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The RasGAP Gene, RASAL2, Is a Tumor and Metastasis Suppressor

Cancer cell, 2013-09, Vol.24 (3), p.365-378

2013

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Exploiting Cancer Cell Vulnerabilities to Develop a Combination Therapy for Ras-Driven Tumors

Cancer cell, 2011-09, Vol.20 (3), p.400-413

2011

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Identification of therapeutic sensitivities in a spheroid drug combination screen of Neurofibromatosis Type I associated High Grade Gliomas

PloS one, 2023-02, Vol.18 (2), p.e0277305-e0277305

2023

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Single cell spatial analysis reveals the topology of immunomodulatory purinergic signaling in glioblastoma

Nature communications, 2022-08, Vol.13 (1), p.4814-4814, Article 4814

2022

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Atypical neurofibromas in neurofibromatosis type 1 are premalignant tumors

Genes chromosomes & cancer, 2011-12, Vol.50 (12), p.1021-1032

2011

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Targeting Refractory Sarcomas and Malignant Peripheral Nerve Sheath Tumors in a Phase I/II Study of Sirolimus in Combination with Ganetespib (SARC023)

Sarcoma, 2020, Vol.2020, p.5784876-8

2020

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A Collaborative Model for Accelerating the Discovery and Translation of Cancer Therapies

Cancer research (Chicago, Ill.), 2017-11, Vol.77 (21), p.5706-5711

2017

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Molecular pathogenesis of multiple gastrointestinal stromal tumors in NF1 patients

Human molecular genetics, 2006-03, Vol.15 (6), p.1015-1023

2006

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The Activation of the WNT Signaling Pathway Is a Hallmark in Neurofibromatosis Type 1 Tumorigenesis

Clinical cancer research, 2014-01, Vol.20 (2), p.358-371

2014

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Imaging Mass Spectrometry Reveals Tumor Metabolic Heterogeneity

iScience, 2020-08, Vol.23 (8), p.101355-101355, Article 101355

2020

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P588: Identification of NF1-associated tumor mutations in plasma cfDNA and its clinical application

Genetics in Medicine Open, 2023, Vol.1 (1), p.100635, Article 100635

2023

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Conservation of hotspots for recombination in low-copy repeats associated with the NF1 microdeletion

Nature genetics, 2006-12, Vol.38 (12), p.1419-1423

2006

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Intestinal Neurofibromatosis Is a Subtype of Familial GIST and Results From a Dominant Activating Mutation in PDGFRA

Gastroenterology (New York, N.Y. 1943), 2006-12, Vol.131 (6), p.1907-1912

2006

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EXTH-29. INTERNEURONS THAT BITE, A CELLULAR THERAPY FOR HIGH GRADE GLIOMA

Neuro-oncology (Charlottesville, Va.), 2023-11, Vol.25 (Supplement_5), p.v230-v230

2023

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PRC2 loss amplifies Ras-driven transcription and confers sensitivity to BRD4-based therapies

Nature (London), 2014-10, Vol.514 (7521), p.247-251

2014

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HGG-14. RAS PATHWAY MEDIATED REGULATION OF HISTONE METHYLTRANSFERASE AND TUMOR SUPPRESSOR SETD2 IN PEDIATRIC HIGH GRADE GLIOMA

Neuro-oncology (Charlottesville, Va.), 2023-06, Vol.25 (Supplement_1), p.i42-i42

2023

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HGG-49. INTERNEURONS THAT BITE: A CELLULAR DELIVERY SYSTEM FOR PEDIATRIC HIGH-GRADE GLIOMA

Neuro-oncology (Charlottesville, Va.), 2024-06, Vol.26 (Suppl 4), p.0-0

2024

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Spheroid Drug Sensitivity Screening in Glioma Stem Cell Lines

Journal of visualized experiments, 2024-02 (204)

2024

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Genomic organization and evolution of the NF1 microdeletion region

Genomics (San Diego, Calif.), 2004-08, Vol.84 (2), p.346-360

2004

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A Deregulated HOX Gene Axis Confers an Epigenetic Vulnerability in KRAS-Mutant Lung Cancers

