovarian neoplasms, yet most patients present with stage IA disease (limited to one ovary). Evidence of bilateral ovarian involvement suggests the presence of a tumor with a propensity for involvement of the contralateral ovary, including benign cystic teratoma, dysgerminoma, or a tumor with components of dysgerminoma (mixed germ cell tumor). These conditions are bilateral in 10 to 12 percent of cases, while the majority of other histologies present as unilateral ovarian masses [7].

Epidemiology — OGCTs arise primarily in young women between 10 and 30 years of age, representing 70 percent of ovarian neoplasms in this age group [4]. Worldwide, the incidence is the highest in Eastern Asia for women under the age of 30, and the highest in Central America for those over 30 [8]. For unclear reasons, from the Surveillance, Epidemiology, and End Results (SEER) in the United States, malignant OGCTs occur more frequently among Hispanic Americans and Asian/Pacific Islanders compared with non-Hispanic White and non-Hispanic Black Americans [9].

Clinical manifestations overview — OGCTs often produce hormones, particularly the beta subunit of human chorionic gonadotropin (hCG) or alpha-fetoprotein (AFP). Patients typically present with one or more of the following signs and symptoms:

●Abdominal enlargement – From the mass itself, ascites, or both.

●Abdominal pain – From rupture or torsion.

●Precocious puberty, abnormal vaginal bleeding – Presumably from hCG production.

●Symptoms of pregnancy – From hCG production.

Eighty-five percent of women with an OGCT have both abdominal pain and an abdominal mass; fever or vaginal bleeding occurs in 10 percent. OGCTs tend to be large (median size, 16 cm). Ascites, rupture (pre- or intraoperative), and torsion are reported in 20, 20, and 5 percent of cases, respectively.

Diagnosis overview — The diagnosis is made by histology at time of surgical excision. The diagnosis is strongly suggested preoperatively by the presence of an adnexal mass on pelvic imaging and an elevated level of an associated tumor marker (eg, hCG, AFP).

For benign cystic mature teratomas, the diagnosis can be made with reasonable confidence using pelvic ultrasonography; however, removal of the cyst is still advised. (See 'Mature teratoma (dermoid)' below.)

Tumor markers — OGCTs are often associated with hormonal or enzymatic activity. Some of these proteins can be measured in the serum, providing a highly sensitive and variably specific marker for the presence of certain histologic components (table 3). Some tumor markers are present in some, but not all tumors of a specific histology. Tumor markers produced by tumor types are as follows:

●hCG – Embryonal cell carcinomas and ovarian choriocarcinomas, mixed germ cell tumors, and some dysgerminomas.

●AFP – Yolk sac tumors, embryonal cell carcinomas and polyembryoma carcinomas, mixed germ cell tumors, and some immature teratomas [10,11]; most dysgerminomas are associated with a normal AFP.

●Lactate dehydrogenase – Dysgerminomas.

Staging and surgical treatment — Malignant germ cell tumors are staged according to the International Federation of Gynecology and Obstetrics (FIGO) staging system for epithelial ovarian cancer (table 4) [12]. In brief, stage I disease is confined to the ovaries, stage II includes extension into other pelvic tissues, stage III refers to disease that has spread beyond the pelvis or to retroperitoneal lymph nodes but remains in the abdomen, and stage IV refers to the presence of distant metastasis or involvement of liver parenchyma.

In virtually all cases, surgery is required for definitive histologic diagnosis, treatment, and staging (if malignant) of OGCTs. Oophorectomy, ovarian cystectomy, or resection of the ovarian mass can be performed, depending on the clinical situation, and tissue sent for frozen section. Confirmation of the diagnosis should be obtained prior to definitive surgical treatment.

The following sections review the pathology and clinical manifestations of the individual types of OGCTs. Treatment of benign OGCTs is also described below, while management of malignant OGCTs is discussed separately. (See "Treatment of malignant germ cell tumors of the ovary".)

TERATOMAS — Teratomas are the most common type of germ cell tumor. Most, but not all, teratomas are benign. The designation teratoma refers to a neoplasm that differentiates toward somatic-type cell populations (typically including cell populations that would normally derive from ectoderm, endoderm, and mesoderm) that can be typical of either adult or embryonic development. The component tissues in a teratoma range from immature to well differentiated and are foreign to the anatomic site in which they are found.

Teratomas are divided into four categories: mature (cystic or solid, benign), immature (malignant), malignant due to a component of another somatic malignant neoplasm, and monodermal or highly specialized.

