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Pulsed focused ultrasound alters the proteomic profile of the tumor microenvironment in a syngeneic mouse model of glioblastoma

Journal of neuro-oncology, 2024-08

2024

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MGMT function determines the differential response of ATR inhibitors with DNA-damaging agents in glioma stem cells for GBM therapy

Neuro-oncology advances, 2024-01, Vol.6 (1), p.vdad165-vdad165

2024

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Neuronal differentiation drives the antitumor activity of mitogen-activated protein kinase kinase (MEK) inhibition in glioblastoma

Neuro-oncology advances, 2023-01, Vol.5 (1), p.vdad132-vdad132

2023

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CNSC-12. NEURONAL DIFFERENTIATION DRIVES THE ANTI-TUMOR EFFICACY OF MEK INHIBITION IN GLIOBLASTOMA

Neuro-oncology (Charlottesville, Va.), 2022-11, Vol.24 (Supplement_7), p.vii24-vii24

2022

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DDDR-13. MGMT FUNCTION DETERMINES THE DIFFERENTIAL RESPONSE OF ATR AND PARP INHIBITORS WITH DNA DAMAGING AGENTS FOR GBM THERAPY

Neuro-oncology (Charlottesville, Va.), 2022-11, Vol.24 (Supplement_7), p.vii101-vii101

2022

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EGFR suppresses p53 function by promoting p53 binding to DNA-PKcs: a noncanonical regulatory axis between EGFR and wild-type p53 in glioblastoma

Neuro-oncology (Charlottesville, Va.), 2022-10, Vol.24 (10), p.1712-1725

2022

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EXTH-06. ATR INHIBITORS AS MONOTHERAPY AND COMBINATORIAL THERAPY WITH TEMOZOLOMIDE IN PRECLINICAL GLIOBLASTOMA MODELS

Neuro-oncology (Charlottesville, Va.), 2021-11, Vol.23 (Supplement_6), p.vi164-vi164

2021

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DDRE-33. PRECLINICAL THERAPEUTIC EFFICACY OF THE NOVEL BLOOD BRAIN BARRIER PENETRANT ATR INHIBITOR LR02 IN GLIOBLASTOMA

Neuro-oncology (Charlottesville, Va.), 2021-11, Vol.23 (Supplement_6), p.vi81-vi81

2021

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PARP-mediated PARylation of MGMT is critical to promote repair of temozolomide-induced O6-methylguanine DNA damage in glioblastoma

Neuro-oncology (Charlottesville, Va.), 2021-01, Vol.23 (6), p.920-931

2021

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Integrated analysis of telomerase enzymatic activity unravels an association with cancer stemness and proliferation

Nature communications, 2021-01, Vol.12 (1), p.139-11, Article 139

2021

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The promise of DNA damage response inhibitors for the treatment of glioblastoma

Neuro-oncology advances, 2021-01, Vol.3 (1), p.vdab015

2021

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DDRE-05. DECREASED EXPRESSION OF DNA DAMAGE RESPONSE PATHWAYS CORRELATES WITH SYNERGISTIC ACTIVITY OF TEMOZOLOMIDE WITH ATR INHIBITORS IN GLIOBLASTOMA

Neuro-oncology (Charlottesville, Va.), 2020-11, Vol.22 (Supplement_2), p.ii62-ii62

2020

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EGFR Amplification Induces Increased DNA Damage Response and Renders Selective Sensitivity to Talazoparib (PARP Inhibitor) in Glioblastoma

Clinical cancer research, 2020-03, Vol.26 (6), p.1395-1407

2020

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CBMT-32. EGFR SUPPRESSES p53 FUNCTION THROUGH DNA-PKcs BINDING TO p53: NOVEL CROSSTALK BETWEEN EGFR AND TP53 IN GLIOBLASTOMA

Neuro-oncology (Charlottesville, Va.), 2019-11, Vol.21 (Supplement_6), p.vi40-vi40

2019

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DRES-02. PARYLATION OF MGMT BY PARP IS REQUIRED FOR MGMT MEDIATED TEMOZOLOMIDE-INDUCED O6-METHYLGUANINE REPAIR: A NOVEL MECHANISM OF MGMT ACTION

Neuro-oncology (Charlottesville, Va.), 2019-11, Vol.21 (Supplement_6), p.vi71-vi72

2019

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Tie2-FGFR1 Interaction Induces Adaptive PI3K Inhibitor Resistance by Upregulating Aurora A/PLK1/CDK1 Signaling in Glioblastoma

Cancer research (Chicago, Ill.), 2019-10, Vol.79 (19), p.5088-5101

2019

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EGFR amplification predicted selective sensitivity to PARP inhibitors with high PARP-DNA trapping potential in human GBM

Journal of clinical oncology, 2019-05, Vol.37 (15_suppl), p.2047-2047

2019

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Buparlisib in Patients With Recurrent Glioblastoma Harboring Phosphatidylinositol 3-Kinase Pathway Activation: An Open-Label, Multicenter, Multi-Arm, Phase II Trial

Journal of clinical oncology, 2019-03, Vol.37 (9), p.741-750

2019

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Wild-type TP53 defined gamma-secretase inhibitor sensitivity and synergistic activity with doxorubicin in GSCs

American journal of cancer research, 2019-01, Vol.9 (8), p.1734-1745

2019

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BRCA1 identified as a modulator of temozolomide resistance in P53 wild-type GBM using a high-throughput shRNA-based synthetic lethality screening

American journal of cancer research, 2019-01, Vol.9 (11), p.2428-2441

2019

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EXTH-11. GLIOBLASTOMA STEM CELL GROWTH DEPENDENCE ON NUTRIENTS: MORE THAN BASAL METABOLIC ACTIVITIES

