Presentation is loading. Please wait.

Presentation is loading. Please wait.

Model of ATM-MPG–mediated therapeutic resistance in pGBM.

Published byAmadeu Filipe Modified over 5 years ago

Similar presentations

Presentation on theme: "Model of ATM-MPG–mediated therapeutic resistance in pGBM."— Presentation transcript:

1 Model of ATM-MPG–mediated therapeutic resistance in pGBM.
Model of ATM-MPG–mediated therapeutic resistance in pGBM. A, Western blot analysis demonstrating MPG knockdown by retroviral shRNA transduction and ATM knockdown by siRNA at 72 hours. Control cells were transduced with shRNA control retrovirus and treated with siRNA scramble controls. B, control or double MPG and ATM knockdown astrocytes were treated with 100 μmol/L temozolomide (TMZ) and assessed for viability at 72 hours. ns, nonsignificance. C, control or double MPG and ATM knockdown astrocytes were targeted by siRNA for DNA damage response genes redundant to either ATM or MPG and treated with 100 μmol/L temozolomide and assessed for viability at 72 hours. All experiments were performed in triplicate with the SEM reported. D, summary model of targeting the BER and ATM pathways for sensitization to alkylating agents. MA, methoxyamine. Sameer Agnihotri et al. Cancer Discovery 2014;4: ©2014 by American Association for Cancer Research

Download ppt "Model of ATM-MPG–mediated therapeutic resistance in pGBM."

Similar presentations

Metabolic reprogramming results in chemosensitivity in IDH1 mutant cells. Metabolic reprogramming results in chemosensitivity in IDH1 mutant cells. A,

Metabolic reprogramming results in chemosensitivity in IDH1 mutant cells. Metabolic reprogramming results in chemosensitivity in IDH1 mutant cells. A,
Enhanced DNA damage in IDH1 mutant glioma cells.

Enhanced DNA damage in IDH1 mutant glioma cells.
Targeting the PARP DNA repair pathway enhanced cytotoxicity induced by chemotherapy. Targeting the PARP DNA repair pathway enhanced cytotoxicity induced.

Targeting the PARP DNA repair pathway enhanced cytotoxicity induced by chemotherapy. Targeting the PARP DNA repair pathway enhanced cytotoxicity induced.
IDH1 mutant glioma cells are sensitive to TMZ

IDH1 mutant glioma cells are sensitive to TMZ
Effects of BRG1 depletion in the proliferation of lung cancer cells with amplification at the MYC family of genes and in MAX-deficient cells, after reconstitution.

Effects of BRG1 depletion in the proliferation of lung cancer cells with amplification at the MYC family of genes and in MAX-deficient cells, after reconstitution.
SCLCs and LCNECs are sensitive to PARP inhibition in vitro.

SCLCs and LCNECs are sensitive to PARP inhibition in vitro.
ETV1 positively regulates KIT expression through direct binding to KIT enhancers in human GIST cells and forms a positive feedback circuit in GIST oncogenesis.

ETV1 positively regulates KIT expression through direct binding to KIT enhancers in human GIST cells and forms a positive feedback circuit in GIST oncogenesis.
CDK4 is required for the hormone-independent growth of ER+ breast cancer cells. CDK4 is required for the hormone-independent growth of ER+ breast cancer.

CDK4 is required for the hormone-independent growth of ER+ breast cancer cells. CDK4 is required for the hormone-independent growth of ER+ breast cancer.
PKCK2 determines TRAIL sensitivity.

PKCK2 determines TRAIL sensitivity.
Volume 10, Issue 4, Pages (October 2006)

Volume 10, Issue 4, Pages (October 2006)
Recombinant OPCML protein effect in vitro.

Recombinant OPCML protein effect in vitro.
Combined inhibition of MAP kinase and KIT signaling destabilizes ETV1 protein and results in enhanced growth suppression of human GIST cells. Combined.

Combined inhibition of MAP kinase and KIT signaling destabilizes ETV1 protein and results in enhanced growth suppression of human GIST cells. Combined.
Proline supplementation during P5CS protein knockdown suppressed GCN2 activation. Proline supplementation during P5CS protein knockdown suppressed GCN2.

Proline supplementation during P5CS protein knockdown suppressed GCN2 activation. Proline supplementation during P5CS protein knockdown suppressed GCN2.
Bortezomib sensitivity correlates with basal NF-κB activity in KP lung adenocarcinoma cell lines. Bortezomib sensitivity correlates with basal NF-κB activity.

Bortezomib sensitivity correlates with basal NF-κB activity in KP lung adenocarcinoma cell lines. Bortezomib sensitivity correlates with basal NF-κB activity.
CHK1 downregulation upon ERG overexpression.

CHK1 downregulation upon ERG overexpression.
Caspase-1 from myeloid cells induces tumor proliferation via MyD88 oncogenic signaling. Caspase-1 from myeloid cells induces tumor proliferation via MyD88.

Caspase-1 from myeloid cells induces tumor proliferation via MyD88 oncogenic signaling. Caspase-1 from myeloid cells induces tumor proliferation via MyD88.
A20 inhibits caspase-8 cleavage and TRAIL-induced apoptosis.

A20 inhibits caspase-8 cleavage and TRAIL-induced apoptosis.
BIRC6 confers resistance against cisplatin and oxaliplatin.

BIRC6 confers resistance against cisplatin and oxaliplatin.
A genome-wide RNAi pooled screen identifies NF1 as a key determinant of RAF inhibitor sensitivity in melanoma cells. A genome-wide RNAi pooled screen identifies.

A genome-wide RNAi pooled screen identifies NF1 as a key determinant of RAF inhibitor sensitivity in melanoma cells. A genome-wide RNAi pooled screen identifies.
MPG is a substrate of ATM, and phosphorylation of MPG is essential for function. MPG is a substrate of ATM, and phosphorylation of MPG is essential for.

MPG is a substrate of ATM, and phosphorylation of MPG is essential for function. MPG is a substrate of ATM, and phosphorylation of MPG is essential for.

Similar presentations

Ads by Google