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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...

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Tumor Treating Field Therapy in Combination with Bevacizumab for the Treatment of Recurrent Glioblastoma
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Tumor-Targeted pan-RAS Inhibition as a Novel Biologic Therapy for Diffuse Midline Glioma.

Stefanie-Grace Sbergio1,2, Huazhu Liang3,4, Lucy Chen1

  • 1The Arthur and Sonia Labatt Brain Tumour Research Centre, Hospital for Sick Children, 686 Bay Street, Toronto, ON, M5G 0A4, Canada.

Neuro-Oncology
|June 29, 2026
PubMed
Summary

A novel biologic therapy effectively targets RAS signaling in diffuse midline glioma (DIPG), a deadly childhood brain cancer. This approach shows promise for treating DIPG by degrading RAS proteins and inducing cancer cell death.

Keywords:
Diffuse Intrinsic Pontine Glioma (DIPG)H3K27-altered Diffuse Midline Glioma (DMG)ImmunotoxinRASRRSP

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A Protocol for Rapid Post-mortem Cell Culture of Diffuse Intrinsic Pontine Glioma (DIPG)

Published on: March 7, 2017

Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Development

Background:

  • Diffuse midline glioma (DIPG) and pediatric high-grade gliomas (pHGG) are leading causes of childhood cancer mortality.
  • RAS/MAPK pathway is upregulated in DIPG, but RAS proteins are difficult therapeutic targets.
  • Current therapeutic options for DIPG are limited.

Purpose of the Study:

  • To investigate RAS dependency in DIPG.
  • To develop a targeted therapy for DIPG by leveraging a novel biologic.
  • To evaluate the efficacy of a targeted RAS-degrading biologic in DIPG models.

Main Methods:

  • Utilized a pan-RAS-cleaving biologic (RRSP-DTB) to assess RAS dependency in DIPG.
  • Employed proteomic profiling to identify cell-surface receptors for targeted delivery.
  • Engineered RRSP to target tumor endothelial marker 8 (TEM8/ANTXR1) for enhanced delivery and RAS degradation.

Main Results:

  • Pan-RAS cleavage confirmed critical RAS/MAPK signaling dependency in DIPG.
  • Targeted RRSP (RRSP-DTT-TEM8) achieved efficient intracellular delivery, complete RAS ablation, and apoptotic cell death in DIPG cells at low picomolar concentrations.
  • In vivo studies showed reduced leptomeningeal disease burden and extended survival in orthotopic DIPG xenograft models.

Conclusions:

  • Demonstrated RAS dependency in DIPG is targetable with a novel, first-in-class pan-RAS biotherapeutic (RRSP-DTT-TEM8).
  • This targeted biologic represents a potential therapeutic strategy for DIPG.
  • Further development of RRSP-DTT-TEM8 could offer a new treatment option for this aggressive childhood brain tumor.