Teratoma pathophysiology: Difference between revisions
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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 | |||
. Many genetic factors are reported to be involved in pathogenesis of teratomas, mature and immature tumors. | |||
Maternal imprinting of the following genes ''are likely involved in development of teratomas:'' | |||
* , insulin like growth factor 2 (IGF II) and its receptor RNA (H-19) | |||
* small nuclear riboprotein (SNRPN) | |||
* ''mas'' proto-oncogene | |||
* tumor suppressor genes ''WT1'' | |||
* | |||
''Microsatellite instability is also reported to be involved in pathogenesis of teratomas; however, further evaluation is required to fully understand the underlying mechanism.'' | |||
''For some tumors like'' sacrococcygeal teratomas, no etiology has been evident yet. Familial predilection is a potential cause for some ovarian derived teratomas. | |||
There have been studies proposing a role of diets high in polyunsaturated fat as a predisposing factor for the growth of teratomas. | |||
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. | |||
==References== | ==References== | ||
Revision as of 02:53, 16 September 2019
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
The exact pathogenesis of [disease name] is not fully understood.
OR
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].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
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
. Many genetic factors are reported to be involved in pathogenesis of teratomas, mature and immature tumors.
Maternal imprinting of the following genes are likely involved in development of teratomas:
- , insulin like growth factor 2 (IGF II) and its receptor RNA (H-19)
- small nuclear riboprotein (SNRPN)
- mas proto-oncogene
- tumor suppressor genes WT1
Microsatellite instability is also reported to be involved in pathogenesis of teratomas; however, further evaluation is required to fully understand the underlying mechanism.
For some tumors like sacrococcygeal teratomas, no etiology has been evident yet. Familial predilection is a potential cause for some ovarian derived teratomas.
There have been studies proposing a role of diets high in polyunsaturated fat as a predisposing factor for the growth of teratomas.
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.