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SU‐C‐303‐01: Activation‐Induced Cytidine Deaminase Confers Cancer Resistance to Radiation Therapy
Author(s) -
Yi S,
La Count S,
Liu J,
Bai X,
Lu L
Publication year - 2015
Publication title -
medical physics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.473
H-Index - 180
eISSN - 2473-4209
pISSN - 0094-2405
DOI - 10.1118/1.4923818
Subject(s) - cytidine deaminase , radiation therapy , cancer research , cancer , apoptosis , cancer cell , medicine , activation induced (cytidine) deaminase , cell , nuclear medicine , biology , immunology , b cell , immunoglobulin class switching , biochemistry , genetics , antibody
Purpose: To study the role of activation‐induced cytidine deaminase (AID) in malignant cell resistance to radiation therapy. Methods: We first developed several small devices that could be used to adopt radiation beams from clinical high dose rate brachy therapy (HDR) or linac‐based megavoltage machines to perform pre‐clinical cell and mouse experiments. Then we used these devices to deliver radiation to AID‐positive and AID‐silenced cancer cells or tumors formed by these cells in mice. Cells and mice bearing tumors received the same dose under the same experimental conditions. For cells, we observed the apoptosis and the cell survival rate over time. For mice bearing tumors, we measured and recorded the tumor sizes every other day for 4 weeks. Results: For cell experiments, we found that the AID‐positive cells underwent much less apoptosis compared with AID‐silenced cells upon radiation. And for mouse experiments, we found that AID‐positive tumors grew significantly faster than the AID‐silenced tumors despite of receiving the same doses of radiation. Conclusion: Our study suggests that AID may confer cancer resistance to radiation therapy, and AID may be a significant biomarker predicting cancer resistance to radiation therapy for certain cancer types