Modeling tumorigenesis in Drosophila: Current Advances and Future Perspectives

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F13%3A10195048" target="_blank" >RIV/00216208:11110/13:10195048 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.5772/55686" target="_blank" >http://dx.doi.org/10.5772/55686</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.5772/55686" target="_blank" >10.5772/55686</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Modeling tumorigenesis in Drosophila: Current Advances and Future Perspectives

Popis výsledku v původním jazyce

Cancer is essentially considered as a genetic disease caused by the accumulation of multiple genetic or epigenetic lesions in tumor-suppressor genes and oncogenes [1]. Although the notion that retinoblastoma could be an inherited disease was already formulated at the end of the 19th Century a solid genetic basis was established with the discovery of both proto-oncogenes, whose gain-of function mutations or altered expression is associated with the cancerous state, and tumor suppressor genes (TSGs), whose inactivation releases the "brakes" inhibiting cell proliferation. Analysis of both proto-oncogenes and TSGs revealed also that cancer results from an alteration of the normal pathway of cell fate and differentiation. The hallmarks of cancer, as laid down by Hanahan and Weinberg to explain the complex biology of cancer, comprise six major developmental changes taking successively place in human tumors. These cancer "characteristics" include sustained proliferative signaling, evasion of

Název v anglickém jazyce

Modeling tumorigenesis in Drosophila: Current Advances and Future Perspectives

Popis výsledku anglicky

Cancer is essentially considered as a genetic disease caused by the accumulation of multiple genetic or epigenetic lesions in tumor-suppressor genes and oncogenes [1]. Although the notion that retinoblastoma could be an inherited disease was already formulated at the end of the 19th Century a solid genetic basis was established with the discovery of both proto-oncogenes, whose gain-of function mutations or altered expression is associated with the cancerous state, and tumor suppressor genes (TSGs), whose inactivation releases the "brakes" inhibiting cell proliferation. Analysis of both proto-oncogenes and TSGs revealed also that cancer results from an alteration of the normal pathway of cell fate and differentiation. The hallmarks of cancer, as laid down by Hanahan and Weinberg to explain the complex biology of cancer, comprise six major developmental changes taking successively place in human tumors. These cancer "characteristics" include sustained proliferative signaling, evasion of

Druh

C - Kapitola v odborné knize

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

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Projekt

<a href="/cs/project/GAP302%2F11%2F1640" target="_blank" >GAP302/11/1640: Morfologické znaky a molekulární determinanty apokrinní sekrece</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2013

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název knihy nebo sborníku

Future Aspects of Tumor Suppressor Gene

ISBN

978-953-51-1063-7

Počet stran výsledku

29

Strana od-do

98-127

Počet stran knihy

221

Název nakladatele

InTech

Místo vydání

Rijeka, Croatia

Kód UT WoS kapitoly

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