Mature teratoma (dermoid) — Most teratomas are cystic and composed of mature differentiated elements (mature); they are better known as dermoid cysts. The mature cystic teratoma accounts for more than 95 percent of all ovarian teratomas and is almost invariably benign [13]. Dermoid cysts are the most common ovarian tumor in women in the second and third decade of life. Mature teratomas at nonovarian sites (eg, vaginal wall) have also been described [14].

In rare instances, a teratoma is solid but is composed entirely of benign-appearing heterogeneous collections of tissue and organized structures derived from all three cell layers. Most mature solid teratomas are unilateral and benign, although peritoneal implants have been described. Grossly, it may be difficult/impossible to differentiate these neoplasms from malignant solid immature teratomas, which are almost always solid, and they therefore may require sampling from multiple sites (see 'Immature teratoma' below). Management is as described above for mature cystic teratomas.

Histopathology — Mature cystic teratomas contain mature tissue of ectodermal (eg, skin, hair follicles, sebaceous glands), mesodermal (eg, muscle, urinary), and endodermal origin (eg, lung, gastrointestinal) [15]. The mechanism by which these cysts develop is possibly by failure of meiosis II or from a premeiotic cell in which meiosis I has failed [16]. They are bilateral in 10 to 17 percent of cases [17].

The characteristic macroscopic appearance of benign cystic teratomas is a multicystic mass that contains hair, teeth, and/or skin that is mixed into sebaceous, thick, sticky, and often foul-smelling material (picture 1). A solid prominence (Rokitansky protuberance) is located at the junction between the teratoma and normal ovarian tissue [2]. The greatest cellular variety is found in the area of this junction, which should therefore be examined carefully by the pathologist to exclude immature/malignant components.

Clinical manifestations — Most women with dermoid cysts are asymptomatic. If present, symptoms depend upon the size of the mass. Torsion is not uncommon. Rupture of dermoid cysts with spillage of sebaceous material into the abdominal cavity can occur, but is uncommon. Shock and hemorrhage are the immediate sequelae of rupture; a marked granulomatous reaction (chemical peritonitis) may subsequently develop and lead to formation of dense adhesions.

A rare condition associated with either mature or immature teratomas is Anti-N-methyl-D-aspartate (NMDA) receptor encephalitis [18]. (See "Paraneoplastic and autoimmune encephalitis", section on 'Anti-NMDA receptor encephalitis'.)

Diagnosis — These tumors have a characteristic ultrasound appearance, which allows reasonably accurate noninvasive diagnosis in many cases [19]. The reported specificity is 98 to 100 percent [19,20]. Definitive diagnosis is made at the time of surgical excision. (See "Ultrasound categorization of adnexal masses".)

Treatment — Ovarian cystectomy is suggested in order to make a definitive diagnosis, preserve ovarian tissue, and avoid potential problems such as torsion, rupture, or development of malignant components. For women who have completed childbearing, salpingo-oophorectomy is also acceptable treatment. Benign cystic teratomas do not recur if surgically resected.

Dermoid cysts may be removed via either laparoscopy or laparotomy. With either approach, the abdomen should be copiously irrigated to avoid a chemical peritonitis from spillage of the sebaceous cyst fluid. (See "Oophorectomy and ovarian cystectomy", section on 'Laparoscopic/minimally invasive surgery cystectomy'.)

Malignant transformation — Malignant transformation occurs in 0.2 to 2 percent of mature cystic teratomas [21-23]. Mature teratomas with malignant transformation comprise 2.9 percent of all malignant OGCTs (table 2) [6]. Although any of the components of a mature cystic teratoma may undergo malignant degeneration, squamous cell carcinoma arising from the ectoderm is the most common secondary neoplasm [17,24].

Risk factors for malignant neoplasm in a mature cystic teratoma include age over 45 years (mean age, 50 years versus 33 years for benign teratomas), tumor diameter greater than 10 cm, rapid growth, and findings on imaging (eg, low-resistance intratumor flow on Doppler) [17,24].

Other possible malignant neoplasms include (but are not limited to) basal cell carcinoma, melanoma, adenocarcinoma, sarcoma, and thyroid carcinoma. When malignant transformation has occurred within a teratoma, treatment must be tailored to the transformed histology.

Monodermal highly specialized teratomas — The specialized or monodermal teratomas are a rare and remarkable subset of teratomas that consist of a predominant mature histologic cell type. The most common of these are struma ovarii and carcinoid (a well-differentiated neuroendocrine neoplasm). They are usually unilateral, although a contralateral teratoma may be present.

