(Q41174750)

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Effects of topoisomerase inhibitors that induce DNA damage response on glucose metabolism and PI3K/Akt/mTOR signaling in multiple myeloma cells.

scientific article published on 15 April 2015

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scholarly article

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19 February 2020

Effects of topoisomerase inhibitors that induce DNA damage response on glucose metabolism and PI3K/Akt/mTOR signaling in multiple myeloma cells (English)

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19 February 2020

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Christof Seidl

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19 February 2020

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Markus Essler

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19 February 2020

Benedikt Feuerecker

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Benedikt Feuerecker

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19 February 2020

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Hans-Richard Demel

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19 February 2020

Guido Piontek

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19 February 2020

Birgit Blechert

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19 February 2020

Anja Pickhard

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19 February 2020

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15 April 2015

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19 February 2020

American Journal of Cancer Research

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19 February 2020

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19 February 2020

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19 February 2020

1649-1664

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19 February 2020

Concurrent inhibition of PI3K and mTORC1/mTORC2 overcomes resistance to rapamycin induced apoptosis by down-regulation of Mcl-1 in mantle cell lymphoma

1 reference

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Modulation of DNA repair by pharmacological inhibitors of the PIKK protein kinase family

1 reference

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3D tumour spheroids as a model to assess the suitability of [18F]FDG-PET as an early indicator of response to PI3K inhibition

1 reference

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Akt: a double-edged sword in cell proliferation and genome stability

1 reference

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Optimal induction of myeloma cell death requires dual blockade of phosphoinositide 3-kinase and mTOR signalling and is determined by translocation subtype

1 reference

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The dual PI3K/mTOR inhibitor NVP-BEZ235 is a potent inhibitor of ATM- and DNA-PKCs-mediated DNA damage responses

1 reference

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Up-regulation of hexokinaseII in myeloma cells: targeting myeloma cells with 3-bromopyruvate

1 reference

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ATP-dependent chromatin remodeling in the DNA-damage response.

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Glycolysis inhibition inactivates ABC transporters to restore drug sensitivity in malignant cells

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The DNA Damage Response: Making It Safe to Play with Knives

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DNA damage-induced modulation of GLUT3 expression is mediated through p53-independent extracellular signal-regulated kinase signaling in HeLa cells

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Glucose deprivation contributes to the development of KRAS pathway mutations in tumor cells

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

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Antimyeloma activity of the orally bioavailable dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor NVP-BEZ235.

1 reference

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Assessing tumor response to therapy

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RAD50, an SMC family member with multiple roles in DNA break repair: how does ATP affect function?

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The novel orally bioavailable inhibitor of phosphoinositol-3-kinase and mammalian target of rapamycin, NVP-BEZ235, inhibits growth and proliferation in multiple myeloma

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Glucose metabolism inhibits apoptosis in neurons and cancer cells by redox inactivation of cytochrome c.

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PKBalpha/Akt1 acts downstream of DNA-PK in the DNA double-strand break response and promotes survival

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Glycolysis inhibition for anticancer treatment

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DNA damage-triggered apoptosis: critical role of DNA repair, double-strand breaks, cell proliferation and signaling

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DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation

1 reference

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Genotoxic exposure is associated with alterations in glucose uptake and metabolism.

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19 February 2020

1 reference

Europe PubMed Central

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19 February 2020

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