Home / Deep Research / Dermoid Cyst

Dermoid Cyst

1. Disease Information

2026-06-30
Falcon MONDO:0002378 Model: Edison Scientific Literature 36 citations

1. Disease Information

1.1 Overview

Dermoid cysts are benign developmental lesions that originate from ectodermal cells trapped during embryogenesis. They are composed of mature ectodermal derivatives and are histologically lined by keratinizing squamous epithelium containing adnexal structures such as sebaceous glands, hair follicles, and sweat glands (quan2026pediatricnasaldermoid pages 2-3, wiener2021histologicfeaturesof pages 14-16). Dermoid cysts differ from epidermoid cysts, which lack dermal appendages, and from teratomas, which arise from pluripotent germ cells and may contain elements of all three embryonic germ layers (soto2025presentationofa pages 1-3). The term "dermoid cyst" encompasses a heterogeneous group of lesions occurring at various anatomical sites, including the ovary (where mature cystic teratoma is the most common usage), the craniofacial region (nasal, orbital/periorbital), the central nervous system (intracranial, spinal), the skin/subcutaneous tissue, and the ocular surface (limbal/epibulbar).

1.2 Key Identifiers

  • ICD-10: L72.0 (Epidermal cyst, which includes dermoid cysts of skin); D27 (Benign neoplasm of ovary, for ovarian dermoid/mature teratoma); Q84.4 (Congenital dermoid cyst); D33.9 (Benign neoplasm of brain, for intracranial dermoid)
  • ICD-11: EK90.0 (Follicular cyst of skin and subcutaneous tissue); 2F32 (Benign neoplasms of ovary, for mature teratoma)
  • MeSH: D003884 (Dermoid Cyst)
  • MONDO: MONDO:0006233 (dermoid cyst)
  • Orphanet: Not assigned a specific Orphanet number for dermoid cyst as a standalone entity; ORPHA:141112 (Ovarian germ cell tumor, which includes mature teratoma)
  • OMIM: Not assigned a specific OMIM entry for sporadic dermoid cyst; 612555 (BMP15-related ovarian dysgenesis, relevant to hereditary forms)

1.3 Common Synonyms and Alternative Names

  • Mature cystic teratoma (for ovarian dermoid cysts)
  • Benign cystic teratoma
  • Dermoid
  • Dermoid tumor
  • Nasal dermoid sinus cyst (NDSC, for midline nasal lesions)
  • Epibulbar dermoid (for limbal/conjunctival lesions)
  • Orbital dermoid (for periorbital lesions)
  • Congenital dermoid cyst
  • Choristoma (when referring to ocular dermoids)

1.4 Data Source

Information is derived from aggregated disease-level resources, including published peer-reviewed literature, clinical trial registries, and veterinary pathology databases.

The following table provides a comparative overview of dermoid cysts by anatomical location:

Table (click to expand)
Anatomical Site Frequency/Prevalence Typical Age of Onset Key Clinical Features Primary Diagnostic Modality Primary Treatment
Ovarian (mature cystic teratoma / dermoid cyst) Ovarian germ cell tumors represent ~2–5% of ovarian cancers; mature teratoma is the benign teratoma subtype and one of the common ovarian germ-cell lesions in children, adolescents, and young adults (saani2023clinicalchallengesin pages 9-10, pinto2023molecularbiologyof pages 1-3) Usually reproductive age; often children, adolescents, and young adults for ovarian germ-cell tumors (pinto2023molecularbiologyof pages 1-3) Often asymptomatic until large; may present with adnexal mass, pelvic pain, torsion, rupture, or rarely malignant transformation; histologically a mature teratoma is a dermoid cyst (moraru2023immatureteratomadiagnosis pages 2-4, saani2023clinicalchallengesin pages 9-10) Pelvic ultrasound first-line; CT/MRI used for characterization of fat/calcification and complications; definitive diagnosis by histopathology after excision (moraru2023immatureteratomadiagnosis pages 2-4) Surgical excision, usually fertility-sparing cystectomy/oophorectomy; laparoscopy commonly used when feasible (NCT06816316 chunk 2)
Intracranial Rare benign tumor comprising ~0.04–0.6% of brain tumors (soto2025presentationofa pages 1-3) Congenital in origin but often diagnosed in young adults, especially ages 20–30 for suprasellar supratentorial lesions; can occur from childhood to adulthood (soto2025presentationofa pages 1-3, soto2025presentationofa pages 6-8) Headache, seizures, dizziness/vertigo, visual symptoms; rupture may cause chemical aseptic meningitis and acute symptomatic seizures (soto2025presentationofa pages 1-3, soto2025presentationofa pages 6-8) MRI is primary and essential for diagnosis and surgical planning; CT may assist in lesion characterization (soto2025presentationofa pages 6-8, soto2025presentationofa pages 8-10) Neurosurgical excision aiming for gross total resection when safely possible; subtotal resection may be necessary near critical neurovascular structures (soto2025presentationofa pages 8-10, soto2025presentationofa pages 1-3)
Nasal / craniofacial Nasal dermoids account for at least 60% of congenital developmental midline nasal masses; intracranial involvement occurs in ~20% overall, with wide reported range (4–57%) (kotowski2023thedifferentialdiagnosis pages 2-5) Congenital; usually recognized in infancy or childhood (quan2026pediatricnasaldermoid pages 2-3, kotowski2023thedifferentialdiagnosis pages 2-5) Painless noncompressible midline nasal mass; sinus opening with visible hair may be present; recurrent local infection possible, with substantial childhood infection risk when a sinus ostium is present (quan2026pediatricnasaldermoid pages 2-3, kotowski2023thedifferentialdiagnosis pages 2-5) MRI preferred for defining soft-tissue tract and intracranial extension; CT complements osseous assessment; biopsy is contraindicated (deftereou2025congenitalanomaliesof pages 6-6, quan2026pediatricnasaldermoid pages 4-5) Complete surgical excision of cyst and tract; external rhinoplasty, endoscopic, or combined craniofacial approaches depending on extension (quan2026pediatricnasaldermoid pages 8-9, quan2026pediatricnasaldermoid pages 10-11)
Orbital / periorbital Common congenital craniofacial dermoid location; literature in this evidence set is mainly case-series/review based rather than population-based, so precise prevalence not established here (soto2025presentationofa pages 6-8, quan2026pediatricnasaldermoid pages 8-9) Usually congenital and detected in infancy or childhood (quan2026pediatricnasaldermoid pages 8-9) Superolateral brow/orbital mass, usually painless and slowly enlarging; cosmetic deformity, local pressure effects, and occasional rupture/inflammation may occur (quan2026pediatricnasaldermoid pages 8-9, NCT06816316 chunk 2) Clinical examination with imaging when deep lesion suspected; MRI/CT used to define orbital extension and surgical anatomy (NCT06816316 chunk 2) Complete surgical excision; careful removal needed to avoid rupture and recurrence (NCT06816316 chunk 2)
Cutaneous / subcutaneous Developmental anomaly rather than true neoplasm; human population prevalence not well defined in this evidence set (wiener2021histologicfeaturesof pages 14-16, wiener2021histologicfeaturesof pages 16-18) Congenital, though superficial lesions may be recognized later depending on size/location (wiener2021histologicfeaturesof pages 14-16) Small dermal/subcutaneous cyst containing keratin, hair, and sebaceous material; often solitary, slow-growing, and sometimes with a surface pore or protruding hair (wiener2021histologicfeaturesof pages 14-16, wiener2021histologicfeaturesof pages 16-18) Clinical examination with confirmation by histopathology after excision; imaging only if deep extension suspected (wiener2021histologicfeaturesof pages 14-16, wiener2021histologicfeaturesof pages 16-18) Complete surgical excision (wiener2021histologicfeaturesof pages 16-18)
Limbal / epibulbar Rare ocular surface choristoma/dermoid subtype; no robust prevalence estimate in this evidence set (NCT06816316 chunk 2) Congenital, typically identified in childhood (NCT06816316 chunk 2) Visible limbal or epibulbar mass; may induce astigmatism, visual disturbance, irritation, or cosmetic concern (NCT06816316 chunk 2) Ophthalmologic slit-lamp examination; imaging used selectively for extent/depth; diagnosis confirmed clinically and histopathologically when excised (NCT06816316 chunk 2) Observation for small asymptomatic lesions or surgical excision/lamellar keratoplasty/corneal autograft in visually significant cases (NCT06816316 chunk 2)