Neuro-oncology (Charlottesville, Va.), 2018-11, Vol.20 (suppl_6), p.vi87-vi87

2018

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DDIS-03. EGFR AMPLIFICATION INDUCED INCREASED DNA DAMAGE RESPONSE AND PREDICTED SELECTIVE SENSITIVITY TO TALAZOPARIB (PARP INHIBITOR) IN GLIOBLASTOMA STEM-LIKE CELLS

Neuro-oncology (Charlottesville, Va.), 2018-11, Vol.20 (suppl_6), p.vi69-vi69

2018

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Abstract 4032: Pharmacogenomic analysis of acquired resistance can reveal effective drug combination in glioblastoma

Cancer research (Chicago, Ill.), 2018-07, Vol.78 (13_Supplement), p.4032-4032

2018

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Activation of WEE1 confers resistance to PI3K inhibition in glioblastoma

Neuro-oncology (Charlottesville, Va.), 2018-01, Vol.20 (1), p.78-91

2018

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DRES-02. FGFR1 DRIVES RESISTANCE TO PI3K INHIBITORS VIA UP-REGULATION OF AURORA A/PLK1/CDK1 AXIS IN GLIOBLASTOMA

Neuro-oncology (Charlottesville, Va.), 2017-11, Vol.19 (suppl_6), p.vi64-vi64

2017

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Pulsed focused ultrasound alters the proteomic profile of the tumor microenvironment in a syngeneic mouse model of glioblastoma

MGMT function determines the differential response of ATR inhibitors with DNA-damaging agents in glioma stem cells for GBM therapy

Neuronal differentiation drives the antitumor activity of mitogen-activated protein kinase kinase (MEK) inhibition in glioblastoma

CNSC-12. NEURONAL DIFFERENTIATION DRIVES THE ANTI-TUMOR EFFICACY OF MEK INHIBITION IN GLIOBLASTOMA

DDDR-13. MGMT FUNCTION DETERMINES THE DIFFERENTIAL RESPONSE OF ATR AND PARP INHIBITORS WITH DNA DAMAGING AGENTS FOR GBM THERAPY

EGFR suppresses p53 function by promoting p53 binding to DNA-PKcs: a noncanonical regulatory axis between EGFR and wild-type p53 in glioblastoma

EXTH-06. ATR INHIBITORS AS MONOTHERAPY AND COMBINATORIAL THERAPY WITH TEMOZOLOMIDE IN PRECLINICAL GLIOBLASTOMA MODELS

DDRE-33. PRECLINICAL THERAPEUTIC EFFICACY OF THE NOVEL BLOOD BRAIN BARRIER PENETRANT ATR INHIBITOR LR02 IN GLIOBLASTOMA

PARP-mediated PARylation of MGMT is critical to promote repair of temozolomide-induced O6-methylguanine DNA damage in glioblastoma

Integrated analysis of telomerase enzymatic activity unravels an association with cancer stemness and proliferation

The promise of DNA damage response inhibitors for the treatment of glioblastoma

DDRE-05. DECREASED EXPRESSION OF DNA DAMAGE RESPONSE PATHWAYS CORRELATES WITH SYNERGISTIC ACTIVITY OF TEMOZOLOMIDE WITH ATR INHIBITORS IN GLIOBLASTOMA

EGFR Amplification Induces Increased DNA Damage Response and Renders Selective Sensitivity to Talazoparib (PARP Inhibitor) in Glioblastoma

CBMT-32. EGFR SUPPRESSES p53 FUNCTION THROUGH DNA-PKcs BINDING TO p53: NOVEL CROSSTALK BETWEEN EGFR AND TP53 IN GLIOBLASTOMA

DRES-02. PARYLATION OF MGMT BY PARP IS REQUIRED FOR MGMT MEDIATED TEMOZOLOMIDE-INDUCED O6-METHYLGUANINE REPAIR: A NOVEL MECHANISM OF MGMT ACTION

Tie2-FGFR1 Interaction Induces Adaptive PI3K Inhibitor Resistance by Upregulating Aurora A/PLK1/CDK1 Signaling in Glioblastoma

EGFR amplification predicted selective sensitivity to PARP inhibitors with high PARP-DNA trapping potential in human GBM

Buparlisib in Patients With Recurrent Glioblastoma Harboring Phosphatidylinositol 3-Kinase Pathway Activation: An Open-Label, Multicenter, Multi-Arm, Phase II Trial

Wild-type TP53 defined gamma-secretase inhibitor sensitivity and synergistic activity with doxorubicin in GSCs

BRCA1 identified as a modulator of temozolomide resistance in P53 wild-type GBM using a high-throughput shRNA-based synthetic lethality screening

EXTH-11. GLIOBLASTOMA STEM CELL GROWTH DEPENDENCE ON NUTRIENTS: MORE THAN BASAL METABOLIC ACTIVITIES

DDIS-03. EGFR AMPLIFICATION INDUCED INCREASED DNA DAMAGE RESPONSE AND PREDICTED SELECTIVE SENSITIVITY TO TALAZOPARIB (PARP INHIBITOR) IN GLIOBLASTOMA STEM-LIKE CELLS

Abstract 4032: Pharmacogenomic analysis of acquired resistance can reveal effective drug combination in glioblastoma

Activation of WEE1 confers resistance to PI3K inhibition in glioblastoma

DRES-02. FGFR1 DRIVES RESISTANCE TO PI3K INHIBITORS VIA UP-REGULATION OF AURORA A/PLK1/CDK1 AXIS IN GLIOBLASTOMA

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