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Matches in Nanopublications for { ?s ?p "[Manipulating the expression of mutant or wild-type PIK3CA or DUSP1 confirmed that this mechanism is responsible for the induction of apoptosis and the inhibition of tumour proliferation in vitro and in vivo, to sensitise cells to AKT target therapy.Conclusion or interpretation:PIK3CA mutations confer sensitivity to AKT target therapy in BLCA by regulating DUSP1 expression and subsequent ERK1/2 dephosphorylation and can potentially serve as a stratifying biomarker for treatment.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine."@en ?g. }

• NP231832.RAcA2zFIvsCIu_NNeQ75G1Z-5-kmnx1bkL69Kyjwcgl7w130_assertion description "[Manipulating the expression of mutant or wild-type PIK3CA or DUSP1 confirmed that this mechanism is responsible for the induction of apoptosis and the inhibition of tumour proliferation in vitro and in vivo, to sensitise cells to AKT target therapy.Conclusion or interpretation:PIK3CA mutations confer sensitivity to AKT target therapy in BLCA by regulating DUSP1 expression and subsequent ERK1/2 dephosphorylation and can potentially serve as a stratifying biomarker for treatment.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP231832.RAcA2zFIvsCIu_NNeQ75G1Z-5-kmnx1bkL69Kyjwcgl7w130_provenance.
• NP232658.RApbE_NKpEGdUg-yY-05lSZI4IPhSXxqzvg6IfPUALfTI130_assertion description "[Manipulating the expression of mutant or wild-type PIK3CA or DUSP1 confirmed that this mechanism is responsible for the induction of apoptosis and the inhibition of tumour proliferation in vitro and in vivo, to sensitise cells to AKT target therapy.Conclusion or interpretation:PIK3CA mutations confer sensitivity to AKT target therapy in BLCA by regulating DUSP1 expression and subsequent ERK1/2 dephosphorylation and can potentially serve as a stratifying biomarker for treatment.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP232658.RApbE_NKpEGdUg-yY-05lSZI4IPhSXxqzvg6IfPUALfTI130_provenance.
• NP1233092.RAvJasnLtA9ZspUgySvYYyXQSB9_dTPHb8eXUxMBf0YYs130_assertion description "[Manipulating the expression of mutant or wild-type PIK3CA or DUSP1 confirmed that this mechanism is responsible for the induction of apoptosis and the inhibition of tumour proliferation in vitro and in vivo, to sensitise cells to AKT target therapy.Conclusion or interpretation:PIK3CA mutations confer sensitivity to AKT target therapy in BLCA by regulating DUSP1 expression and subsequent ERK1/2 dephosphorylation and can potentially serve as a stratifying biomarker for treatment.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP1233092.RAvJasnLtA9ZspUgySvYYyXQSB9_dTPHb8eXUxMBf0YYs130_provenance.
• NP621809.RAwH13spEkGFEU-IVq96421CSV5XAYAU_UkeRIo1e2iFk130_assertion description "[Manipulating the expression of mutant or wild-type PIK3CA or DUSP1 confirmed that this mechanism is responsible for the induction of apoptosis and the inhibition of tumour proliferation in vitro and in vivo, to sensitise cells to AKT target therapy.Conclusion or interpretation:PIK3CA mutations confer sensitivity to AKT target therapy in BLCA by regulating DUSP1 expression and subsequent ERK1/2 dephosphorylation and can potentially serve as a stratifying biomarker for treatment.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP621809.RAwH13spEkGFEU-IVq96421CSV5XAYAU_UkeRIo1e2iFk130_provenance.
• NP620740.RAKUEq3QKVDL4U-hGvyYIucmcfVvkiZP7g6a0-Is1WrS0130_assertion description "[Manipulating the expression of mutant or wild-type PIK3CA or DUSP1 confirmed that this mechanism is responsible for the induction of apoptosis and the inhibition of tumour proliferation in vitro and in vivo, to sensitise cells to AKT target therapy.Conclusion or interpretation:PIK3CA mutations confer sensitivity to AKT target therapy in BLCA by regulating DUSP1 expression and subsequent ERK1/2 dephosphorylation and can potentially serve as a stratifying biomarker for treatment.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP620740.RAKUEq3QKVDL4U-hGvyYIucmcfVvkiZP7g6a0-Is1WrS0130_provenance.
• NP1233086.RA7OgnmJ2H2aaYDMooqn6QdtwXsBEiF7X-ZS6Zu_mvID0130_assertion description "[Manipulating the expression of mutant or wild-type PIK3CA or DUSP1 confirmed that this mechanism is responsible for the induction of apoptosis and the inhibition of tumour proliferation in vitro and in vivo, to sensitise cells to AKT target therapy.Conclusion or interpretation:PIK3CA mutations confer sensitivity to AKT target therapy in BLCA by regulating DUSP1 expression and subsequent ERK1/2 dephosphorylation and can potentially serve as a stratifying biomarker for treatment.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP1233086.RA7OgnmJ2H2aaYDMooqn6QdtwXsBEiF7X-ZS6Zu_mvID0130_provenance.
• NP1233087.RAw8YfzGGzKAow3m8CT-LQkZsHi5XrP-KDOIMhKM_dvpc130_assertion description "[Manipulating the expression of mutant or wild-type PIK3CA or DUSP1 confirmed that this mechanism is responsible for the induction of apoptosis and the inhibition of tumour proliferation in vitro and in vivo, to sensitise cells to AKT target therapy.Conclusion or interpretation:PIK3CA mutations confer sensitivity to AKT target therapy in BLCA by regulating DUSP1 expression and subsequent ERK1/2 dephosphorylation and can potentially serve as a stratifying biomarker for treatment.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP1233087.RAw8YfzGGzKAow3m8CT-LQkZsHi5XrP-KDOIMhKM_dvpc130_provenance.
• NP1233089.RAxl6UmBj-y3OqSjTRxEkDyYJVRsbo8bR62hWsXG70OVc130_assertion description "[Manipulating the expression of mutant or wild-type PIK3CA or DUSP1 confirmed that this mechanism is responsible for the induction of apoptosis and the inhibition of tumour proliferation in vitro and in vivo, to sensitise cells to AKT target therapy.Conclusion or interpretation:PIK3CA mutations confer sensitivity to AKT target therapy in BLCA by regulating DUSP1 expression and subsequent ERK1/2 dephosphorylation and can potentially serve as a stratifying biomarker for treatment.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP1233089.RAxl6UmBj-y3OqSjTRxEkDyYJVRsbo8bR62hWsXG70OVc130_provenance.