Cancer cell, 2020-05, Vol.37 (5), p.705-719.e6

2020

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MAPK Pathway Suppression Unmasks Latent DNA Repair Defects and Confers a Chemical Synthetic Vulnerability in BRAF-, NRAS -, and NF1 -Mutant Melanomas

Cancer discovery, 2019-04, Vol.9 (4), p.526-545

2019

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Loss of RasGAP Tumor Suppressors Underlies the Aggressive Nature of Luminal B Breast Cancers

Cancer discovery, 2017-02, Vol.7 (2), p.202-217

2017

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Oncogenic Deregulation of EZH2 as an Opportunity for Targeted Therapy in Lung Cancer

Cancer discovery, 2016-09, Vol.6 (9), p.1006-1021

2016

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Abstract LB-113: MAPK pathway suppression unmasks latent DNA repair defects and confers a chemical synthetic vulnerability in BRAF , NRAS and NF1- mutant melanomas

Cancer research (Chicago, Ill.), 2019-07, Vol.79 (13_Supplement), p.LB-113-LB-113

2019

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PATH-21. TELOMERE LENGTH ANALYSIS OF CNS TUMORS IN THE PEDIATRIC BRAIN TUMOR ATLAS

Neuro-oncology (Charlottesville, Va.), 2020-12, Vol.22 (Supplement_3), p.iii428-iii428

2020

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The RasGAP Gene, RASAL2, Is a Tumor and Metastasis Suppressor

Exploiting Cancer Cell Vulnerabilities to Develop a Combination Therapy for Ras-Driven Tumors

Identification of therapeutic sensitivities in a spheroid drug combination screen of Neurofibromatosis Type I associated High Grade Gliomas

Single cell spatial analysis reveals the topology of immunomodulatory purinergic signaling in glioblastoma

Atypical neurofibromas in neurofibromatosis type 1 are premalignant tumors

Targeting Refractory Sarcomas and Malignant Peripheral Nerve Sheath Tumors in a Phase I/II Study of Sirolimus in Combination with Ganetespib (SARC023)

A Collaborative Model for Accelerating the Discovery and Translation of Cancer Therapies

Molecular pathogenesis of multiple gastrointestinal stromal tumors in NF1 patients

The Activation of the WNT Signaling Pathway Is a Hallmark in Neurofibromatosis Type 1 Tumorigenesis

Imaging Mass Spectrometry Reveals Tumor Metabolic Heterogeneity

P588: Identification of NF1-associated tumor mutations in plasma cfDNA and its clinical application

Conservation of hotspots for recombination in low-copy repeats associated with the NF1 microdeletion

Intestinal Neurofibromatosis Is a Subtype of Familial GIST and Results From a Dominant Activating Mutation in PDGFRA

EXTH-29. INTERNEURONS THAT BITE, A CELLULAR THERAPY FOR HIGH GRADE GLIOMA

PRC2 loss amplifies Ras-driven transcription and confers sensitivity to BRD4-based therapies

HGG-14. RAS PATHWAY MEDIATED REGULATION OF HISTONE METHYLTRANSFERASE AND TUMOR SUPPRESSOR SETD2 IN PEDIATRIC HIGH GRADE GLIOMA

HGG-49. INTERNEURONS THAT BITE: A CELLULAR DELIVERY SYSTEM FOR PEDIATRIC HIGH-GRADE GLIOMA

Spheroid Drug Sensitivity Screening in Glioma Stem Cell Lines

Genomic organization and evolution of the NF1 microdeletion region

A Deregulated HOX Gene Axis Confers an Epigenetic Vulnerability in KRAS-Mutant Lung Cancers

MAPK Pathway Suppression Unmasks Latent DNA Repair Defects and Confers a Chemical Synthetic Vulnerability in BRAF-, NRAS -, and NF1 -Mutant Melanomas

Loss of RasGAP Tumor Suppressors Underlies the Aggressive Nature of Luminal B Breast Cancers

Oncogenic Deregulation of EZH2 as an Opportunity for Targeted Therapy in Lung Cancer

Abstract LB-113: MAPK pathway suppression unmasks latent DNA repair defects and confers a chemical synthetic vulnerability in BRAF , NRAS and NF1- mutant melanomas

PATH-21. TELOMERE LENGTH ANALYSIS OF CNS TUMORS IN THE PEDIATRIC BRAIN TUMOR ATLAS

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