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''':<ref name="LimOliva2018">{{cite journal|last1=Lim|first1=Diana|last2=Oliva|first2=Esther|title=Ovarian sex cord-stromal tumours: an update in recent molecular advances|journal=Pathology|volume=50|issue=2|year=2018|pages=178–189|issn=00313025|doi=10.1016/j.pathol.2017.10.008}}</ref><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><ref name="LiBao2018">{{cite journal|last1=Li|first1=Jiaheng|last2=Bao|first2=Riqiang|last3=Peng|first3=Shiwei|last4=Zhang|first4=Chunping|title=The molecular mechanism of ovarian granulosa cell tumors|journal=Journal of Ovarian Research|volume=11|issue=1|year=2018|issn=1757-2215|doi=10.1186/s13048-018-0384-1}}</ref><ref name="pmid29409506">{{cite journal |vauthors=Li J, Bao R, Peng S, Zhang C |title=The molecular mechanism of ovarian granulosa cell tumors |journal=J Ovarian Res |volume=11 |issue=1 |pages=13 |date=February 2018 |pmid=29409506 |pmc=5802052 |doi=10.1186/s13048-018-0384-1 |url=}}</ref><ref name="pmid27858560">{{cite journal |vauthors=Schultz KA, Harris AK, Schneider DT, Young RH, Brown J, Gershenson DM, Dehner LP, Hill DA, Messinger YH, Frazier AL |title=Ovarian Sex Cord-Stromal Tumors |journal=J Oncol Pract |volume=12 |issue=10 |pages=940–946 |date=October 2016 |pmid=27858560 |pmc=5063189 |doi=10.1200/JOP.2016.016261 |url=}}</ref><ref name="BoussiosMoschetta2017">{{cite journal|last1=Boussios|first1=Stergios|last2=Moschetta|first2=Michele|last3=Zarkavelis|first3=George|last4=Papadaki|first4=Alexandra|last5=Kefas|first5=Aristides|last6=Tatsi|first6=Konstantina|title=Ovarian sex-cord stromal tumours and small cell tumours: Pathological, genetic and management aspects|journal=Critical Reviews in Oncology/Hematology|volume=120|year=2017|pages=43–51|issn=10408428|doi=10.1016/j.critrevonc.2017.10.007}}</ref> | '''FOXL2''':<ref name="LimOliva2018">{{cite journal|last1=Lim|first1=Diana|last2=Oliva|first2=Esther|title=Ovarian sex cord-stromal tumours: an update in recent molecular advances|journal=Pathology|volume=50|issue=2|year=2018|pages=178–189|issn=00313025|doi=10.1016/j.pathol.2017.10.008}}</ref><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><ref name="LiBao2018">{{cite journal|last1=Li|first1=Jiaheng|last2=Bao|first2=Riqiang|last3=Peng|first3=Shiwei|last4=Zhang|first4=Chunping|title=The molecular mechanism of ovarian granulosa cell tumors|journal=Journal of Ovarian Research|volume=11|issue=1|year=2018|issn=1757-2215|doi=10.1186/s13048-018-0384-1}}</ref><ref name="pmid29409506">{{cite journal |vauthors=Li J, Bao R, Peng S, Zhang C |title=The molecular mechanism of ovarian granulosa cell tumors |journal=J Ovarian Res |volume=11 |issue=1 |pages=13 |date=February 2018 |pmid=29409506 |pmc=5802052 |doi=10.1186/s13048-018-0384-1 |url=}}</ref><ref name="pmid27858560">{{cite journal |vauthors=Schultz KA, Harris AK, Schneider DT, Young RH, Brown J, Gershenson DM, Dehner LP, Hill DA, Messinger YH, Frazier AL |title=Ovarian Sex Cord-Stromal Tumors |journal=J Oncol Pract |volume=12 |issue=10 |pages=940–946 |date=October 2016 |pmid=27858560 |pmc=5063189 |doi=10.1200/JOP.2016.016261 |url=}}</ref><ref name="BoussiosMoschetta2017">{{cite journal|last1=Boussios|first1=Stergios|last2=Moschetta|first2=Michele|last3=Zarkavelis|first3=George|last4=Papadaki|first4=Alexandra|last5=Kefas|first5=Aristides|last6=Tatsi|first6=Konstantina|title=Ovarian sex-cord stromal tumours and small cell tumours: Pathological, genetic and management aspects|journal=Critical Reviews in Oncology/Hematology|volume=120|year=2017|pages=43–51|issn=10408428|doi=10.1016/j.critrevonc.2017.10.007}}</ref><ref name="LeungFuller2016">{{cite journal|last1=Leung|first1=Dilys T.H.|last2=Fuller|first2=Peter J.|last3=Chu|first3=Simon|title=Impact of FOXL2 mutations on signaling in ovarian granulosa cell tumors|journal=The International Journal of Biochemistry & Cell Biology|volume=72|year=2016|pages=51–54|issn=13572725|doi=10.1016/j.biocel.2016.01.003}}</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 17:00, 10 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 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 crucial role in ovarian development
- It regulates the ovarian granulosa cell proliferation, follicle development and ovarian hormones synthesis
- Almost all like 97% of 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 making it a pathognomonic feature.
- The phosphorylation modification of FOXL2 in particular is responsible to the growth of 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
- ↑ Lim, Diana; Oliva, Esther (2018). "Ovarian sex cord-stromal tumours: an update in recent molecular advances". Pathology. 50 (2): 178–189. doi:10.1016/j.pathol.2017.10.008. ISSN 0031-3025.
- ↑ 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.
- ↑ Li, Jiaheng; Bao, Riqiang; Peng, Shiwei; Zhang, Chunping (2018). "The molecular mechanism of ovarian granulosa cell tumors". Journal of Ovarian Research. 11 (1). doi:10.1186/s13048-018-0384-1. ISSN 1757-2215.
- ↑ Li J, Bao R, Peng S, Zhang C (February 2018). "The molecular mechanism of ovarian granulosa cell tumors". J Ovarian Res. 11 (1): 13. doi:10.1186/s13048-018-0384-1. PMC 5802052. PMID 29409506.
- ↑ Schultz KA, Harris AK, Schneider DT, Young RH, Brown J, Gershenson DM, Dehner LP, Hill DA, Messinger YH, Frazier AL (October 2016). "Ovarian Sex Cord-Stromal Tumors". J Oncol Pract. 12 (10): 940–946. doi:10.1200/JOP.2016.016261. PMC 5063189. PMID 27858560.
- ↑ Boussios, Stergios; Moschetta, Michele; Zarkavelis, George; Papadaki, Alexandra; Kefas, Aristides; Tatsi, Konstantina (2017). "Ovarian sex-cord stromal tumours and small cell tumours: Pathological, genetic and management aspects". Critical Reviews in Oncology/Hematology. 120: 43–51. doi:10.1016/j.critrevonc.2017.10.007. ISSN 1040-8428.
- ↑ Leung, Dilys T.H.; Fuller, Peter J.; Chu, Simon (2016). "Impact of FOXL2 mutations on signaling in ovarian granulosa cell tumors". The International Journal of Biochemistry & Cell Biology. 72: 51–54. doi:10.1016/j.biocel.2016.01.003. ISSN 1357-2725.