Germ cell tumor pathophysiology: Difference between revisions

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*The [[pathophysiology]] of [[germ cell tumors]] is different based on the [[classification]] of [[germ cell tumors]]
*The [[pathophysiology]] of [[germ cell tumors]] is different based on the [[classification]] of [[germ cell tumors]]
*Each of the distinct entities of [[germ cell tumor]] has a different [[pathogenesis]]
*Each of the distinct entities of [[germ cell tumor]] has a different [[pathogenesis]]
*[[Germ cell tumors]] are [[classified]] as;
 
**[[Gonadal]]
 
***[[Seminoma]]
== '''Dysgerminoma''' ==
***[[Dysgerminoma]]
The [[pathophysiology]] of [[ovarian]] [[germ cell]] [[tumors]] depends on the [[histological]] subtype. Their common origin is believed to be from the [[primordial germ cells]] that [[Transformation|transformed]] [[Pathology|pathologically]] in different stages of development. It is difficult to distinguish subtypes of ovarian germ cell tumor on gross [[pathology]] alone. The majority of [[ovarian]] [[germ cell]] [[tumors]] have a [[solid]] and [[cystic]]<nowiki/>appearance with areas of [[hemorrhage]] and [[necrosis]]. On microscopic [[pathology]], [[ovarian]] [[germ cell]] [[tumors]] may be characterized by a uniform “fried egg” appearance ([[dysgerminoma]]), presence of Schiller-Duval bodies ([[yolk sac tumor]]), presence of embryonic-like neural, [[gastrointestinal]], and/or cartilaginous tissue ([[teratoma]]), or mixed histopathological features (embryonal cell carcinoma).
***[[Germinoma]]
<br />
** Extragonadal
***[[Embryonic]]
**** Mature/Immature teratoma
*** Extraembryonic
**** Chorionic carcinoma/Yolk sac tumor <br />


== '''Testicular Seminoma''' ==
== '''Testicular Seminoma''' ==
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**
**


== '''Dysgerminoma''' ==
The [[pathophysiology]] of [[ovarian]] [[germ cell]] [[tumors]] depends on the [[histological]] subtype. Their common origin is believed to be from the [[primordial germ cells]] that [[Transformation|transformed]] [[Pathology|pathologically]] in different stages of development. It is difficult to distinguish subtypes of ovarian germ cell tumor on gross [[pathology]] alone. The majority of [[ovarian]] [[germ cell]] [[tumors]] have a [[solid]] and [[cystic]]<nowiki/>appearance with areas of [[hemorrhage]] and [[necrosis]]. On microscopic [[pathology]], [[ovarian]] [[germ cell]] [[tumors]] may be characterized by a uniform “fried egg” appearance ([[dysgerminoma]]), presence of Schiller-Duval bodies ([[yolk sac tumor]]), presence of embryonic-like neural, [[gastrointestinal]], and/or cartilaginous tissue ([[teratoma]]), or mixed histopathological features (embryonal cell carcinoma).
<br />
== '''Germinoma''' ==
== '''Germinoma''' ==
On microscopic histopathological analysis, uniform cells that resemble [[primordial germ cells]], consisting of large, round cells with vesicular nuclei and clear or finely granular cytoplasm that is eosinophilic are characteristic findings of germinoma. Genes involved in the pathogenesis of germinoma include gains of 1p, 8p, and 12q and losses of 13q and 18q, duplication of the short arm of chromosome 12, loss of 1p and 6q, alterations in sex chromosomes in children, alterations of the ''p14'' gene, mutations of the ''c-kit'' gene, aberrations of ''CCND2'' (12P13), and ''RB1'', and gain-of-function mutations of ''KIT''. The progression to germinoma usually involves the mutations of the ''KIT/RAS'' signalling or ''AKT1''/mtor pathways and cyclin/''CDK-RB-E2F'' pathway if ''CCND2''(12P13) and ''RB1'' genes are aberrated<br />
On microscopic histopathological analysis, uniform cells that resemble [[primordial germ cells]], consisting of large, round cells with vesicular nuclei and clear or finely granular cytoplasm that is eosinophilic are characteristic findings of germinoma. Genes involved in the pathogenesis of germinoma include gains of 1p, 8p, and 12q and losses of 13q and 18q, duplication of the short arm of chromosome 12, loss of 1p and 6q, alterations in sex chromosomes in children, alterations of the ''p14'' gene, mutations of the ''c-kit'' gene, aberrations of ''CCND2'' (12P13), and ''RB1'', and gain-of-function mutations of ''KIT''. The progression to germinoma usually involves the mutations of the ''KIT/RAS'' signalling or ''AKT1''/mtor pathways and cyclin/''CDK-RB-E2F'' pathway if ''CCND2''(12P13) and ''RB1'' genes are aberrated<br />

Revision as of 16:45, 13 August 2019


Dysgerminoma

The pathophysiology of ovarian germ cell tumors depends on the histological subtype. Their common origin is believed to be from the primordial germ cells that transformed pathologically in different stages of development. It is difficult to distinguish subtypes of ovarian germ cell tumor on gross pathology alone. The majority of ovarian germ cell tumors have a solid and cysticappearance with areas of hemorrhage and necrosis. On microscopic pathology, ovarian germ cell tumors may be characterized by a uniform “fried egg” appearance (dysgerminoma), presence of Schiller-Duval bodies (yolk sac tumor), presence of embryonic-like neural, gastrointestinal, and/or cartilaginous tissue (teratoma), or mixed histopathological features (embryonal cell carcinoma).

Testicular Seminoma

Germinoma

On microscopic histopathological analysis, uniform cells that resemble primordial germ cells, consisting of large, round cells with vesicular nuclei and clear or finely granular cytoplasm that is eosinophilic are characteristic findings of germinoma. Genes involved in the pathogenesis of germinoma include gains of 1p, 8p, and 12q and losses of 13q and 18q, duplication of the short arm of chromosome 12, loss of 1p and 6q, alterations in sex chromosomes in children, alterations of the p14 gene, mutations of the c-kit gene, aberrations of CCND2 (12P13), and RB1, and gain-of-function mutations of KIT. The progression to germinoma usually involves the mutations of the KIT/RAS signalling or AKT1/mtor pathways and cyclin/CDK-RB-E2F pathway if CCND2(12P13) and RB1 genes are aberrated

Infantile testis teratomas

Yolk sac tumors

References