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Task 3D Tissue Models for Study of Intercellular Signaling Stimulated by High Energy Particles (Completed)
Last Published:  07/27/17 09:48:12 AM (Central)
Task Book: Entry
Principal Investigator: Held, Kathryn
Short Title: 3-D Intercellular
Responsible HRP Element: Space Radiation
Collaborating Org(s):
Funding Status: Completed - Task completed and produced a deliverable
Procurement Mechanism(s):
Solicited
Aims:
  1. We will quantify apoptosis, proliferation and differentiation, as early hallmarks of cancer, in 3D epithelial tissue models of skin, a tissues in which radiation is known to cause cancer.
  2. A novel aspect of our studies is to test the hypothesis that radiation can alter the ability of dendritic cells to participate in immune surveillance and that radiation-induced persistent oxidative stress is part of the underlying mechanism.
  3. Studies comparing radiation and bystander effects in normal, pre-cancerous and neoplastic epithelial cells will be conducted. An important component of anti-cancer processes in epithelial tissues is the immune system, including dendritic cells which are critically involved in immune surveillance against cancer.
  4. We will quantify apoptosis, proliferation and differentiation, as early hallmarks of cancer, in 3D epithelial tissue models of colon, a tissue in which radiation is known to cause cancer.
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 02: How can experimental models of tumor development for the other tissues (bladder, ovary, brain, esophagus, skin, etc.) 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 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?
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