Sexcord/ stromal ovarian tumors pathophysiology: Difference between revisions
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*The recent advancing analyses have made us understand the pathophysiology of some of these tumor subtypes | *The recent advancing analyses have made us understand the pathophysiology of some of these tumor subtypes | ||
*Mutations mainly involving DICER1, STK11, and FOXL2 influence the development of some of these neoplasms | *Mutations mainly involving DICER1, STK11, and FOXL2 influence the development of some of these neoplasms | ||
'''FOXL2''': | '''FOXL2'''<ref name="pmid27813081">{{cite journal |vauthors=Fuller PJ, Leung D, Chu S |title=Genetics and genomics of ovarian sex cord-stromal tumors |journal=Clin. Genet. |volume=91 |issue=2 |pages=285–291 |date=February 2017 |pmid=27813081 |doi=10.1111/cge.12917 |url=}}</ref>: | ||
*FOXL2 is a tumor suppressor gene | *FOXL2 is a tumor suppressor gene | ||
*It is a member of the forkhead box (FOX) family of evolutionarily conserved transcription factors | *It is a member of the forkhead box (FOX) family of evolutionarily conserved transcription factors | ||
Revision as of 18:11, 8 March 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
Physiology
The normal physiology of [name of process] can be understood as follows:
Pathogenesis
- The exact pathogenesis of [disease name] is not completely understood.
OR
- It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
Genetics
- The recent advancing analyses have made us understand the pathophysiology of some of these tumor subtypes
- Mutations mainly involving DICER1, STK11, and FOXL2 influence the development of some of these neoplasms
FOXL2[1]:
- FOXL2 is a tumor suppressor gene
- It is a member of the forkhead box (FOX) family of evolutionarily conserved transcription factors
- It plays a fundamental and essential role in ovarian development
- Almost all adult granulosa cell tumors are characterized by missense somatic point mutations (402 C→G) in FOXL2 gene
- Infact this mutation is a sensitive and specific biomarker for adult granulosa cell tumors
- Importantly this mutation alter's antiproliferative pathways and also limit the apoptosis, as a result contributing to the pathogenesis of adult granulosa cell tumors
Associated Conditions
Conditions associated with [disease name] include:
- [Condition 1]
- [Condition 2]
- [Condition 3]
Gross Pathology
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ Fuller PJ, Leung D, Chu S (February 2017). "Genetics and genomics of ovarian sex cord-stromal tumors". Clin. Genet. 91 (2): 285–291. doi:10.1111/cge.12917. PMID 27813081.