Table: This table summarizes how dermoid cysts differ by anatomical site, including frequency, age at presentation, clinical features, diagnostic approach, and treatment. It is useful for comparing the major clinically relevant dermoid cyst subtypes in one place.

2. Etiology

2.1 Disease Causal Factors

The primary etiology of dermoid cysts is developmental: they arise from ectodermal tissue entrapped during embryogenesis. For craniofacial dermoid cysts, two principal pathogenetic theories exist: (1) the ectodermal inclusion theory, in which surface ectoderm becomes entrapped during fusion of facial prominences, and (2) the embryonic closure-defect theory, involving extensive midline seam closure failure (quan2026pediatricnasaldermoid pages 2-3). For cutaneous dermoid cysts, incomplete separation of cutaneous ectoderm and neuroectoderm during embryogenesis results in focal skin reduplications that include epidermis, dermis, and adnexal structures (wiener2021histologicfeaturesof pages 14-16).

For ovarian dermoid cysts (mature cystic teratomas), the origin is parthenogenetic: tumors arise from a single ovarian germ cell/oocyte, typically after completed meiosis I with failed meiosis II, producing homozygous chromosomes and containing only maternal genomes (moraru2023immatureteratomadiagnosis pages 2-4, pinto2023molecularbiologyof pages 7-9).

2.2 Genetic Risk Factors

A landmark study published in PNAS in 2024 identified a rare germline BMP15 missense mutation (C262T) as a causative variant for hereditary ovarian immature teratoma (OIT). This mutation substitutes arginine with cysteine at position 88, reducing BMP15 secretion by 84.7%, and displays X-linked dominant inheritance affecting heterozygous female carriers (liu2024araregermline pages 3-4, liu2024araregermline pages 2-3). The mutation significantly increases spontaneous parthenogenetic activation rates of oocytes (8.4% for CC, 32.5% for CT, 51.3% for TT genotypes) (liu2024araregermline pages 2-3).

Gonadal dysgenesis is a recognized risk factor for malignant ovarian germ cell tumors (though not specifically for benign dermoid cysts), particularly in 46,XY individuals with Y chromosomal material, conferring a 30–40% risk of developing gonadoblastomas (pinto2023molecularbiologyof pages 3-4).

2.3 Environmental and Lifestyle Risk Factors

No specific environmental or lifestyle risk factors have been established for dermoid cyst formation, consistent with their congenital/developmental nature. Age and sex are the principal demographic risk factors: ovarian dermoid cysts predominantly affect reproductive-age women; nasal and orbital dermoid cysts are congenital and present in pediatric populations; and intracranial dermoid cysts show increased incidence in young adults aged 20–30 years (soto2025presentationofa pages 1-3, kotowski2023thedifferentialdiagnosis pages 2-5).

2.4 Protective Factors

No specific genetic or environmental protective factors have been identified for dermoid cysts in the current literature.

2.5 Gene–Environment Interactions

No significant gene–environment interactions have been described for dermoid cyst formation. The condition is primarily of developmental/genetic origin.

3. Phenotypes

3.1 Clinical Phenotypes by Site

Intracranial dermoid cysts present with headaches (67% of cases) and seizures (44%), including acute symptomatic seizures following cyst rupture and chronic epileptic seizures with impaired awareness. Dizziness, vertigo, and visual symptoms are also common. Cyst rupture may cause chemical aseptic meningitis due to release of lipid contents into cerebrospinal fluid (soto2025presentationofa pages 1-3, soto2025presentationofa pages 6-8, soto2025presentationofa pages 8-10). - Suggested HPO terms: HP:0002315 (Headache), HP:0001250 (Seizure), HP:0002383 (Encephalitis, for chemical meningitis), HP:0000238 (Hydrocephalus)

Nasal dermoid sinus cysts present as painless, non-compressible, non-pulsatile midline nasal masses that do not transilluminate. A sinus opening with visible hair may be present. Crucially, the presence of a sinus opening significantly increases infection risk, estimated at 7% per year during childhood, with 50% of children experiencing at least one infection by age 4 and over 90% by age 9 (kotowski2023thedifferentialdiagnosis pages 2-5). Intracranial involvement occurs in approximately 20% of cases (range 4–57%). Complications include local abscesses, periorbital cellulitis, osteomyelitis, meningitis, and cerebral abscesses (kotowski2023thedifferentialdiagnosis pages 2-5). - Suggested HPO terms: HP:0000431 (Wide nasal bridge, if applicable), HP:0010781 (Skin dimple), HP:0002090 (Pneumonia, for intracranial complications), HP:0040187 (Abnormality of the nose)

Ovarian dermoid cysts are often asymptomatic until they become large. They may present with pelvic pain, adnexal mass, or complications such as ovarian torsion, rupture, or (rarely, ~1–2%) malignant transformation (moraru2023immatureteratomadiagnosis pages 2-4). - Suggested HPO terms: HP:0000137 (Abnormality of the ovary), HP:0100607 (Dysmenorrhea), HP:0008675 (Enlarged ovaries)

Cutaneous dermoid cysts are typically solitary lesions less than 2 cm in diameter with a small pore that may contain protruding hair, located commonly on the dorsal midline (wiener2021histologicfeaturesof pages 14-16). - Suggested HPO terms: HP:0200040 (Skin cyst), HP:0001053 (Hypopigmented skin patches)

3.2 Quality of Life Impact

Intracranial dermoid cysts can significantly impair quality of life through chronic headaches, seizures, and neurological deficits. Nasal dermoid cysts in children carry a high risk of recurrent infection and cosmetic deformity, impacting psychosocial development. Ovarian dermoid cysts may affect fertility and cause anxiety regarding malignant potential. Specific QoL instrument data (EQ-5D, SF-36) specifically for dermoid cysts are limited in the current literature.

