Abstract
Head and neck cancer encompass different malignancies that develop in and around the throat, larynx, nose, sinuses and mouth. Most head and neck cancers are squamous cell carcinomas (HNSCC) that arise in the flat squamous cells that makeup the thin layer of tissue on the surface of anatomical structures in the head and neck. Each year, HNSCC is diagnosed in more than 600,000 people worldwide, with about 50,000 new cases. HNSCC is considered extremely curable if detected early. But the problem remains in treatment of inoperable cases, residues or late stages. Circadian rhythm regulation has a big role in developing various carcinomas, and head and neck tumors are no exception. A number of studies have reported that alteration in clock gene expression is associated with several cancers, including HNSCC. Analyses on circadian clock genes and their association with HNSCC have shown that expression of PER1, PER2, PER3, CRY1, CRY2, CKIε, TIM, and BMAL1 are deregulated in HNSCC tissues. This review paper comprehensively presents data on deregulation of circadian genes in HNSCC and critically evaluates their potential diagnostics and prognostics role in this type of pathology.
Highlights
Head and neck cancer are malignant tumors of the throat, larynx, nose, sinuses and mouth
We propose that further investigation and understanding of clock gene involvement, and circadian clock regulation, in tumor development might contribute to novel insights into cancer pathogenesis
The regulations of central and peripheral circadian oscillators involve transcriptional-translational feedback loops that consist of so-called core circadian clock genes such as PERIOD (PER1, PER2 and PER3), CRYPTOCHROME (CRY1 and CRY2), CLOCK, NPAS2, BMAL1, retinoic acid-related orphan nuclear receptors RORα and REV-ERBα, CASEIN KINASE 1є (CK1є), and TIMELESS (TIM) [41,43,45,46]
Summary
Head and neck cancer are malignant tumors of the throat, larynx, nose, sinuses and mouth. The majority of cases, up to 90%, fall into the category of head and neck squamous cell carcinomas (HNSCC). Targeted therapies of HNSCC, for example epidermal growth factor receptor (EGFR) kinase inhibitors or monoclonal antibodies directed on PD-1 (programmed cell death-1) or vascular endothelial growth factor (VEGF), have been tested in such cases and represent an additional option in tumor spread control. These targeted therapy options require additional studies [7,8]. We propose that further investigation and understanding of clock gene involvement, and circadian clock regulation, in tumor development might contribute to novel insights into cancer pathogenesis
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