Task A Novel Biological Countermeasure and Mitigator of High LET-Induced Cancer Progression (Completed)
Last Published:  07/31/18 09:30:09 AM (Central)
Short Title: Biological Countermeasure Mitigator
Responsible HRP Element: Space Radiation
Collaborating Org(s):
Funding Status: Completed - Task completed and produced a deliverable
Procurement Mechanism(s):
Solicited
Aims:
  1. To use a lung cancer susceptible mouse model that develops significantly more invasive lung tumors when high LET is provided in fractionated/protracted doses over 5 to 10 days (e.g 0.2 Gy x 5 days or 0.1 Gy x 10 days 56Fe 1GeV, compared to single acute 1 Gy 56Fe). Our objective is to determine if pretreatment with BARD prior to acute or fractionated IR reduces the number of invasive (e.g. more lethal) cancers. We will examine at least 3 different ions.
  2. To test Bardoxylone methyl (BARD) as a Biological Countermeasures (BCM) in mouse models exposed to SPE simulations. As part of the UT Southwestern Lung NSCOR and the Georgetown GI NSCOR, we have lung cancer and colon cancer susceptible mice that have been treated with solar particle simulations. We propose to test if providing BARD to these animals before irradiation reduces the incidence or progression of cancer.
  3. To test BARD as a radiation mitigator by providing it to mice within 60 minutes after irradiation. We will compare SPE simulations (total body exposure 2 Gy Protons) and at least two other ions (56Fe at 600 meV, LET 175 and 28Si at 300 MeV LET 70).
Resources (None Listed)
Mappings
RiskRisk of Radiation Carcinogenesis
GapCancer 01: How can experimental models of tumor development for the major tissues (lung, colon, stomach, breast, liver, and leukemias) be developed to represent the major processes in radiation carcinogenesis and extrapolated to human risk and clinical outcome projections?
GapCancer 03: How can experimental models of carcinogenesis be applied to reduce the uncertainties in radiation quality effects from SPE’s and GCR, including effects on tumor spectrum, burden, latency and progression (e.g., tumor aggression and metastatic potential)?
GapCancer 04: How can models of cancer risk be applied to reduce the uncertainties in dose-rate dependence of risks from SPE's and GCR?
GapCancer 05: How can models of cancer risk be applied to reduce the uncertainties in individual radiation sensitivity including genetic and epigenetic factors from SPE and GCR?
GapCancer 06: How can models of cancer risk be applied to reduce the uncertainties in the age and sex dependence of cancer risks from SPE's and GCR?
GapCancer 07: How can systems biology approaches be used to integrate research on the molecular, cellular, and tissue mechanisms of radiation damage to improve the prediction of the risk of cancer and to evaluate the effectiveness of countermeasures? How can epidemiology data and scaling factors support this approach?
GapCancer 08: What are the most effective medical or dietary countermeasures to mitigate cancer risks from exposure to SPE and GCR? What side effects should be tolerated versus mission risks?Can medical countermeasures that provide mitigation across multiple cancer types or across multiple radiation risk areas be identified (degenerative tissue risks or CNS in addition to cancer)?
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