Pediatric Teratomas and Other Germ Cell Tumors 

  • Author: E Stanton Adkins III, MD; Chief Editor: Max J Coppes, MD, PhD, MBA   more...
 
Updated: Dec 2, 2011
 

Background

Teratomas (from Greek terato meaning "a monster" and onkoma meaning "swelling or mass") and other germ cell tumors are relatively common solid neoplasms in children. They may occur in both gonadal and extragonadal locations. Locations and specific tumor types depend on the age of the child. The tumors are grouped together because they all appear to arise from postmeiotic germ cells. Most of the malignant tumors produce markers that can be serologically assessed.

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Pathophysiology

Several theories about the origin of these tumors are recognized. The best evidence suggests that most are due to abnormal differentiation of fetal germ cells that arise from the fetal yolk sac. Normal migration of these germ cells may cause gonadal tumors, whereas abnormal migration produces extragonadal tumors. Teratomas are typically found in the midline or gonads. Frequencies of the most common sites are as follows:

  • Sacrococcygeal - 40%
  • Ovary - 25%
  • Testicle - 12%
  • Brain - 5%
  • Other (including the neck and mediastinum) - 18%

By definition, teratomas include components derived from all 3 embryonic layers: ectoderm, endoderm, and mesoderm. These tissues are foreign to the location in which they are found. Teratomas may be classified as mature or immature on the basis of the presence of immature neuroectodermal elements within the tumor. Mature tumors (grade 0) have no immature elements. In grade 1 tumors, immature elements are limited to one low-power field per slide; in grade 2 tumors, less than 4 fields are present per slide; and in grade 3 tumors, more than 4 fields are present per slide.

In the past, survival was linked to the degree of immaturity in the teratoma. Close histologic evaluation of immature teratomas reveals a good correlation between the degree of immaturity and the presence of microscopic foci of frankly malignant elements. These malignant elements are typically yolk sac tumors but may also represent primitive neuroectodermal tumor (PNET). Charoenkwan et al (2002) found overexpression of p53 in the more aggressive immature teratomas at all sites.[1]

The risk of recurrence also appears to be related to the degree of immaturity. Recurrence in a completely resected mature teratoma is less than 10%; in an immature teratoma, recurrence may be as high as 33%. The likelihood of recurrence depends on the site of the tumor as well as the completeness of resection. The German MAKEI trials suggest that the recurrence rate for immature teratomas can be decreased to 9.5% with chemotherapy.[2] Sacrococcygeal teratomas are more likely to recur than those in the ovary or other sites. Molecular biologic and cytogenetic studies are providing a firmer scientific basis to these observations.

In 1965, Teilum first suggested the germ cell origin of gonadal tumors.[3] Since that time, the pathologic classification scheme has evolved to its present state. Germ cells undergo neoplastic transformation as follows:

  • Suppressed differentiation
    • Seminoma
    • Dysgerminoma
  • Differentiation
    • Initial - Embryonal carcinoma
    • Embryonic - Mature teratoma and immature teratoma
    • Extraembryonic - Choriocarcinoma and endodermal sinus tumor (yolk sac tumor)

Mutter describes genetic imprinting as a major factor in the development of some of these tumors.[4] The developmentally expressed genes insulinlike growth factor 2 (IGF II) and its receptor RNA (H-19); small nuclear riboprotein (SNRPN); mas proto-oncogene; and the tumor suppressor genes WT1 and MASH2 are imprinted, depending on their maternal or paternal origin. Mutter suggests that these genes or the cells have only the maternal imprint because many teratomas arise from a parthenogenetically activated egg. Therefore, maternally active genes are present in higher-than-usual concentrations, and maternally inactive products are present at lesser concentrations if at all. These abnormalities may account for the lack of organization of the 3 germ cell layers.

Oosterhuis et al suggest that tumors may be grouped on the basis of their chromosomal abnormalities as follows:[5]

  • Group 1 includes immature teratomas and yolk sac tumors. The immature teratomas are usually diploid, whereas yolk sac tumors may be diploid, tetraploid, or aneuploid. The chromosomal aberrations include overrepresentation of chromosomes X, 1, 3, 8, 12, and 14 and underrepresentation of Y and X. Deletions in 1p and rearrangements of 3q and 6q may be present. Isochromosome 12p (i12p) has been found. An abnormal number of centromeres is frequent in both diploid and aneuploid tumors.
  • Group 2 includes most nonseminomatous malignant germ cell tumors and typically includes numeric abnormalities in X, 7, 8, 12, and 21 as excess and deletions of Y, 11, 13, or 18. Once again, isochromosomes 12p with other aberrations of 12p and 1p are present.
  • Group 3 includes mature teratomas or mature cystic teratomas. Numeric abnormalities, including extra X, 7, 12, and 15, have been found. No chromosomal structural anomalies have been found.
  • Group 4 includes spermatocytic seminoma, a type usually confined to older men. The cytogenetics of this group have not been characterized. As with abnormalities and imprinting patterns, these chromosomal rearrangements can lead to overproduction of certain gene products and underproduction of others; these lead to the abnormal growth characteristics of the tumor.