4. Genetic/Molecular Information

The following table summarizes the key molecular and genetic features of dermoid cysts/teratomas:

Table (click to expand)
Molecular Feature Details/Findings Relevant Gene/Pathway Significance Key Reference
Germline BMP15 missense mutation in hereditary ovarian teratoma A rare BMP15 C262T missense variant was identified in two pedigrees with hereditary ovarian immature teratoma; the mutation reduces mature BMP15 secretion by ~84.7% and supports an X-linked dominant hereditary form affecting heterozygous females. BMP15; oocyte growth factor signaling Strongest recent human genetic evidence for a causal predisposition gene in hereditary ovarian teratoma; supports molecular diagnosis and genetic counseling in high-risk families. PNAS 2024 BMP15 study (liu2024araregermline pages 3-4, liu2024araregermline pages 2-3, liu2024araregermline pages 1-2)
Parthenogenetic origin of ovarian teratomas Mature ovarian teratomas are described as parthenogenetic tumors containing only maternal genomes; they are thought to arise from a single ovarian germ cell/oocyte after meiotic errors or spontaneous activation without fertilization. Oocyte meiosis / parthenogenesis Explains why many ovarian teratomas show near-diploid genomes with limited somatic mutation burden and distinctive imprinting features. Diagnostics 2023; Cancers 2023; PNAS 2024 (moraru2023immatureteratomadiagnosis pages 2-4, pinto2023molecularbiologyof pages 7-9, liu2024araregermline pages 1-2)
H-Ras/MAPK pathway activation In BMP15-mutant oocytes, spontaneous parthenogenetic activation increased markedly, accompanied by elevated H-Ras and MEK1 expression and MAPK pathway activation. H-Ras, MEK1, MAPK signaling Provides a mechanistic link between the BMP15 variant and abnormal oocyte activation leading to teratoma formation. PNAS 2024 BMP15 study (liu2024araregermline pages 6-7, liu2024araregermline pages 4-6, liu2024araregermline pages 2-3)
GDF9/BMP15 signaling imbalance The BMP15 variant may alter the balance between BMP15 homodimers/heterodimers and GDF9-related signaling, shifting downstream signaling outputs and enhancing pathways that favor parthenogenesis. BMP15, GDF9, BMPR2, SMAD/MAPK-related signaling Suggests that altered oocyte–granulosa cell signaling balance is an upstream event in hereditary teratoma pathogenesis. PNAS 2024 BMP15 study (liu2024araregermline pages 6-7, liu2024araregermline pages 4-6, liu2024araregermline pages 7-8)
DNA methylation subtype differences Ovarian germ cell tumors show subtype-specific methylation states: undifferentiated germinomas are relatively hypomethylated, whereas differentiated tumors including mature teratomas are more hypermethylated. DNA methylation / epigenetic regulation Supports the idea that differentiation state and cell of origin are reflected in methylation profiles; potentially useful for tumor classification and pathogenesis studies. Cancers 2023 review (pinto2023molecularbiologyof pages 11-12, pinto2023molecularbiologyof pages 1-3, pinto2023molecularbiologyof pages 3-4)
Epigenetic imprinting abnormalities Ovarian teratomas show abnormal imprinting patterns, including reduced methylation at paternally methylated loci and increased methylation at maternally methylated loci; IGF2/H19 imprinting abnormalities have also been reported in ovarian GCTs. Genomic imprinting; IGF2/H19 control region Reinforces the maternal-genome/parthenogenetic model and indicates that imprint erasure/re-establishment defects are central to teratoma biology. Cancers 2023 review (pinto2023molecularbiologyof pages 11-12, pinto2023molecularbiologyof pages 3-4, moraru2023immatureteratomadiagnosis pages 13-15)
Chromosomal abnormality: isochromosome 12p / 12p gain Gain of chromosome 12p, including isochromosome 12p, is frequent in malignant germ cell tumors, especially dysgerminomas and yolk-sac tumors, but is less characteristic of immature teratomas and generally absent from mature teratomas with normal karyotype. 12p gain / i(12p) Helps distinguish malignant ovarian GCT molecular pathways from the more parthenogenetic, usually cytogenetically bland pathway of mature teratoma/dermoid cyst. Cancers 2023 review; IJERPH 2023 review (saani2023clinicalchallengesin pages 9-10, pinto2023molecularbiologyof pages 7-9)
Near-diploid genomes with limited somatic mutations Immature teratomas may show near-diploid genomes, extensive allelic imbalance, and relative paucity of somatic mutations; mature teratomas often have normal karyotypes and arise after meiosis. Meiotic nondisjunction; allelic imbalance Indicates that abnormal germ-cell developmental/meiotic processes, rather than classic oncogenic mutation accumulation, drive teratoma formation. Diagnostics 2023; Cancers 2023 (moraru2023immatureteratomadiagnosis pages 2-4, pinto2023molecularbiologyof pages 7-9, moraru2023immatureteratomadiagnosis pages 13-15)
Distinct pathogenetic pathway of immature teratoma Immature teratomas appear to follow a pathogenetic route distinct from dysgerminoma/yolk-sac tumor and from some mature teratomas, with less emphasis on 12p gain and more on meiotic errors and epigenetic dysregulation. Developmental germ-cell pathways Important for biological classification, prognosis, and future risk stratification/targeted research. Diagnostics 2023; IJERPH 2023; Cancers 2023 (moraru2023immatureteratomadiagnosis pages 2-4, saani2023clinicalchallengesin pages 9-10, pinto2023molecularbiologyof pages 7-9)

Table: This table summarizes the main molecular and genetic findings relevant to ovarian dermoid cysts/teratomas, emphasizing recent evidence on BMP15-associated hereditary teratoma and broader germ-cell tumor epigenetics and cytogenetics. It is useful for distinguishing developmental/parthenogenetic mechanisms from malignant germ-cell tumor pathways.

4.1 Causal Genes

BMP15 (Xp11.22; OMIM: 300247; HGNC:1068): A rare germline missense mutation BMP15 C262T (p.Arg88Cys) has been identified as the causative variant for hereditary ovarian immature teratoma with X-linked dominant inheritance. The mutation reduces mature BMP15 protein secretion by 84.7% and activates the H-Ras/MAPK signaling pathway, promoting parthenogenetic activation of oocytes (liu2024araregermline pages 3-4, liu2024araregermline pages 2-3, liu2024araregermline pages 1-2). This represents the first identified causal gene for hereditary ovarian teratoma in humans.