●Struma ovarii – Struma ovarii is a teratoma predominantly composed of mature thyroid tissue [15]. The secretion of thyroid hormones results in clinical hyperthyroidism in 25 to 35 percent of patients. Struma ovarii is uncommon, comprising approximately 2.7 percent of ovarian teratomas. It is often associated with a mature cystic teratoma and rarely with a cystadenoma. Most cases of struma ovarii are benign and can be managed by excision of the ovary or by unilateral salpingo-oophorectomy. However, malignant change may occur in struma ovarii, but it is exceedingly rare [25,26]. (See "Struma ovarii".)

●Carcinoid neoplasms – Ovarian carcinoid neoplasms are rare [27]. Primary ovarian carcinoid neoplasms are usually unilateral, localized to the ovary, and indistinguishable histologically from metastasis. They have similar appearances to those that arise in any other site (eg, gastrointestinal or respiratory). They are comprised of nests and cords of relatively bland cells (uniform cells without nuclear atypia) with endocrine features and a fine vascular network. Some carcinoid neoplasms secrete bioactive polypeptides and amines, producing a constellation of symptoms, predominantly flushing and diarrhea (table 5). Carcinoid syndrome develops in approximately one-third of cases, and it can develop without hepatic metastases due to direct venous drainage from the ovary into the systemic circulation (see "Clinical characteristics of well-differentiated neuroendocrine (carcinoid) tumors arising in the gastrointestinal and genitourinary tracts", section on 'Ovary' and "Clinical features of carcinoid syndrome", section on 'Clinical features'). 5-hydroxyindoleacetic acid, a metabolite of serotonin (figure 2), is excreted in the urine and can be used to confirm the diagnosis of carcinoid syndrome and as a marker of disease activity in patients with advanced disease or the carcinoid syndrome. (See "Diagnosis of carcinoid syndrome and tumor localization", section on 'Biochemical testing for carcinoid syndrome'.)

Carcinoid tumors metastatic to the ovary are even more rare; they tend to be bilateral and arise from primary ileal carcinoid tumors [28]. In such cases, disseminated abdominal disease is common.

●Mixed struma ovarii and carcinoid – The presence of a mixed struma ovarii and carcinoid is even more rare. These lesions usually follow a benign course.

Immature teratoma — Immature teratomas are also called malignant teratoma, teratoblastoma, or embryonal teratoma [15]. They comprise less than 1 percent of ovarian teratomas and are most common in the first two decades of life. They comprise 35.6 percent of all malignant OGCTs (table 2) [6].

Histopathology — These neoplasms are typically composed of tissue from the three germ cell layers: ectoderm, mesoderm, and endoderm, arranged in a haphazard manner. Histologically, there are varying amounts of immature tissue, most frequently with neural differentiation, although immature stromal elements can also be present.

Immature teratomas are the only OGCTs that are histologically graded. The grade of differentiation (ranging from I [well differentiated] to III [poorly differentiated]) is based upon the proportion of tissue in histologic sections containing immature neural elements [29]. Grade is an important indicator of the risk for extraovarian spread. The presence of foci of yolk sac tumor in immature teratomas generally reflects more aggressive behavior and a worse outcome [30].

Clinical manifestations — The clinical presentation is similar to that of other OGCTs (incidentally discovered adnexal mass, abdominal enlargement or pain). In some cases, alpha-fetoprotein or lactate dehydrogenase may be elevated.

A rare condition associated with either mature or immature teratomas is anti-N-methyl-D-aspartate (NMDA) receptor encephalitis. (See "Paraneoplastic and autoimmune encephalitis", section on 'Anti-NMDA receptor encephalitis'.)

Treatment is discussed in detail separately. (See "Treatment of malignant germ cell tumors of the ovary".)

DYSGERMINOMA — Although dysgerminomas are relatively uncommon among all ovarian neoplasms (accounting for only an approximate 2 percent), they account for 32.8 percent of malignant OGCTs (table 2) [6]. The majority of cases (75 percent) arise in adolescents and young adults, in whom they account for approximately one-third of all ovarian malignant neoplasms [31]. Because of their predilection for young women, they are one of the more common ovarian malignant neoplasms detected during pregnancy. Nevertheless, dysgerminoma can occur at any age; case reports have described patients with dysgerminoma between 7 months and 70 years of age.

Histopathology — Although dysgerminomas are considered to be malignant, the degree of histologic atypia is variable, and only an approximate one-third behave aggressively. The neoplasm is composed of undifferentiated germ cells, large vesicular cells with clear cytoplasm, well-defined cell boundaries, and centrally placed regular nuclei; the overall appearance is sometimes described as resembling "fried eggs" (picture 2). The stroma is infiltrated by clusters of small lymphocytes and frequently contains granulomas. Dysgerminoma is the ovarian counterpart of testicular seminoma; histologically it has a similar appearance. (See "Anatomy and pathology of testicular tumors".)

