Abstract
Radiotherapy is commonly used in patients with oral cavity and pharyngeal cancers, usually resulting in irreversible salivary hypofunction. Currently management of radiation damage to salivary glands still remains a great challenge. Recent studies show that activation of mammalian target of rapamycin (mTOR) occurs in salivary gland lesions, making it possible to apply mTOR inhibitor for treatment. Our results indicate inhibition of mTOR by rapamycin significantly alleviated irradiation-induced salivary hypofunction by restoring 46% salivary flow rate and protecting histological structures in swine. Furthermore, rapamycin protected human submandibular gland cell line (HSG) from irradiation-induced cell depletion and loss of cell proliferation capacity. These findings lay the foundation for a new clinical application of rapamycin to prevent irradiation-induced salivary hypofunction.
Highlights
It is estimated that the incidence rate of lip, oral cavity and pharynx cancers was 48.1 per 10,000 in China in 2015 [1]
To determine the dose of rapamycin to achieve this rapamycin blood levels, nine minipigs were dived into 3 groups (n = 3 per group), which received 0.05, 0.1 or 0.15 mg/kg injection dose per day for 5 continuous days separately
These results indicate that rapamycin treatment remarkably protects the secretion function of parotid gland in minipigs after fractionated irradiation
Summary
It is estimated that the incidence rate of lip, oral cavity and pharynx cancers was 48.1 per 10,000 in China in 2015 [1]. Radiotherapy is commonly used to treat the majority of patients with oral cavity and pharyngeal cancers, but often results in radiation exposure of the normal salivary gland, inducing irreversible irradiationinduced hypofunction. The new radiotherapy technology image guide radiation therapy (IGRT) and various radio-protectants, such as Amifostine or Tempol, could significantly alleviate irradiation-induced salivary gland injury [6,7,8,9], these therapies are not widely available and remain palliative in essence. Treatment with an adenoviral vector encoding fibroblast growth factor-2 (AdFGF2) resulted in the protection of parotid microvascular endothelial cells from IR damage and significantly limited the decline of parotid salivary flow [14]. Viral vector-mediated gene transfer is a relatively complicated process, and needs further investigations such as long-term efficiency, safety and other factors
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