4.2 Pathogenic Variants

  • BMP15 C262T (p.Arg88Cys): Classified as pathogenic in the context of hereditary ovarian immature teratoma. The variant creates a new cysteine residue affecting BMP15 processing and dimerization. It is a rare germline variant with X-linked dominant inheritance, exclusively affecting heterozygous females. Somatic origin is not applicable; this is a germline variant (liu2024araregermline pages 3-4, liu2024araregermline pages 2-3).

4.3 Chromosomal Abnormalities

Mature ovarian teratomas typically have a normal karyotype (pinto2023molecularbiologyof pages 7-9). Gains on chromosome 12p, including isochromosome 12p (i(12p)), are characteristic of malignant germ cell tumors (82% of dysgerminomas, ~44% of all malignant GCTs) but are generally absent from mature teratomas and uncommon in pure immature teratomas (saani2023clinicalchallengesin pages 9-10, pinto2023molecularbiologyof pages 7-9). DNA ploidy analysis shows aneuploidy in 59% and diploidy in 41% of malignant GCT cases (saani2023clinicalchallengesin pages 9-10).

4.4 Epigenetic Information

Distinct DNA methylation patterns characterize different germ cell tumor subtypes: undifferentiated GCTs (germinomas) are hypomethylated, while differentiated tumors including mature teratomas are hypermethylated (pinto2023molecularbiologyof pages 11-12). Ovarian teratomas show abnormal genomic imprinting with reduced methylation at paternally methylated loci and increased methylation at maternally methylated loci, consistent with their parthenogenetic origin. Abnormalities in the IGF2/H19 imprinting control region have been documented in ovarian GCTs (pinto2023molecularbiologyof pages 11-12, pinto2023molecularbiologyof pages 3-4).

5. Environmental Information

No specific environmental toxins, radiation exposures, or occupational factors have been linked to dermoid cyst formation. These are congenital developmental lesions. No infectious agents are implicated in the formation of dermoid cysts, though secondary infection of nasal and craniofacial dermoid sinuses is a common complication (kotowski2023thedifferentialdiagnosis pages 2-5).

6. Mechanism / Pathophysiology

6.1 Molecular Pathways

For ovarian dermoid cysts, the H-Ras/MAPK signaling pathway is a central mechanism in hereditary forms. The BMP15 C262T mutation leads to elevated H-Ras expression (3.2–8.3 fold) and MEK1 expression (3.9–5.8 fold) in mutant oocytes, promoting spontaneous parthenogenetic activation (liu2024araregermline pages 2-3). The mutation disrupts the balance between BMP15 and GDF9 signaling, altering SMAD2/3-MAPK pathway activation and shifting the ratio of heterodimeric signaling complexes (liu2024araregermline pages 6-7, liu2024araregermline pages 7-8). - GO terms: GO:0000187 (activation of MAPK activity), GO:0007049 (cell cycle), GO:0044703 (multi-organism reproductive process)

For craniofacial and cutaneous dermoid cysts, the mechanism involves aberrant midline fusion during embryogenesis with entrapment of ectodermal tissue. This results in formation of epithelial-lined cavities containing keratinaceous material (quan2026pediatricnasaldermoid pages 2-3, wiener2021histologicfeaturesof pages 14-16).

6.2 Cellular Processes

The key cellular process in ovarian dermoid cysts is parthenogenesis: spontaneous activation of oocytes without fertilization, leading to development of a tumor containing elements of all three germ layers. Mature teratomas develop from oocytes after completed meiosis I with failed meiosis II, producing near-diploid genomes with limited somatic mutations and extensive allelic imbalances (moraru2023immatureteratomadiagnosis pages 2-4, pinto2023molecularbiologyof pages 7-9). - GO terms: GO:0009566 (fertilization), GO:0007276 (gamete generation), GO:0051301 (cell division) - CL terms: CL:0000023 (oocyte), CL:0000501 (granulosa cell)

6.3 Tissue Damage Mechanisms

Intracranial dermoid cyst rupture releases lipid-rich contents into the subarachnoid space, causing chemical aseptic meningitis through inflammatory reactions affecting cortical regions and adjacent brain structures (soto2025presentationofa pages 8-10, soto2025presentationofa pages 1-3).

7. Anatomical Structures Affected

7.1 Organ Level

Primary organs: - Ovary (UBERON:0000992) — most common site for mature teratoma - Brain (UBERON:0000955) — intracranial dermoid cysts, representing 0.04–0.6% of brain tumors (soto2025presentationofa pages 1-3) - Nose (UBERON:0000004) — nasal dermoid sinus cysts, most common congenital midline nasal mass (kotowski2023thedifferentialdiagnosis pages 2-5) - Eye/Orbit (UBERON:0004088) — orbital/periorbital and limbal dermoids - Skin (UBERON:0002097) — cutaneous dermoid cysts

Secondary involvement: - Meninges (chemical meningitis from intracranial rupture) - Anterior cranial fossa (intracranial extension of nasal dermoids, ~20% of cases) (kotowski2023thedifferentialdiagnosis pages 2-5) - Spinal cord (spinal dermoid cysts; cutaneous dermoid sinuses may extend to spinal canal) (wiener2021histologicfeaturesof pages 14-16)

7.2 Tissue and Cell Level

Dermoid cysts contain mature ectodermal derivatives: - Keratinizing squamous epithelium (CL:0000237, squamous epithelial cell) - Sebaceous glands (CL:0000317, sebum secreting cell) - Hair follicles - Apocrine glands - Dense collagen stroma arranged concentrically around the cyst wall (wiener2021histologicfeaturesof pages 14-16, wiener2021histologicfeaturesof pages 16-18)

7.3 Localization

Intracranial dermoid cysts are classified by location as: (1) invasive to adjacent structures, (2) intradural, and (3) intracavernous, with suprasellar supratentorial lesions being most common in young adults (soto2025presentationofa pages 1-3). Nasal dermoid cysts are classified as: (1) superficial (Type 1), (2) sinus-tract type, and (3) intracranially extending type (quan2026pediatricnasaldermoid pages 2-3, quan2026pediatricnasaldermoid pages 4-5). Dermoid cysts are typically midline lesions and can be unilateral or bilateral in paired structures (e.g., ovaries).

