Dual inhibition of DNA damage repair in DIPG

  • Hashizume, Rintaro (PD/PI)
  • Gius, David R (Co-Investigator)
  • Zou, Lihua (Co-Investigator)

Project: Research project

Project Details

Description

For a child is diagnosed with a diffuse intrinsic pontine glioma so called DIPG, the options for treatment are scarce and so are the chances for survival. This aggressive brain tumor generally strikes children who are 6 years old and younger, with most surviving less than a year after diagnosis. The only known effective treatment is the use of radiation. Yet, even with radiation therapy most children show tumor progression within the year after radiation therapy. Given this reality, there is a desperately need to identify the drug that increase the anti-tumor activity of radiation, as a mean to improve treatment outcome for these children. DNA damage is thought to be the most toxic effect caused by radiation, and we and others showed that the majority of the DNA damage caused by radiation are repaired within 24 hours of treatment. This DNA damage repair is possibly responsible for the tumor progression observed in DIPG after radiation therapy, thereby ultimately taking no survival benefits to the patients. We recently performed a genetic screening in DIPG cells collected from patient tumor and found specific therapeutic targets which is important for DNA damage repair. This research will study whether targeted inhibition of DNA damage repair increase DNA damage by radiation, leading to increased radiation toxicity in DIPG. Successful results from this research will find a new effective therapy which increases the anti-tumor activity of radiation, in turn, will ultimately leads to improved treatment outcomes for children with highly malignant and currently incurable cancer.
StatusFinished
Effective start/end date7/1/206/30/21

Funding

  • St. Baldrick's Foundation (696235)

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