The autophagy pathway is the process whereby cells keep cellular homeostasis and respond to stress via recycling their damaged cellular proteins, organelles, and other cellular components. In the context of cancer, autophagy is a dual-edge sword pro- and anti-tumorigenic role depending on the oncogenic context and stage of tumorigenesis. Cancer cells have a higher dependency on autophagy compared with normal cells because of cellular damages and high demands for energy. The carbon, nitrogen, and molecular oxygen are building blocks for highly proliferative cancer cells which extremely depend on glutaminolysis and aerobic glycolysis; when a cancer cell is restricted to glucose and glutamine, it initiates to activate a stress response pathway using autophagy. Oncogenic tyrosine kinases (OncTKs) and receptor tyrosine kinases (RTKs) activation result in autophagy modulation through activation of the PI3K/AKT/mTORC1 and RAS/MAPK signaling pathways. Targeted inhibition of tyrosine kinases (TKs) and RTKs have recently been considered as cancer therapy but drug resistance and cancer relapse continue to be a major limitation of tyrosine kinase inhibitors (TKIs). Manipulation of autophagy pathway along with TKIs may be a promising strategy to circumvent unknown existing drug-resistance mechanisms that may emerge in a treated patient. In this way, clinical trials are ongoing to modulate autophagy to treat cancer. This review aims to summarize the combination therapy of autophagy affecting compounds with anticancer drugs which target cell signaling pathways, metabolism mechanisms, and epigenetics modification to improve therapeutic efficacy against cancers.

Human telomerase reverse transcriptase (hTERT) is an enzyme that is critically involved in elongating and maintaining telomeres length to control cell life span and replicative potential. Telomerase activity is continuously expressed in human germ-line cells and most cancer cells, whereas it is suppressed in most somatic cells. In normal cells, by reducing telomerase activity and progressively shortening the telomeres, the cells progress to the senescence or apoptosis process. However, in cancer cells, telomere lengths remain constant due to telomerase's reactivation, and cells continue to proliferate and inhibit apoptosis, and ultimately lead to cancer development and human death due to metastasis. Studies demonstrated that several DNA and RNA oncoviruses could interact with telomerase by integrating their genome sequence within the host cell telomeres specifically. Through the activation of the hTERT promoter and lengthening the telomere, these cells contributes to cancer development. Since oncoviruses can activate telomerase and increase hTERT expression, there are several therapeutic strategies based on targeting the telomerase of cancer cells like telomerase-targeted peptide vaccines, hTERT-targeting dendritic cells (DCs), hTERT-targeting gene therapy, and hTERT-targeting CRISPR/Cas9 system that can overcome tumor-mediated toleration mechanisms and specifically apoptosis in cancer cells. This study reviews available data on the molecular structure of telomerase and the role of oncoviruses and telomerase interaction in cancer development and telomerase-dependent therapeutic approaches to conquest the cancer cells.

Autophagy is a finely tuned process in the regulation of innate immunity to avoid excessive inflammatory responses and inflammasome signaling. In contrast, the results of recent studies have shown that autophagy may disease-dependently contribute to the pathogenesis of liver diseases, such as fibrosis, cirrhosis, and hepatocellular carcinoma (HCC) during hepatitis B virus (HBV) infection. HBV has learned to subvert the cell's autophagic machinery to promote its replication. Given the great impact of the autophagy mechanism on the HBV infection and HCC, recognizing these factors may be offered new hope for human intervention and treatment of chronic HBV. This review focuses on recent findings viewing the dual role of autophagy plays in the pathogenesis of HBV infected hepatocytes.

Background: Head and neck cancers (HNC) constitute the sixth common type of malignancies worldwide and can affect a wide range of anatomical regions. The role of the herpes simplex virus (HSV) in oral squamous cell carcinoma (OSCC) has been previously investigated. Objectives: The objective of the current study was to evaluate the molecular epidemiology of herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) in patients with HNC. Methods: A total of 156 patients with HNC were chosen including 90 biopsies and 66 formalin-fixed paraffin-embedded (FFPE) samples. HNC was confirmed and affected different anatomical regions. HSV detection was performed by a polymerase chain reaction (PCR) and HSV typing was assessed by a multiplex PCR. Results: The 156 HNC specimens included 35 (22.4%) larynx, 29 (18.6%) tongue, 6 (3.8%) glands (parotid and tonsil), 12 (7.6%) nasopharynx, 9 (5.7%) pharynx, 33 (21%) vocal cord, 3 (1.9%) palatine, glottis 17 (10.8%), nasal 2 (1.3%), mandibular 4 (2.5%), lip 4 (2.5%), neck 1 (0.6%), and face 1 (0.6%). The mean ± SD of the patients’ age was 60.3 ± 12.65, where 121 (77.1%) were male. The HSV was detected in 4 (2.6%) samples and 75% of HSV positive samples were HSV-1. Conclusions: The rate of HSV infection in Iranian patients with HNC was 2.6% with the majority being HSV-1 (75%). As a preliminary study in Iranian patients with HNC, cancer location was not statistically significant. Further investigations are needed to assess the role of HSV in HNC.