The origin of ovarian teratomas.

Parrington, J. M.; West, L. F.; Povey, Sue

doi:10.1136/jmg.21.1.4

Cited by 86 publications

(47 citation statements)

References 21 publications

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“…They are considered to stem from parthenotes, which develop from aberrant activated oocytes in the absence of fertilization (Edson et al, 2009, Parrington et al, 1984. Search for genetic defects facilitating the formation of teratomas in humans is impeded by the exceedingly rare frequency of familial teratomas (Nezhat et al, 2010).…”

Section: Abstract: Teratoma Ovary Stat1 Folliculogenesismentioning

confidence: 99%

MMTV-neu mice deficient in STAT1 are susceptible to develop ovarian teratomas

Hannesdóttir

Daschil²,

Philipp³

et al. 2012

Int. J. Dev. Biol.

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Signal transducer and activator of transcription 1 (STAT1) serves in the protection of the organism against pathogens and other harmful insults. It is implicated in innate immune response, immunosurveillance, tumor-suppression, and the response to genotoxic as well as oxidative stress. We report here that 9 of 140 examined STAT1 deficient mouse mammary tumor virus-neu (MMTV-neu) mice developed differentiated ovarian teratomas, which histologically resemble benign dermatoid cysts. Conventional karyotyping revealed diploidy without structural rearrangements of the chromosomes. STAT1 proficient MMTV-neu mice with the same genetic background (FVB/N), and STAT1 deficient C57BL/6 mice failed to develop this type of tumor. This indicates that STAT1 deficiency promotes teratoma formation and this depends on MMTV-neu expression and/or the genetic background. Since ovarian teratomas are considered to develop as a consequence of alterations in the maturation of oocytes and follicular cells, we compared the ovaries from non-tumor bearing STAT1 deficient and proficient MMTV-neu mice. No detectable alterations in the number and proportion of the different follicular developmental stages were detected, implying the absence of non-redundant functions of STAT1 in normal folliculogenesis, as well as in follicular atresia. However, strong staining for STAT1 was detectable in granulosa and theca cells. These results point to a role for STAT1 in protecting from teratoma formation in a later step of tumorigenesis, e.g. by inducing apoptosis and eliminating premature or aberrantly formed follicles which have the potential to transform into teratomas. KEY WORDS: teratoma, ovary, STAT1, folliculogenesisBenign cystic teratomas belong to the most common ovarian tumors developing in women of the reproductive age. They are considered to stem from parthenotes, which develop from aberrant activated oocytes in the absence of fertilization (Edson et al., 2009, Parrington et al., 1984. Search for genetic defects facilitating the formation of teratomas in humans is impeded by the exceedingly rare frequency of familial teratomas (Nezhat et al., 2010). In mice, spontaneous development of teratomas is rare and only a few reports have documented a link between the expression of a particular gene and teratoma formation. One of these genes encodes the serine kinase c-mos, which is required for meiosis II arrest in activated non fertilized oocytes. Due to failure to arrest, mos deficient mice exhibit a high frequency of parthenotes (Colledge et al., 1994, Hirao andEppig, 1997), and a small percentage of these parthenotes are Abbreviations used in this paper: hGC, human chorionic gonadotropin; MMTV, mouse mammary tumor virus; STAT, signal transducer and activator of transcription. postulated to transform into teratomas. Bcl-2 represents a second gene linked to teratoma formation. There, its inhibin-alpha directed over-expression in granulosa cells of the ovary (Hsu et al., 1996), but not its expression in oocytes (Morita et al., 1999), induces ...

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Section: Abstract: Teratoma Ovary Stat1 Folliculogenesismentioning

confidence: 99%

MMTV-neu mice deficient in STAT1 are susceptible to develop ovarian teratomas

Hannesdóttir

Daschil²,

Philipp³

et al. 2012

Int. J. Dev. Biol.

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“…Multiple uniparental chromosomes occur in human tumors. Interestingly, such genotypes are mainly associated with abnormal embryonal development, as seen in ovarian teratomas or trophoblastic diseases (15,17,18). Therefore, it seems that HCRs may be the genetic basis for nonseminoma morphology transition.…”

Section: Resultsmentioning

confidence: 99%

“…Cell fusion or abnormal fertilization is believed to lead to clonal proliferation in human diseases with a similar phenotype to nonseminomas (e.g., ovarian teratomas and trophoblastic diseases; refs. [15][16][17][18]. In both cases, uniparental chromosomes are frequently generated by recombination of two or more sets of chromosomes from haploid cells of a same parental origin (15,17,18).…”

Section: Resultsmentioning

confidence: 99%

Association between Large-scale Genomic Homozygosity without Chromosomal Loss and Nonseminomatous Germ Cell Tumor Development

Lu¹,

Yang²,

Noël³

et al. 2005

Cancer Research

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The genotype of a tumor determines its biology and clinical behavior. The genetic alterations associated with the unique embryonal morphology of nonseminomatous subtypes of testicular germ cell tumors remain to be established. Using single nucleotide polymorphism microarray analysis, we found in all of the 15 nonseminomas analyzed, large-scale chromosomal homozygosities, most of which were not associated with relative chromosome loss. This unusual genotype, distinguishing nonseminoma from seminomas and other human tumors, may be associated with the special embryonal development morphologic transition of this malignancy. Based on these genetic data, we hypothesized a new potential origin of nonseminomas through sperm fusion. Nonrandom involvement of certain chromosomes also suggests that genes on these chromosome regions may play an important role in nonseminoma development. (Cancer Res 2005; 65(20): 9137-41)

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“…Instead, heterozygous centromeric markers and other chromosomal heteromorphisms were reported in a subset of tumors. 3,[9][10][11][12] In most previous studies, however, the teratomas were grown in culture prior to genetic analysis; the disadvantage of this approach consists of the potential selection of only a subgroup of teratoma cells, whereas other tumor compartmentsin particular those with slow growth and high degree of differentiation-may escape analytical characterization.…”

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confidence: 99%