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Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
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Targeted therapy for BRAFV600E malignant astrocytoma.

Theodore P Nicolaides1, Huifang Li, David A Solomon

  • 1University of California, San Francisco, San Francisco, CA 94158, USA.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|November 1, 2011
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Activating BRAF(V600E) mutations occur in 10% of pediatric malignant astrocytomas (MA). BRAF(V600E)-specific inhibitors show promise for treating these aggressive brain tumors.

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Area of Science:

  • Neuro-oncology
  • Molecular biology
  • Cancer genetics

Background:

  • Malignant astrocytomas (MA) are aggressive pediatric brain tumors with poor prognoses.
  • Activating BRAF(V600E) mutations are found in a subset of MAs, particularly in children.

Purpose of the Study:

  • To determine the incidence of BRAF(V600E) in pediatric MA patient cohorts.
  • To evaluate the therapeutic effects of BRAF blockade in preclinical MA models with BRAF(V600E) and wild-type BRAF.

Main Methods:

  • BRAF(V600E) mutation analysis in two pediatric MA cohorts.
  • In vitro studies using MA cell lines to assess BRAF shRNA knockdown and pharmacologic inhibition (PLX4720).
  • In vivo efficacy studies using orthotopic MA xenografts in mice.

Main Results:

  • BRAF(V600E) mutations were identified in 10-11% of pediatric MAs.
  • BRAF(V600E)-specific inhibitor PLX4720 demonstrated antiproliferative effects on mutant cells in vitro.
  • PLX4720 reduced tumor growth and improved survival in mice with BRAF(V600E) MA xenografts, but was ineffective or tumor-promoting in wild-type xenografts.

Conclusions:

  • Approximately 10% of pediatric malignant astrocytomas harbor activating BRAF(V600E) mutations.
  • BRAF(V600E)-specific inhibitors warrant clinical evaluation for treating pediatric MA patients with this mutation.