Grossly, dysgerminoma appears as a lobulated mass that is firm and cream colored or pale tan (picture 3) [2].

Dysgerminomas may develop within a gonadoblastoma (a benign or in situ germ cell ovarian neoplasm composed of germ cells and sex cord stroma) in phenotypic females who have a Y chromosome. Included in this group are patients with pure gonadal dysgenesis 46XY, mixed gonadal dysgenesis 45X/46XY, or complete androgen insensitivity (formerly called testicular feminization) 46XY. Occasional patients may have features of Turner syndrome. These latter patients may have a 45X, 45X/46XX, or 45X/46XY karyotype. (See "Clinical manifestations and diagnosis of Turner syndrome", section on 'Risk of malignancy'.)

The first two patients with unique gonadal tumors were described in 1953, at which time the term gonadoblastoma was introduced [32]. These tumors may produce either testosterone or estrogens. Clinical presentation may include developmental abnormalities of the genitalia, primary amenorrhea, or virilization. Although gonadoblastoma may be overgrown by dysgerminoma, as occurs in approximately 50 percent of cases, other malignant germ cell components may predominate, including yolk sac tumor, immature teratoma, embryonal carcinoma, or choriocarcinoma. Thus, karyotyping is recommended for all patients with the operative finding of gonadoblastoma, with or without a coexistent malignant germ cell tumor, or young patients who present with an ovarian mass or masses and either primary amenorrhea or abnormalities of the genitalia.

It is important to determine whether a gonadoblastoma is present, since oophorectomy should be performed in these patients to prevent the development of gonadal neoplasia, although the age at which the procedure is performed depends upon the underlying etiology [33,34]. Women at risk for having dysgenetic gonads ideally should be identified preoperatively; frozen section is not reliable.

Clinical manifestations — The growth of dysgerminomas is usually rapid; as a result, patients often present with abdominal enlargement and pain due to rupture with hemoperitoneum or torsion. Menstrual abnormalities may occur if the tumor is hormonally active.

Dysgerminomas can contain syncytiotrophoblastic giant cells that produce placental alkaline phosphatase, and lactate dehydrogenase [35,36]. Serial measurements of these markers can be useful for monitoring disease (table 3). In addition, 3 to 5 percent of dysgerminomas produce human chorionic gonadotropin. In general, dysgerminomas do not produce alpha-fetoprotein, although borderline elevations (<16 ng/mL) are described in case series, but most often in the setting of mixed germ cell tumors that contain a yolk sac element.

Seventy-five percent of women with dysgerminomas present with stage I disease (table 4); the contralateral ovary is involved in 10 to 15 percent [37,38]. Bilateral ovarian disease is more common with dysgerminoma than with any other malignant OGCT.

Surgery is performed for definitive diagnosis, staging, and initial treatment. For a unilateral neoplasm confined to the ovary without capsular involvement or rupture, simple salpingo-oophorectomy is curative in over 95 percent. Treatment is discussed in detail separately. (See "Treatment of malignant germ cell tumors of the ovary".)

YOLK SAC TUMOR — Yolk sac tumors make up 14 to 20 percent of all malignant OGCTs (table 2) [6,39]. The name was chosen because the tumor structure is similar to that of the endodermal sinuses of the rat yolk sac and is derived from the primitive yolk sac. These neoplasms usually occur in young girls and women; the median age at presentation is 23 years and one-third of patients are premenarchal [40,41].

Histopathology — Histologically, these epithelial neoplasms consist of tubules or spaces lined by single layers of flattened cuboidal cells, reticular stroma, and scattered globules (picture 4) [42]. Invaginated papillary structures with a central vessel (Schiller-Duval bodies) are found within some of the spaces (picture 5) [2].

Clinical manifestations — Patients with yolk sac tumors often present with abdominal pain and a pelvic mass, similar to dysgerminomas. The pain may be acute and is commonly misdiagnosed as appendicitis.

Tumor growth can be very rapid and aggressive with extensive intraperitoneal dissemination. Serum alpha-fetoprotein levels are elevated in a significant number of patients and, if elevated, are useful for monitoring the response to treatment and for posttreatment surveillance [43,44]. Serum lactate dehydrogenase may also be elevated [45].

Treatment of yolk sac tumors is discussed in detail elsewhere.

EMBRYONAL CARCINOMA — Embryonal carcinoma accounts for 4 percent of malignant OGCTs (table 2) [6,46]. It resembles the more common embryonal carcinoma of the testis and is one of the most aggressive ovarian malignant neoplasms. The average age at diagnosis is 15 years. (See "Anatomy and pathology of testicular tumors".)