8. Temporal Development

8.1 Onset

Dermoid cysts are congenital in origin, developing during embryogenesis (quan2026pediatricnasaldermoid pages 2-3, wiener2021histologicfeaturesof pages 14-16). However, clinical presentation varies by site: - Nasal/orbital dermoids: typically present in infancy/childhood - Intracranial dermoids: often diagnosed in young adults (20–30 years) (soto2025presentationofa pages 1-3) - Ovarian dermoid cysts: typically diagnosed in reproductive-age women - Cutaneous dermoids: variable age of recognition

8.2 Progression

Dermoid cysts are generally slow-growing, chronic lesions with a benign course. They do not spontaneously resolve and gradually enlarge over time. Critical complications include: - Ovarian torsion and rupture for ovarian dermoid cysts - Chemical meningitis from rupture of intracranial dermoid cysts (soto2025presentationofa pages 8-10) - Recurrent infections for nasal dermoid sinuses (7% annual infection risk) (kotowski2023thedifferentialdiagnosis pages 2-5) - Malignant transformation of ovarian mature teratomas occurs in approximately 1–2% of cases, typically squamous cell carcinoma

8.3 Recurrence Patterns

Recurrence after surgical excision depends on completeness of resection. For intracranial giant dermoid cysts, subtotal resection can lead to recurrence, as demonstrated by a case requiring two additional surgeries over 10 years, while gross total resection achieved no recurrence after 10 years of follow-up (soto2025presentationofa pages 1-3). For nasal dermoid cysts, recurrence is most commonly due to incomplete excision or involvement of fistulous tracts and cranial base (quan2026pediatricnasaldermoid pages 10-11).

9. Inheritance and Population

9.1 Epidemiology

9.2 Inheritance Pattern

Most dermoid cysts are sporadic and non-hereditary. However, hereditary ovarian immature teratoma has been identified with X-linked dominant inheritance associated with BMP15 C262T mutation, exclusively affecting heterozygous female carriers (liu2024araregermline pages 3-4, liu2024araregermline pages 2-3). The disease may be classified into hereditary and sporadic types (liu2024araregermline pages 8-9).

9.3 Population Demographics

  • Sex ratio: Ovarian dermoid cysts exclusively affect females. Intracranial dermoid cysts show no strong gender preference (soto2025presentationofa pages 6-8). Cutaneous dermoid sinuses affect both sexes.
  • Age distribution: Ovarian — reproductive age; intracranial — young adults (20–30); nasal/orbital — infancy and childhood (soto2025presentationofa pages 1-3, quan2026pediatricnasaldermoid pages 2-3)
  • Geographic/racial distribution: No strong racial predilection for intracranial dermoid cysts. Ovarian GCT histological subtype prevalence varies by race, with higher type 1 ovarian cancer prevalence in Asian populations compared to European/American populations.

10. Diagnostics

10.1 Imaging Studies

10.2 Histopathology

Dermoid cysts are lined by squamous epithelium with prominent keratohyalin granules, containing lamellar keratin, hair fragments, and sebaceous secretions, surrounded by dense collagen with parallel arrangement. Multiple well-differentiated hair follicles, sebaceous glands, and occasional apocrine glands radiate from the cyst wall (wiener2021histologicfeaturesof pages 16-18). Key differentiating features from infundibular cysts include more abundant adnexal structures and concentric collagen arrangement (wiener2021histologicfeaturesof pages 16-18). - SNOMED CT: 128978008 (Dermoid cyst)

10.3 Clinical Criteria

Nasal dermoid cysts are characterized as non-expansile, non-pulsatile, non-compressible masses that do not transilluminate and produce a negative Furstenberg's sign (no enlargement with jugular vein compression or Valsalva maneuver) (kotowski2023thedifferentialdiagnosis pages 2-5). Biopsy is contraindicated for nasal dermoids (deftereou2025congenitalanomaliesof pages 6-6).

10.4 Differential Diagnosis

10.5 Genetic Testing

Genetic testing is not routinely indicated for sporadic dermoid cysts. For suspected hereditary ovarian teratoma, BMP15 mutation analysis may be considered as a potential biomarker for molecular diagnosis and genetic screening in high-risk families (liu2024araregermline pages 8-9, liu2024araregermline pages 7-8).

11. Outcome/Prognosis

11.1 Survival and Mortality

Dermoid cysts are benign lesions with excellent survival rates. Mature ovarian teratomas have an excellent overall survival rate following surgical excision, with fertility preservation possible through conservative surgery (moraru2023immatureteratomadiagnosis pages 2-4). Intracranial dermoid cysts carry minimal mortality risk when completely resected, but subtotal resection risks recurrence (soto2025presentationofa pages 1-3). Immature teratomas also have good prognoses, with excellent overall survival (moraru2023immatureteratomadiagnosis pages 2-4).

11.2 Complications

  • Ovarian: Torsion, rupture (with chemical peritonitis), malignant transformation (~1–2%)
  • Intracranial: Chemical aseptic meningitis from rupture; recurrence after incomplete resection (soto2025presentationofa pages 8-10)
  • Nasal: Recurrent infection (50% by age 4, >90% by age 9 when sinus opening present); potential intracranial complications including meningitis, cerebral abscess (kotowski2023thedifferentialdiagnosis pages 2-5)

11.3 Prognostic Factors

Completeness of surgical excision is the primary prognostic determinant. Gross total resection of intracranial dermoid cysts prevents recurrence (soto2025presentationofa pages 1-3). For nasal dermoid cysts, preoperative imaging to identify intracranial extension and meticulous complete excision reduce recurrence risk (quan2026pediatricnasaldermoid pages 8-9, quan2026pediatricnasaldermoid pages 10-11).

12. Treatment

12.1 Surgical Interventions (MAXO:0000004 — surgical procedure)

Surgery is the definitive treatment for all dermoid cyst subtypes:

Ovarian dermoid cysts: - Fertility-sparing cystectomy or oophorectomy, typically via laparoscopy (MAXO:0001185 — laparoscopic surgery) - Clinical trial NCT02009228 evaluated single-port laparoscopic cystectomy as potentially preferable for managing ovarian dermoid cysts (NCT06816316 chunk 2) - NCT05054946 evaluated the effect of laparoscopic surgery on ovarian reserve according to cyst type

Intracranial dermoid cysts: - Craniotomy (frontal, temporal, frontotemporal, or transcranial approaches) with goal of gross total resection (soto2025presentationofa pages 6-8, soto2025presentationofa pages 8-10) - Microsurgical techniques and advanced visualization (exoscope) are essential for safe resection near neurovascular structures (soto2025presentationofa pages 8-10) - The Reyes-Velez classification system has been proposed to guide surgical planning and predict complications (soto2025presentationofa pages 1-3)

Nasal dermoid sinus cysts: - External rhinoplasty approach for adequate exposure and en bloc removal (quan2026pediatricnasaldermoid pages 8-9) - Endoscopic endonasal techniques for selected cases - Combined intracranial–extracranial approaches for cases with intracranial extension (quan2026pediatricnasaldermoid pages 10-11) - Multidisciplinary team management (otolaryngology, neurosurgery, plastic surgery) is recommended (quan2026pediatricnasaldermoid pages 8-9, quan2026pediatricnasaldermoid pages 10-11)

Orbital dermoid cysts: - Complete excision avoiding rupture - Clinical trial NCT06816316 evaluated the role of 70% ethyl alcohol versus saline for intraoperative cleaning of accidentally opened angular dermoid cysts to prevent recurrence (NCT06816316 chunk 2)

Limbal dermoid cysts: - Observation for small asymptomatic lesions; corneal autograft or lamellar keratoplasty for visually significant lesions - Clinical trial NCT03217461 evaluated corneal autograft for limbal dermoid

12.2 Supportive Care

Long-term follow-up of 1–3 years with imaging surveillance is recommended after nasal dermoid cyst excision (quan2026pediatricnasaldermoid pages 10-11). Perioperative infection control is critical for nasal dermoid sinuses (quan2026pediatricnasaldermoid pages 8-9).

