Complex analysis of the p53 tumor suppressor in lung carcinoma
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00209775%3A_____%2F16%3AN0000021" target="_blank" >RIV/00209775:_____/16:N0000021 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/00216224:14310/16:00089204 RIV/65269705:_____/16:00064344
Výsledek na webu
<a href="https://www.spandidos-publications.com/or/35/3" target="_blank" >https://www.spandidos-publications.com/or/35/3</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.3892/or.2015.4533" target="_blank" >10.3892/or.2015.4533</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Complex analysis of the p53 tumor suppressor in lung carcinoma
Popis výsledku v původním jazyce
Lung cancer is the leading cause of cancer-related deaths worldwide. The p53 tumor suppressor is a transcription factor controlling expression of its target genes in response to various stress stimuli. Mutations of the TP53 gene occur very frequently in lung carcinomas and they play an important role in both oncogenic transformation of lung epithelial cells and lung carcinoma progression. We determined the TP53 status in 42 samples of squamous cell lung carcinoma (SQCC) and 56 samples of lung adenocarcinoma (AC) by the functional analysis FASAY and its variant called split assay. Altogether, we detected 64 TP53 mutations in 63 patients and analyzed them by cDNA and gDNA sequencing. The TP53 mutations were found in 76.2% (32/42) of SQCC cases, and 55.4% (31/56) of ACs. Immunoblotting revealed the p53 protein accumulation in 18 samples (42.9%) among SQCC cases and 19 samples (33.9%) among AC cases. Using fluorescence in situ hybridization we detected loss of the TP53-specific 17p13.3 locus in 23 from 41 analyzed SQCC samples (56.1%) and in 20 from 54 analyzed AC samples (37.0%). We did not find any statistically significant differences in overall and disease-free survival in relation to TP53 status.
Název v anglickém jazyce
Complex analysis of the p53 tumor suppressor in lung carcinoma
Popis výsledku anglicky
Lung cancer is the leading cause of cancer-related deaths worldwide. The p53 tumor suppressor is a transcription factor controlling expression of its target genes in response to various stress stimuli. Mutations of the TP53 gene occur very frequently in lung carcinomas and they play an important role in both oncogenic transformation of lung epithelial cells and lung carcinoma progression. We determined the TP53 status in 42 samples of squamous cell lung carcinoma (SQCC) and 56 samples of lung adenocarcinoma (AC) by the functional analysis FASAY and its variant called split assay. Altogether, we detected 64 TP53 mutations in 63 patients and analyzed them by cDNA and gDNA sequencing. The TP53 mutations were found in 76.2% (32/42) of SQCC cases, and 55.4% (31/56) of ACs. Immunoblotting revealed the p53 protein accumulation in 18 samples (42.9%) among SQCC cases and 19 samples (33.9%) among AC cases. Using fluorescence in situ hybridization we detected loss of the TP53-specific 17p13.3 locus in 23 from 41 analyzed SQCC samples (56.1%) and in 20 from 54 analyzed AC samples (37.0%). We did not find any statistically significant differences in overall and disease-free survival in relation to TP53 status.
Klasifikace
Druh
J<sub>x</sub> - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)
CEP obor
FD - Onkologie a hematologie
OECD FORD obor
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Návaznosti výsledku
Projekt
<a href="/cs/project/NT13784" target="_blank" >NT13784: Komplexní analýza mutantů p53 u lymfoproliferativních onemocnění</a><br>
Návaznosti
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Ostatní
Rok uplatnění
2016
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Oncology reports
ISSN
1021-335X
e-ISSN
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Svazek periodika
35
Číslo periodika v rámci svazku
3
Stát vydavatele periodika
GR - Řecká republika
Počet stran výsledku
9
Strana od-do
1859-1867
Kód UT WoS článku
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EID výsledku v databázi Scopus
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