Histopathology — Histologically, this neoplasm is epithelial and therefore forms nests and may form papillary or gland-like structures. Many atypical mitotic figures are usually present, reflecting the high proliferative activity of the neoplastic cells. Multinucleated giant cells resembling syncytial cells may be present; these are the cells that produce human chorionic gonadotropin (hCG) [15].

Clinical manifestations — Patients with embryonal carcinoma usually present with an abdominal or pelvic mass and abdominal pain [47]. Most of these neoplasms produce hCG, while some also make alpha-fetoprotein (table 3).

Treatment is discussed separately. (See "Treatment of malignant germ cell tumors of the ovary".)

MIXED GERM CELL TUMORS — Mixed germ cell neoplasms consist of two or more admixed types of OGCTs. They account for 5.3 percent of all malignant OGCTs (table 2) [6]. Components of dysgerminoma mixed with a yolk sac tumor are found most commonly. In cases in which a dysgerminoma component is present, the contralateral ovary is involved 10 percent of the time. The neoplasms may secrete tumor markers, such as lactate dehydrogenase, alpha-fetoprotein, or human chorionic gonadotropin, depending upon the type of tissue present.

Treatment is discussed separately. (See "Treatment of malignant germ cell tumors of the ovary".)

POLYEMBRYOMA — Polyembryoma is composed of embryoid bodies that morphologically resemble normal embryos [2]. This malignant germ cell neoplasm is very rare and, in most instances, is associated with other germ cell elements such as immature teratoma. It usually occurs in young girls and may present with signs of pseudopuberty.

Polyembryoma is a very aggressive tumor with extensive local infiltration and distant metastasis [48]. Serum human chorionic gonadotropin and alpha-fetoprotein concentrations may be elevated.

Treatment is discussed separately. (See "Treatment of malignant germ cell tumors of the ovary".)

CHORIOCARCINOMA — Nongestational choriocarcinoma is a rare and highly malignant type of OGCT [49]. Choriocarcinomas are more commonly of placental than ovarian origin; the estimated incidence of a primary ovarian choriocarcinoma is 1 in 369,000,000. They comprise 2.1 percent of all malignant OGCTs (table 2) [6]. A choriocarcinoma of ovarian origin derives from an extraembryonic differentiation of malignant germ cells. This highly malignant germ cell epithelial neoplasm differentiates towards trophoblastic structures and often contains other malignant germ cell elements.

Nongestational ovarian choriocarcinoma is histologically identical to primary gestational choriocarcinoma associated with pregnancy [50-52]. The two entities can be distinguished by DNA analysis; the presence of paternal DNA within the tumor indicates a gestational (placental) origin [53]. (See "Gestational trophoblastic disease: Pathology", section on 'Choriocarcinoma'.)

All choriocarcinomas produce human chorionic gonadotropin (hCG), which may cause isosexual precocity in young girls and irregular vaginal bleeding of uterine origin. Serum levels of hCG are useful for monitoring response to treatment.

Like gestational choriocarcinomas, those arising in the ovary tend to develop early hematogenous metastasis to several different sites, including lung, liver, brain, bone, vagina, and other viscera. In contrast to gestational choriocarcinomas, those arising in the ovary are relatively chemoresistant.

Treatment is discussed separately.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Ovarian, fallopian tube, and peritoneal cancer".)

SUMMARY AND RECOMMENDATIONS

●Ovarian germ cell tumors are derived from primordial germ cells of the ovary (figure 1). They may be benign or malignant. These neoplasms comprise approximately 20 to 25 percent of ovarian neoplasms overall, but account for only an approximate 5 percent of all malignant ovarian neoplasms. (See 'Introduction' above.)

●Ovarian germ cell tumors arise primarily in young women between 10 and 30 years of age; they represent 70 percent of ovarian neoplasms in this age group. (See 'Introduction' above.)

●Ovarian germ cell tumors often produce tumor markers (table 3). (See 'Tumor markers' above.)

●The most common ovarian germ cell tumor is the benign mature cystic teratoma (dermoid cyst), which can be bilateral. Approximately 1 percent contain a secondary malignancy arising from one of the components, usually a squamous cell cancer. Ovarian cystectomy or oophorectomy provides definitive diagnosis and treatment. (See 'Mature teratoma (dermoid)' above.)

●Dysgerminoma is the most common malignant ovarian germ cell tumor. Bilateral ovarian disease is more common than with any other ovarian germ cell tumor. These tumors are less likely to produce tumor markers than other malignant germ cell tumors (table 3), but lactate dehydrogenase is often elevated. (See 'Dysgerminoma' above.)