Preserving Salivary Gland Function After Radioiodine Therapy for Thyroid Cancer

$311,360P50FY2015CANIH

Ohio State University, Columbus OH

Investigators

Linked publications & trials

Paper 38688277 Paper 38062777 Paper 34638434 Paper 34238982 Paper 33974556 Paper 33536187 Paper 33449450 Paper 32798993 Paper 32772084 Paper 32769997 Paper 32761153 Paper 32216548 Paper 32051256 Paper 31446085 Paper 31154940 Paper 31097454 Paper 30820785 Paper 30747051 Paper 30654714 Paper 30552230 Paper 30419129 Paper 30350351 Paper 30305013 Paper 30265861 Paper 30135308 Paper 30088223 Paper 30076554 Paper 29768105 Paper 29495389 Paper 29454064 Paper 29310570 Paper 29300379 Paper 29132255 Paper 29121253 Paper 29105562 Paper 29066476 Paper 28987384 Paper 28920557 Paper 28911154 Paper 28591772 Paper 28510122 Paper 28195142 Paper 28049826 Paper 27965276 Paper 27935748 Paper 27785980 Paper 27736322 Paper 27673361 Paper 27610696 Paper 27604949 Paper 27575943 Paper 27542854 Paper 27533304 Paper 27459529 Paper 27296473 Paper 27127178 Paper 26581005 Paper 26549818 Paper 26494382 Paper 26418285 Paper 26274343 Paper 25918370 Paper 25795775 Paper 25710562 Paper 25546157 Paper 25338077 Paper 25303483 Paper 25234361 Paper 24911281 Paper 24617864 Paper 24241281 Paper 24238055 Paper 24030941 Paper 19190587

Abstract

Radioiodine (131I) targets thyroid tissues and has been an effective and standard treatment for differentiated thyroid cancers for many years. However, the Na +/| symporter (NIS), which mediates active iodide uptake into thyroid follicular cells, is also abundantly expressed in salivary ductal cells. Accordingly, many 131I-treated thyroid cancer survivors suffer from life-long morbidity of 131I-induced salivary gland (SG) dysfunction, including recurrent sialadenitis, persistent xerostomia, and progressive susceptibility to dental caries and periodontal disease. In this proposal, we aim to explore novel approaches to prevent 131I-induced SG damage in thyroid cancer patients, and to identify protective saliva biomarkers for patients' susceptibility to progressive 131I-induced SG dysfunction. Two specific aims are identified: (1) Transient silencing/inhibition of salivary NIS to eliminate salivary 131I accumulation during radioiodine therapy; and (2) Identify protective saliva biomarkers and underlying pathobiology for 131I-induced SG dysfunction. Upon successful completion of the proposed studies, our novel prevention strategy promises to eliminate 131I-induced SG damage or at least dramatically reduce its occurrence among thyroid cancer survivors who will receive 131I therapy. We will be able to use quantifiable saliva biomarkers or SG anatomic changes to monitor the onset and progression of SG dysfunction induced by 131I such that personalized intervention strategies can be applied to patients in a timely manner. We will determine whether saliva biomarkers detected in the early stage of salivary dysfunction induced by 131I are predictive of future progression to chronic disease. We may also distinguish patients who are more susceptible or resistant to develop life-long morbidity of 131I-induced SG dysfunction for differential clinical management.

View original record on NIH RePORTER →