CDK4/6 and PDGFRA signaling as therapeutic targets in diffuse intrinsic pontine glioma

Christine Marie Hoeman, Chen Shen, Oren Josh Becher*

*Corresponding author for this work

Research output: Contribution to journalReview article

2 Citations (Scopus)

Abstract

Diffuse intrinsic pontine gliomas (DIPGs) are incurable childhood brain tumors, whereby the standard of care is focal radiation, a treatment that provides temporary relief for most patients. Surprisingly, decades of clinical trials have failed to identify additional therapies that can prolong survival in this disease. In this conference manuscript, we discuss how genetic engineered mouse modeling techniques with the use of a retroviral gene delivery system can help dissect the complex pathophysiology of this disease. With this approach, autochthonous murine DIPG models can be readily induced to (1) help interrogate the function of novel genetic alterations in tumorigenesis, (2) identify candidate cells of origin for this disease, (3) address how region-specific differences in the central nervous system influence the process of gliomagenesis, and (4) evaluate novel therapeutics in an immunocompetent model.

Original languageEnglish (US)
Article number191
JournalFrontiers in Oncology
Volume8
Issue numberMAY
DOIs
StatePublished - May 31 2018

Fingerprint

Glioma
Gene Transfer Techniques
Manuscripts
Standard of Care
Brain Neoplasms
Carcinogenesis
Therapeutics
Central Nervous System
Clinical Trials
Radiation
Survival

Keywords

  • CDK4/6
  • Diffuse intrinsic pontine glioma
  • K27M
  • PDGF-A
  • PDGFRA
  • Platelet-derived growth factor-B

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

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title = "CDK4/6 and PDGFRA signaling as therapeutic targets in diffuse intrinsic pontine glioma",
abstract = "Diffuse intrinsic pontine gliomas (DIPGs) are incurable childhood brain tumors, whereby the standard of care is focal radiation, a treatment that provides temporary relief for most patients. Surprisingly, decades of clinical trials have failed to identify additional therapies that can prolong survival in this disease. In this conference manuscript, we discuss how genetic engineered mouse modeling techniques with the use of a retroviral gene delivery system can help dissect the complex pathophysiology of this disease. With this approach, autochthonous murine DIPG models can be readily induced to (1) help interrogate the function of novel genetic alterations in tumorigenesis, (2) identify candidate cells of origin for this disease, (3) address how region-specific differences in the central nervous system influence the process of gliomagenesis, and (4) evaluate novel therapeutics in an immunocompetent model.",
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author = "Hoeman, {Christine Marie} and Chen Shen and Becher, {Oren Josh}",
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CDK4/6 and PDGFRA signaling as therapeutic targets in diffuse intrinsic pontine glioma. / Hoeman, Christine Marie; Shen, Chen; Becher, Oren Josh.

In: Frontiers in Oncology, Vol. 8, No. MAY, 191, 31.05.2018.

Research output: Contribution to journalReview article

TY - JOUR

T1 - CDK4/6 and PDGFRA signaling as therapeutic targets in diffuse intrinsic pontine glioma

AU - Hoeman, Christine Marie

AU - Shen, Chen

AU - Becher, Oren Josh

PY - 2018/5/31

Y1 - 2018/5/31

N2 - Diffuse intrinsic pontine gliomas (DIPGs) are incurable childhood brain tumors, whereby the standard of care is focal radiation, a treatment that provides temporary relief for most patients. Surprisingly, decades of clinical trials have failed to identify additional therapies that can prolong survival in this disease. In this conference manuscript, we discuss how genetic engineered mouse modeling techniques with the use of a retroviral gene delivery system can help dissect the complex pathophysiology of this disease. With this approach, autochthonous murine DIPG models can be readily induced to (1) help interrogate the function of novel genetic alterations in tumorigenesis, (2) identify candidate cells of origin for this disease, (3) address how region-specific differences in the central nervous system influence the process of gliomagenesis, and (4) evaluate novel therapeutics in an immunocompetent model.

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