Hara et al suggest that the MAGE gene family of tumor rejection antigens may also be involved in the pathogenesis of these tumors.[6] These genes appear to be more active in pure seminoma or mixed type of seminomatous elements than in other germ cell tumors. In their limited study of 22 patients, MAGE expression was not correlated with disease progression. It is likely to be only an indicator of maturity or differentiation of the tissues.

The concept of teratoma with malignant transformation indicates the development of non–germ cell malignancies within a teratoma. Among 641 patients in the MAKEI protocols 83/86/89/96, 9 patients were identified with this finding.[7] Five patients presented with a carcinoma, 2 patients presented with glial tumors, and 2 patients presented with embryonal tumors. Resection and chemotherapy were typically used. Because these tumors are quite rare, response to treatment is difficult to generalize.[8]

When platinum-based chemotherapy–resistant tumors are evaluated, between one third and one half of tumors exhibit microsatellite instability.

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Epidemiology

Frequency

United States

Sacrococcygeal teratoma occurs in 1 in 30,000-70,000 live births. The female-to-male predominance is 4:1. Ovarian teratomas are almost as common, whereas testicular teratomas are about one third less frequent. The overall incidence of malignant germ cell tumors is approximately 3% of all childhood malignancies, or approximately 3 cases per million population per year. The frequency of all germ cell tumors has increased over the last several decades.

International

No significant geographic predilection is recognized.

Mortality/Morbidity

The mortality rate for congenital teratomas depends on gestational age and the size and location of the tumors. Survival of preterm infants younger than 30 weeks' gestation with sacrococcygeal teratoma is only 7%, whereas the survival for infants older than 30 weeks' gestation is 75%.

Rapid early growth is associated with the yolk-sac phenotype and carries a poorer prognosis.[9] Early tumors are frequently large relative to the size of the infant and may induce congestive heart failure. Cervical teratomas may frequently lead to airway problems and death when they are large.

Prior to recent chemotherapeutic successes, the 10-year survival rate for malignant germ cell tumors ranged from 25% for embryonal carcinoma to 75% for dysgerminoma. Today, overall survival rates are greater than 90%.

Race

No racial predispositions for these tumors are known.

Sex

Sacrococcygeal teratoma has a 4:1 female-to-male predominance. In other germ cell tumors, the female-to-male ratio is roughly 2:1 in children.

