About: The combined status of ATM and p53 link tumor development with therapeutic response

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An Entity of Type : http://linked.opendata.cz/ontology/domain/vavai/Vysledek, within Data Space : linked.opendata.cz associated with source document(s)

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rdf:type	skos:Concept http://linked.opendata.cz/ontology/domain/vavai/Vysledek
Description	While the contribution of specific tumor suppressor networks to cancer development has been the subject of considerable recent study, it remains unclear how alterations in these networks are integrated to influence the response of tumors to anti-cancer treatments. Here, we show that mechanisms commonly used by tumors to bypass early neoplastic checkpoints ultimately determine chemotherapeutic response and generate tumor-specific vulnerabilities that can be exploited with targeted therapies. Specifically, evaluation of the combined status of ATM and p53, two commonly mutated tumor suppressor genes, can help to predict the clinical response to genotoxic chemotherapies. We show that in p53-deficient settings, suppression of ATM dramatically sensitizes tumors to DNA-damaging chemotherapy, whereas, conversely, in the presence of functional p53, suppression of ATM or its downstream target Chk2 actually protects tumors from being killed by genotoxic agents. Furthermore, ATM-deficient cancer cells display str While the contribution of specific tumor suppressor networks to cancer development has been the subject of considerable recent study, it remains unclear how alterations in these networks are integrated to influence the response of tumors to anti-cancer treatments. Here, we show that mechanisms commonly used by tumors to bypass early neoplastic checkpoints ultimately determine chemotherapeutic response and generate tumor-specific vulnerabilities that can be exploited with targeted therapies. Specifically, evaluation of the combined status of ATM and p53, two commonly mutated tumor suppressor genes, can help to predict the clinical response to genotoxic chemotherapies. We show that in p53-deficient settings, suppression of ATM dramatically sensitizes tumors to DNA-damaging chemotherapy, whereas, conversely, in the presence of functional p53, suppression of ATM or its downstream target Chk2 actually protects tumors from being killed by genotoxic agents. Furthermore, ATM-deficient cancer cells display str (en)
Title	The combined status of ATM and p53 link tumor development with therapeutic response The combined status of ATM and p53 link tumor development with therapeutic response (en)
skos:prefLabel	The combined status of ATM and p53 link tumor development with therapeutic response The combined status of ATM and p53 link tumor development with therapeutic response (en)
skos:notation	RIV/61989592:15110/09:00009729!RIV10-MSM-15110___
http://linked.open...avai/riv/aktivita	Z
http://linked.open...avai/riv/aktivity	Z(MSM6198959216)
http://linked.open...iv/cisloPeriodika	16
http://linked.open...vai/riv/dodaniDat	2010
http://linked.open...aciTvurceVysledku	Bártek, Jiří
http://linked.open.../riv/druhVysledku	J - Článek v odborném periodiku
http://linked.open...iv/duvernostUdaju	S - Úplné a pravdivé údaje nepodléhající ochraně podle zvláštních právních předpisů
http://linked.open...titaPredkladatele	Univerzita Palackého v Olomouci / Lékařská fakulta
http://linked.open...dnocenehoVysledku	307550
http://linked.open...ai/riv/idVysledku	RIV/61989592:15110/09:00009729
http://linked.open...riv/jazykVysledku	eng - angličtina
http://linked.open.../riv/klicovaSlova	Cancer; ATM; p53; DNA-PK; chemotherapy; mouse models (en)
http://linked.open.../riv/klicoveSlovo	Cancer p53 ATM chemotherapy mouse models DNA-PK
http://linked.open...odStatuVydavatele	US - Spojené státy americké
http://linked.open...ontrolniKodProRIV	[7E5E55E24F34]
http://linked.open...i/riv/nazevZdroje	Genes & development
http://linked.open...in/vavai/riv/obor	EB
http://linked.open...ichTvurcuVysledku	1 (xsd:int)
http://linked.open...cetTvurcuVysledku	9 (xsd:int)
http://linked.open...UplatneniVysledku	2009
http://linked.open...v/svazekPeriodika	23
http://linked.open...iv/tvurceVysledku	Bártek, Jiří Blomqvist, Carl Nevanlinna, Heli Bartková, Jiřina Jiang, Hai Tommiska, Johanna Hemann, Michael T. Reinhardt, H. Christian Yaffe, Michael B.
http://linked.open...n/vavai/riv/zamer	Modulation of signalling and regulatory pathways in normal and cancer cells
issn	1549-5477
number of pages	5 (xsd:int)
http://localhost/t...ganizacniJednotka	15110

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