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Review
. 2018;23(3-4):139-151.
doi: 10.1615/CritRevOncog.2018027598.

Current State of Knowledge on Salivary Gland Cancers

H Helen Lin  1 , Kirsten H Limesand  2 , David K Ann  1
Affiliations
Review

Current State of Knowledge on Salivary Gland Cancers

H Helen Lin et al. Crit Rev Oncog. 2018.

Abstract

Salivary gland cancers (SGCs), categorized as head and neck cancers (HNCs), constitute about 6% of head and neck cancer diagnoses based on estimate by American Head and Neck Society. Salivary gland tumors originate from different glandular cell types and are thus morphologically diverse. These tumors arise from any of the three major and various minor salivary glands. The incidence of SGCs has slowly increased during the last four decades. The etiology of SGCs is mostly unknown; however, specific gene mutations are associated with certain types of salivary tumors. Treatment options include surgical resection, radiation therapy (RT), chemotherapy, and multimodality therapy. HNC patients treated with RT often develop xerostomia and salivary hypofunction due to damaged salivary glands. In this review, we discuss etiology of SGCs, present findings on the role of autophagy in salivary tumorigenesis, review adverse effects of radiation treatment, and examine remedies for restoration of salivary function.

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Figures

FIG. 1:
FIG. 1:
Rising long-term SEER incident rates of SGC spanning 40 yr, from 1975 to 2015. Data were extracted from the SEER*Explorer interactive website (https://seer.cancer.gov/explorer/; updated April 16, 2018) of the National Cancer Institute. All ethnicities and age groups of both sexes were included in nine SEER areas (San Francisco, Connecticut, Detroit, Hawaii, Iowa, New Mexico, Seattle, Utah, and Atlanta). Rates are per 100,000 individuals, and annual percent-change estimates were calculated from underlying rates using Joinpoint Trend Analysis software (https://surveillance.cancer.gov/joinpoint; version 4.6, February 2018, National Cancer Institute; created by SEER. cancer.gov/explorer/application.php on 07/23/2018).
FIG. 2:
FIG. 2:
Role of autophagy during tumor initiation and progression. Autophagy suppresses but does not prevent tumor initiation in oncogenic KRAS-induced SDC. Once premalignant cells progress to malignant cells, autophagy has a protective role against unfavorable tumor microenvironment, such as hypoxia and poor nutrient supply, to promote tumor progression. Similar observations have been reported in oncogenic KRAS-induced pancreatic, lung, and colorectal cancers.
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