Age

  • Sacrococcygeal teratomas
    • Sacrococcygeal teratomas are congenital.
    • Those with a significant external component, as shown below, are identified at birth. Tumors without an external component (Altman type 4) are discovered later. Sacrococcygeal teratoma in a female neonate. This Sacrococcygeal teratoma in a female neonate. This particular tumor is largely external with no intrapelvic extension.
    • When the tumors are resected before the patient is aged 2 months, 7-10% are malignant. After that age, the risk of malignancy greatly increases to more than 50% by age one year.
  • Ovarian tumors
    • The incidence of ovarian germ cell tumors, as shown below, increases with age and peaks around age 15-19 years.This is an ovarian mixed germ cell tumor in a 13-yThis is an ovarian mixed germ cell tumor in a 13-year-old girl. This tumor caused right lower quadrant pain. It is largely cystic in composition. No calcifications are observed within the mass.
    • When girls younger than 15 years were examined, fewer than 10% of tumors occurred in girls younger than 5 years, 20% of tumors were found in girls aged 5-9 years, and more than 70% of tumors were found in girls aged 10-14 years.[10]
    • Benign ovarian tumors, largely teratomas, predominate.
    • Roughly 70% of malignant ovarian tumors in childhood are germ cell tumors, one quarter are epithelial, and the remainder are stromal tumors. The ratio of germ cell tumors to epithelial malignancies decreases with increasing patient age.
    • Chromosomal abnormalities also appear to be related to age at presentation for teratomas. In girls less than 5 years old, no chromosomal abnormalities were found, whereas older girls often have gains of 12p and chromosomes 7 and 8.
  • Testicular tumors
    • Testicular germ cell tumors in childhood are split between teratomas and yolk sac tumors (see image below). They are more common from birth to age 5 years. From age 6 years until puberty, testicular tumors are exceedingly uncommon. Thereafter, the incidence increases, with a more adultlike tumor pattern with seminomas gradually becoming the predominant histology. Yolk sac tumor of the testis. The tumor is metastaYolk sac tumor of the testis. The tumor is metastatic to the retroperitoneum. It encases the aorta and renal arteries. The vena cava and renal veins are displaced anteriorly by the mass.
    • Both teratomas and yolk sac tumors may be associated with contralateral in situ dysgenesis in 9% of patients compared with 0.5% of otherwise healthy males. Contralateral tumors are often found. These are occasionally synchronous but are more often metachronous. Ongoing surveillance of the contralateral testis is therefore needed.
    • Among malignant germ cell tumors, yolk sac tumors predominate until patients are aged 14 years. Few tumors of any type are diagnosed in children aged 5-9 years. For malignant teratomas, yolk sac tumors, and all germ cell tumors, rates by age group are as follows:
      • Age group 0-4 years - 0.45 case, 3.66 cases, and 4.16 cases per million population
      • Age group 5-9 years - 0.12 case, 0.12 case, and 0.12 case per million population
      • Age group 10-14 years - 0.05 case, 1.30 case, and 1.77 case per million population
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Contributor Information and Disclosures
Author

E Stanton Adkins III, MD  Clinical Associate Professor, Departments of Pediatrics and Surgery, University of South Carolina School of Medicine

E Stanton Adkins III, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Surgeons, American Medical Association, and American Pediatric Surgical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Rebeccah Brown, MD  Associate Director of Trauma Services, Associate Professor, Department of Clinical Surgery and Pediatrics, Cincinnati Children's Hospital Medical Center and University of Cincinnati Hospital

Rebeccah Brown, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, and American Medical Women's Association

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Deborah F Billmire, MD  Associate Professor, Department of Surgery, Indiana University Medical Center

Deborah F Billmire, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American College of Surgeons, American Pediatric Surgical Association, Phi Beta Kappa, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

H Biemann Othersen Jr, MD  Professor of Surgery and Pediatrics, Emeritus Head, Division of Pediatric Surgery, Medical University of South Carolina

H Biemann Othersen Jr, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Association for the Surgery of Trauma, American Burn Association, American Cancer Society, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, American Society for Parenteral and Enteral Nutrition, American Surgical Association, American Thoracic Society, British Association of Paediatric Surgeons, Society for Surgery of the Alimentary Tract, Society of Critical Care Medicine, South Carolina Medical Association, Southeastern Surgical Congress, Southern Medical Association, Southern Society for Pediatric Research, and Southern Thoracic Surgical Association

Disclosure: Nothing to disclose.

Chief Editor

Max J Coppes, MD, PhD, MBA  Senior Vice President, Center for Cancer and Blood Disorders, Children's National Medical Center; Professor of Medicine, Oncology, and Pediatrics, Georgetown University School of Medicine; Clinical Professor of Pediatrics, George Washington University School of Medicine and Health Sciences

Max J Coppes, MD, PhD, MBA is a member of the following medical societies: American Association for Cancer Research, American Society of Pediatric Hematology/Oncology, and Society for Pediatric Research

Disclosure: Nothing to disclose.

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Sacrococcygeal teratoma in a female neonate. This particular tumor is largely external with no intrapelvic extension.
This is an ovarian mixed germ cell tumor in a 13-year-old girl. This tumor caused right lower quadrant pain. It is largely cystic in composition. No calcifications are observed within the mass.
Ovarian yolk sac tumor at surgery.
Yolk sac tumor of the testis. The tumor is metastatic to the retroperitoneum. It encases the aorta and renal arteries. The vena cava and renal veins are displaced anteriorly by the mass.
Esophagram in an infant with massive thoracic germ cell tumor. Note how the esophagus is displaced posteriorly and laterally by the left mediastinal tumor.
Chest radiograph of the patient in Media file 5 after treatment with chemotherapy. The size of the tumor has not decreased.
CT scan of the chest in the patient in Media file 6. The carina is displaced posteriorly and to the right. The vena cava is displaced anteriorly, and the aorta is compressed between the mass and the spine.
 
 
 
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