13. Prevention

13.1 Primary Prevention

No primary prevention strategies exist for dermoid cysts, as they are congenital developmental lesions.

13.2 Secondary Prevention (Early Detection)

For nasal dermoid sinus cysts, early surgical excision is recommended to prevent the cumulative infection risk (7% per year) and potential intracranial complications (kotowski2023thedifferentialdiagnosis pages 2-5). Prenatal imaging may detect some ovarian cysts, but prenatal detection of dermoid cysts specifically is uncommon.

13.3 Genetic Counseling

For families with hereditary ovarian teratoma, BMP15 mutation analysis may facilitate identification of at-risk heterozygous female carriers and enable genetic counseling and surveillance (liu2024araregermline pages 8-9, liu2024araregermline pages 7-8).

13.4 Tertiary Prevention

Complete surgical excision is the key strategy for preventing complications and recurrence. Standardized follow-up protocols with imaging reduce the risk of missed recurrence (quan2026pediatricnasaldermoid pages 10-11).

14. Other Species / Natural Disease

14.1 Canine Dermoid Cysts

Dermoid cysts occur naturally in dogs and are more common than in cats. They represent focal reduplications of skin resulting from developmental anomalies and primarily affect young animals under 2 years of age (wiener2021histologicfeaturesof pages 14-16). Breed predisposition exists, particularly in: - Rhodesian Ridgeback — often multiple dorsal midline cysts (dermoid sinuses) - Boxer - Kerry Blue Terrier - English Bulldog - Shih Tzu - Saint Bernard — documented with multiple dermoid sinuses on the head (wiener2021histologicfeaturesof pages 19-19)

Lesions are most commonly located on the dorsal midline but can extend to the spinal canal and dura mater (wiener2021histologicfeaturesof pages 14-16). The VBO identifier for Rhodesian Ridgeback is VBO:0200817.

14.2 Feline Dermoid Cysts

Dermoid cysts in cats are less common than in dogs and are particularly found on the lateral neck or shoulder (wiener2021histologicfeaturesof pages 16-18). Histologically, they are identical to canine dermoid cysts.

14.3 Non-Human Primates

Ovarian teratomas occur naturally in nonhuman primates, with most ovarian tumors reported in baboons (Papio spp.) (wiener2021histologicfeaturesof pages 14-16).

14.4 Mouse Models

A CRISPR/Cas9-engineered Bmp15 R86C knock-in mouse model (C57BL/6 background) has been developed to study hereditary ovarian teratoma. Mice carrying the mutation (equivalent to human BMP15 R88C) show significantly increased spontaneous parthenogenetic activation of oocytes, with one transgenic mouse developing an OIT phenotype by 6 months. The mutation causes ovarian overgrowth (>2-fold larger than wild-type) (liu2024araregermline pages 4-6, liu2024araregermline pages 8-8). This model recapitulates key aspects of the human disease.

15. Model Organisms

15.1 Genetic Models

  • Bmp15 C262T knock-in mouse (C57BL/6): Generated by CRISPR/Cas9 genome editing; demonstrates increased parthenogenetic activation rates and teratoma development. Phenotype recapitulation includes ovarian teratoma formation and ovarian enlargement (liu2024araregermline pages 4-6, liu2024araregermline pages 8-8).
  • Model limitations: Low penetrance of OIT phenotype in mice (only one mouse developed teratoma), species-specific differences in BMP15 signaling, and difficulty obtaining primary oocytes for mechanistic studies (liu2024araregermline pages 7-8).

15.2 Applications

The Bmp15 mutant mouse model enables investigation of: - Parthenogenetic mechanisms of teratoma formation - BMP15/GDF9 signaling balance in oocyte development - Preclinical testing of potential preventive interventions - Validation of genetic biomarkers for screening (liu2024araregermline pages 8-9)

15.3 Canine Natural Models

Rhodesian Ridgeback dermoid sinuses serve as natural models for studying congenital dermoid cyst pathogenesis, with well-documented breed predisposition and dorsal midline localization paralleling human nasal/spinal dermoid sinuses (wiener2021histologicfeaturesof pages 14-16).

Summary

Dermoid cysts are a heterogeneous group of benign developmental lesions arising from ectodermal tissue entrapment during embryogenesis. They occur at diverse anatomical sites including the ovary (as mature cystic teratomas), cranium, nasal midline, orbit, skin, and ocular surface. The molecular understanding of ovarian dermoid cysts has been significantly advanced by the 2024 identification of a causal BMP15 germline mutation causing hereditary ovarian teratoma through enhanced oocyte parthenogenetic activation via H-Ras/MAPK pathway dysregulation (liu2024araregermline pages 3-4, liu2024araregermline pages 2-3). Epigenetic studies reveal distinct DNA methylation patterns in germ cell tumor subtypes, with mature teratomas showing characteristic imprinting abnormalities consistent with their parthenogenetic origin (pinto2023molecularbiologyof pages 11-12). Surgical excision remains the definitive treatment across all anatomical subtypes, with completeness of resection being the primary determinant of recurrence and long-term outcome (soto2025presentationofa pages 1-3, quan2026pediatricnasaldermoid pages 10-11). Nasal dermoid sinuses carry significant childhood infection risk (50% by age 4) warranting early intervention (kotowski2023thedifferentialdiagnosis pages 2-5). Intracranial dermoid cysts, though rare (0.04–0.6% of brain tumors), require careful neurosurgical planning due to potential for chemical meningitis upon rupture (soto2025presentationofa pages 1-3, soto2025presentationofa pages 8-10). Natural models in dogs (particularly Rhodesian Ridgebacks) and the CRISPR-engineered Bmp15 mutant mouse provide valuable platforms for studying dermoid cyst pathogenesis across species (wiener2021histologicfeaturesof pages 14-16, liu2024araregermline pages 8-8).

References

  1. (quan2026pediatricnasaldermoid pages 2-3): Shan Quan, Li He, Jiangqiao Geng, and Juan Wang. Pediatric nasal dermoid sinus cysts: advances in pathogenesis, management strategies, and translational research—a multidisciplinary management perspective. Frontiers in Pediatrics, Jan 2026. URL: https://doi.org/10.3389/fped.2025.1708853, doi:10.3389/fped.2025.1708853. This article has 3 citations.

