eISSN: 1509-572x
ISSN: 1641-4640
Folia Neuropathologica
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1/2015
vol. 53
 
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abstract:

Erk activation as a possible mechanism of transformation of subependymal nodule into subependymal giant cell astrocytoma

Monika Siedlecka
,
Stanislaw Szlufik
,
Wieslawa Grajkowska
,
Marcin Roszkowski
,
Jarosław Jóźwiak

Folia Neuropathol 2015; 53 (1): 8-14
Online publish date: 2015/03/24
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Introduction: Subependymal nodule (SEN) and subependymal giant cell astrocytoma (SEGA) are brain lesions frequently found in tuberous sclerosis (TS). As about 10-15% of SENs enlarge and transform into SEGAs, we examined here the possible mechanism of the phenomenon.

Material and methods: Using Western blot we studied 1 SEN and 3 SEGA samples; SEN and 1 SEGA came from the same TS patient. We evaluated e.g. the activation of the phosphorylated forms of proteins belonging to Akt, Erk and mTOR pathways.

Results: Differences in Erk pathway activation between SEN and SEGA were found. There was no upregulation of p-Erk, p-Mek or p-RSK1 in the SEN specimen, whilst we found these proteins to be significantly uptriggered in SEGA samples. Also, for the first time, we found p-Akt, p-GSK3 and p-PDK1 upregulated in both SEN and SEGA from the same TS patient.

Conclusions: Our current study shows for the first time the possible mechanism of SEN/SEGA transformation, where Erk pathway hyperactivation seems to be significant. We hypothesize that SEN/SEGA transformation may depend on Erk potentiation.
keywords:

subependymal giant cell astrocytoma, subependymal nodule, Erk, tuberous sclerosis

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