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| {{CMG}}; {{AE}} {{G.D.}} | | {{CMG}}; {{AE}} {{G.D.}} |
| ==Overview== | | ==Overview== |
| The exact pathogenesis of [disease name] is not fully understood. | | The exact pathogenesis of teratoma may be understood by the pathology migration of primodial germ cells from the yolk sac to primitive gonads. |
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| It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
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| [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
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| Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
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| [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
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| The progression to [disease name] usually involves the [molecular pathway].
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| The pathophysiology of [disease/malignancy] depends on the histological subtype. | | The pathophysiology of [disease/malignancy] depends on the histological subtype. |
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| ==Pathophysiology== | | ==Pathophysiology== |
| There have been several theories about the causes of teratoma. Mounting evidence suggests most are due to abnormal differentiation of fetal germ cells that arise from the fetal yolk sac.<ref name="urlMedscape Log In">{{cite web |url=https://reference.medscape.com/medline/abstract/15017564 |title=Medscape Log In |format= |work= |accessdate=}}</ref>
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| Many genetic factors are reported to be involved in pathogenesis of teratomas, mature and immature tumors.
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| Maternal imprinting of the following genes ''are likely involved in development of teratomas:''<ref name="urlMedscape Log In">{{cite web |url=https://reference.medscape.com/medline/abstract/17080332 |title=Medscape Log In |format= |work= |accessdate=}}</ref>
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| * , insulin like growth factor 2 (IGF II) and its receptor RNA (H-19)
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| * small nuclear riboprotein (SNRPN)
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| * ''mas'' proto-oncogene
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| * tumor suppressor genes ''WT1''
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| ''Microsatellite instability is also reported to be involved in pathogenesis of teratomas; however, further evaluation is required to fully understand the underlying mechanism.''
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| ''For some tumors like'' sacrococcygeal teratomas, no etiology has been evident yet. Familial predilection is a potential cause for some ovarian derived teratomas.
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| There have been studies proposing a role of diets high in polyunsaturated fat as a predisposing factor for the growth of teratomas.
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| Disorders of sex development (DSDs) have also been associated with development of germ cell tumors. Gonadoblastoma, a type of teratoma, is frequently seen in Turner syndrome. Klinefelter syndrome is associated with development of extragonadal malignant germ cell tumors.<ref name="urlMedscape Log In">{{cite web |url=https://reference.medscape.com/medline/abstract/12632341 |title=Medscape Log In |format= |work= |accessdate=}}</ref>
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| ==References== | | ==References== |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Gertrude Djouka, M.D.[2]
Overview
The exact pathogenesis of teratoma may be understood by the pathology migration of primodial germ cells from the yolk sac to primitive gonads.
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
References
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