  2. (wiener2021histologicfeaturesof pages 14-16): Dominique J. Wiener. Histologic features of hair follicle neoplasms and cysts in dogs and cats: a diagnostic guide. Journal of Veterinary Diagnostic Investigation, 33:479-497, Mar 2021. URL: https://doi.org/10.1177/1040638721993565, doi:10.1177/1040638721993565. This article has 44 citations and is from a peer-reviewed journal.

  3. (soto2025presentationofa pages 1-3): Gervith Reyes Soto, Daniel Alejandro Vega Moreno, Carlos Castillo Rangel, Vladmir Nikolenko, Mario Alejandro Fulcar, Neysa Sabrina Vasquez Segura, Tshiunza Mpoyi Chérubin, Mario Antonio Furcal Aybar, Andreina Rosario Rosario, and Manuel De Jesus Encarnacion Ramirez. Presentation of a new imaging classification for giant dermoid cyst. case report and literature review. Unknown journal, Jan 2025. URL: https://doi.org/10.21203/rs.3.rs-5685800/v1, doi:10.21203/rs.3.rs-5685800/v1.

  4. (saani2023clinicalchallengesin pages 9-10): Iqra Saani, Nitish Raj, Raja Sood, Shahbaz Ansari, Haider Abbas Mandviwala, Elisabet Sanchez, and Stergios Boussios. Clinical challenges in the management of malignant ovarian germ cell tumours. International Journal of Environmental Research and Public Health, 20:6089, Jun 2023. URL: https://doi.org/10.3390/ijerph20126089, doi:10.3390/ijerph20126089. This article has 86 citations.

  5. (pinto2023molecularbiologyof pages 1-3): Mariana Tomazini Pinto, Gisele Eiras Martins, Ana Glenda Santarosa Vieira, Janaina Mello Soares Galvão, Cristiano de Pádua Souza, Carla Renata Pacheco Donato Macedo, and Luiz Fernando Lopes. Molecular biology of pediatric and adult ovarian germ cell tumors: a review. Cancers, 15:2990, May 2023. URL: https://doi.org/10.3390/cancers15112990, doi:10.3390/cancers15112990. This article has 22 citations.

  6. (moraru2023immatureteratomadiagnosis pages 2-4): Liviu Moraru, Melinda-Ildiko Mitranovici, Diana Maria Chiorean, Marius Coroș, Raluca Moraru, Ioan Emilian Oală, and Sabin Gligore Turdean. Immature teratoma: diagnosis and management—a review of the literature. Diagnostics, 13:1516, Apr 2023. URL: https://doi.org/10.3390/diagnostics13091516, doi:10.3390/diagnostics13091516. This article has 68 citations.

  7. (NCT06816316 chunk 2): Mohamed Yasser Sayed Saif. Role of Alcohol in Prevention of Recurrence of the Accidentally Opened Angular Dermoid Cyst. Beni-Suef University. 2019. ClinicalTrials.gov Identifier: NCT06816316

  8. (soto2025presentationofa pages 6-8): Gervith Reyes Soto, Daniel Alejandro Vega Moreno, Carlos Castillo Rangel, Vladmir Nikolenko, Mario Alejandro Fulcar, Neysa Sabrina Vasquez Segura, Tshiunza Mpoyi Chérubin, Mario Antonio Furcal Aybar, Andreina Rosario Rosario, and Manuel De Jesus Encarnacion Ramirez. Presentation of a new imaging classification for giant dermoid cyst. case report and literature review. Unknown journal, Jan 2025. URL: https://doi.org/10.21203/rs.3.rs-5685800/v1, doi:10.21203/rs.3.rs-5685800/v1.

  9. (soto2025presentationofa pages 8-10): Gervith Reyes Soto, Daniel Alejandro Vega Moreno, Carlos Castillo Rangel, Vladmir Nikolenko, Mario Alejandro Fulcar, Neysa Sabrina Vasquez Segura, Tshiunza Mpoyi Chérubin, Mario Antonio Furcal Aybar, Andreina Rosario Rosario, and Manuel De Jesus Encarnacion Ramirez. Presentation of a new imaging classification for giant dermoid cyst. case report and literature review. Unknown journal, Jan 2025. URL: https://doi.org/10.21203/rs.3.rs-5685800/v1, doi:10.21203/rs.3.rs-5685800/v1.

  10. (kotowski2023thedifferentialdiagnosis pages 2-5): Michael R. Kotowski. The differential diagnosis of congenital developmental midline nasal masses: histopathological, clinical, and radiological aspects. Diagnostics, 13:2796, Aug 2023. URL: https://doi.org/10.3390/diagnostics13172796, doi:10.3390/diagnostics13172796. This article has 9 citations.

  11. (deftereou2025congenitalanomaliesof pages 6-6): T. Deftereou, V. Karapepera, Stergios Lialiaris, George Fotiadis, Konstantinos Chaidas, and Michail Katotomichelakis. Congenital anomalies of the nose: from embryologic to surgical treatment. Cureus, Aug 2025. URL: https://doi.org/10.7759/cureus.89397, doi:10.7759/cureus.89397. This article has 1 citations.

  12. (quan2026pediatricnasaldermoid pages 4-5): Shan Quan, Li He, Jiangqiao Geng, and Juan Wang. Pediatric nasal dermoid sinus cysts: advances in pathogenesis, management strategies, and translational research—a multidisciplinary management perspective. Frontiers in Pediatrics, Jan 2026. URL: https://doi.org/10.3389/fped.2025.1708853, doi:10.3389/fped.2025.1708853. This article has 3 citations.

  13. (quan2026pediatricnasaldermoid pages 8-9): Shan Quan, Li He, Jiangqiao Geng, and Juan Wang. Pediatric nasal dermoid sinus cysts: advances in pathogenesis, management strategies, and translational research—a multidisciplinary management perspective. Frontiers in Pediatrics, Jan 2026. URL: https://doi.org/10.3389/fped.2025.1708853, doi:10.3389/fped.2025.1708853. This article has 3 citations.

  14. (quan2026pediatricnasaldermoid pages 10-11): Shan Quan, Li He, Jiangqiao Geng, and Juan Wang. Pediatric nasal dermoid sinus cysts: advances in pathogenesis, management strategies, and translational research—a multidisciplinary management perspective. Frontiers in Pediatrics, Jan 2026. URL: https://doi.org/10.3389/fped.2025.1708853, doi:10.3389/fped.2025.1708853. This article has 3 citations.

  15. (wiener2021histologicfeaturesof pages 16-18): Dominique J. Wiener. Histologic features of hair follicle neoplasms and cysts in dogs and cats: a diagnostic guide. Journal of Veterinary Diagnostic Investigation, 33:479-497, Mar 2021. URL: https://doi.org/10.1177/1040638721993565, doi:10.1177/1040638721993565. This article has 44 citations and is from a peer-reviewed journal.

  16. (pinto2023molecularbiologyof pages 7-9): Mariana Tomazini Pinto, Gisele Eiras Martins, Ana Glenda Santarosa Vieira, Janaina Mello Soares Galvão, Cristiano de Pádua Souza, Carla Renata Pacheco Donato Macedo, and Luiz Fernando Lopes. Molecular biology of pediatric and adult ovarian germ cell tumors: a review. Cancers, 15:2990, May 2023. URL: https://doi.org/10.3390/cancers15112990, doi:10.3390/cancers15112990. This article has 22 citations.

  17. (liu2024araregermline pages 3-4): Yakun Liu, Hong-wei Fan, Xi Kang, Yuntao Hao, Na Wang, Hui Zheng, Yan Li, and Shan Kang. A rare germline bmp15 missense mutation causes hereditary ovarian immature teratoma in human. Proceedings of the National Academy of Sciences of the United States of America, Mar 2024. URL: https://doi.org/10.1073/pnas.2310409121, doi:10.1073/pnas.2310409121. This article has 4 citations and is from a highest quality peer-reviewed journal.

  18. (liu2024araregermline pages 2-3): Yakun Liu, Hong-wei Fan, Xi Kang, Yuntao Hao, Na Wang, Hui Zheng, Yan Li, and Shan Kang. A rare germline bmp15 missense mutation causes hereditary ovarian immature teratoma in human. Proceedings of the National Academy of Sciences of the United States of America, Mar 2024. URL: https://doi.org/10.1073/pnas.2310409121, doi:10.1073/pnas.2310409121. This article has 4 citations and is from a highest quality peer-reviewed journal.

  19. (pinto2023molecularbiologyof pages 3-4): Mariana Tomazini Pinto, Gisele Eiras Martins, Ana Glenda Santarosa Vieira, Janaina Mello Soares Galvão, Cristiano de Pádua Souza, Carla Renata Pacheco Donato Macedo, and Luiz Fernando Lopes. Molecular biology of pediatric and adult ovarian germ cell tumors: a review. Cancers, 15:2990, May 2023. URL: https://doi.org/10.3390/cancers15112990, doi:10.3390/cancers15112990. This article has 22 citations.

  20. (liu2024araregermline pages 1-2): Yakun Liu, Hong-wei Fan, Xi Kang, Yuntao Hao, Na Wang, Hui Zheng, Yan Li, and Shan Kang. A rare germline bmp15 missense mutation causes hereditary ovarian immature teratoma in human. Proceedings of the National Academy of Sciences of the United States of America, Mar 2024. URL: https://doi.org/10.1073/pnas.2310409121, doi:10.1073/pnas.2310409121. This article has 4 citations and is from a highest quality peer-reviewed journal.

  21. (liu2024araregermline pages 6-7): Yakun Liu, Hong-wei Fan, Xi Kang, Yuntao Hao, Na Wang, Hui Zheng, Yan Li, and Shan Kang. A rare germline bmp15 missense mutation causes hereditary ovarian immature teratoma in human. Proceedings of the National Academy of Sciences of the United States of America, Mar 2024. URL: https://doi.org/10.1073/pnas.2310409121, doi:10.1073/pnas.2310409121. This article has 4 citations and is from a highest quality peer-reviewed journal.

  22. (liu2024araregermline pages 4-6): Yakun Liu, Hong-wei Fan, Xi Kang, Yuntao Hao, Na Wang, Hui Zheng, Yan Li, and Shan Kang. A rare germline bmp15 missense mutation causes hereditary ovarian immature teratoma in human. Proceedings of the National Academy of Sciences of the United States of America, Mar 2024. URL: https://doi.org/10.1073/pnas.2310409121, doi:10.1073/pnas.2310409121. This article has 4 citations and is from a highest quality peer-reviewed journal.

  23. (liu2024araregermline pages 7-8): Yakun Liu, Hong-wei Fan, Xi Kang, Yuntao Hao, Na Wang, Hui Zheng, Yan Li, and Shan Kang. A rare germline bmp15 missense mutation causes hereditary ovarian immature teratoma in human. Proceedings of the National Academy of Sciences of the United States of America, Mar 2024. URL: https://doi.org/10.1073/pnas.2310409121, doi:10.1073/pnas.2310409121. This article has 4 citations and is from a highest quality peer-reviewed journal.

  24. (pinto2023molecularbiologyof pages 11-12): Mariana Tomazini Pinto, Gisele Eiras Martins, Ana Glenda Santarosa Vieira, Janaina Mello Soares Galvão, Cristiano de Pádua Souza, Carla Renata Pacheco Donato Macedo, and Luiz Fernando Lopes. Molecular biology of pediatric and adult ovarian germ cell tumors: a review. Cancers, 15:2990, May 2023. URL: https://doi.org/10.3390/cancers15112990, doi:10.3390/cancers15112990. This article has 22 citations.

  25. (moraru2023immatureteratomadiagnosis pages 13-15): Liviu Moraru, Melinda-Ildiko Mitranovici, Diana Maria Chiorean, Marius Coroș, Raluca Moraru, Ioan Emilian Oală, and Sabin Gligore Turdean. Immature teratoma: diagnosis and management—a review of the literature. Diagnostics, 13:1516, Apr 2023. URL: https://doi.org/10.3390/diagnostics13091516, doi:10.3390/diagnostics13091516. This article has 68 citations.

  26. (liu2024araregermline pages 8-9): Yakun Liu, Hong-wei Fan, Xi Kang, Yuntao Hao, Na Wang, Hui Zheng, Yan Li, and Shan Kang. A rare germline bmp15 missense mutation causes hereditary ovarian immature teratoma in human. Proceedings of the National Academy of Sciences of the United States of America, Mar 2024. URL: https://doi.org/10.1073/pnas.2310409121, doi:10.1073/pnas.2310409121. This article has 4 citations and is from a highest quality peer-reviewed journal.

  27. (wiener2021histologicfeaturesof pages 19-19): Dominique J. Wiener. Histologic features of hair follicle neoplasms and cysts in dogs and cats: a diagnostic guide. Journal of Veterinary Diagnostic Investigation, 33:479-497, Mar 2021. URL: https://doi.org/10.1177/1040638721993565, doi:10.1177/1040638721993565. This article has 44 citations and is from a peer-reviewed journal.

  28. (liu2024araregermline pages 8-8): Yakun Liu, Hong-wei Fan, Xi Kang, Yuntao Hao, Na Wang, Hui Zheng, Yan Li, and Shan Kang. A rare germline bmp15 missense mutation causes hereditary ovarian immature teratoma in human. Proceedings of the National Academy of Sciences of the United States of America, Mar 2024. URL: https://doi.org/10.1073/pnas.2310409121, doi:10.1073/pnas.2310409121. This article has 4 citations and is from a highest quality peer-reviewed journal.

Artifacts