Barzilai University Medical Center

80 Research Day 2020 Barzilai University Medical Center 57 EXPRESSION OF MITOCHONDRIAL VOLTAGE-DEPENDENT ANION CHANNEL 1 (VDAC1) IN MALIGNANT AND PREMALIGNANT LESIONS IN THE ORAL CAVITY Jacob Pettesh 1 , Alejandro Livoff 2,3 , Oded Nahlieli 3,4 , Eli Michaeli 1 , Irit Allon 2,3 1 Unit of Oral Medicine, Barzilai University Medical Center, Ashkelon, Israel 2 Institute of Pathology, Barzilai University Medical Center, Ashkelon, Israel 3 Faculty of Health Studies, Ben Gurion University of the Negev, Beer Sheva, Israel 4 Department of Oral and Maxillofacial Surgery, Barzilai University Medical Center, Ashkelon, Israel Background Head and neck cancer accounts for more than 650,000 cases and 330,000 deaths annually, out of which Oral Squamous Cell Carcinoma (OSCC) is the most prevalent type. Premalignant lesions, which appear clinically as white and/or red lesions in the oral cavity, may precede the development of OSCC. Identifying prognostic biomarkers or therapy targets for OSCC is of great importance in order to better predict tumor behavior and response to treatment. The mitochondrial voltage-dependent anion channel 1(VDAC1), located at the outer mitochondrial membrane, plays a role in cellular activities and metabolic and survival pathways, including mitochondria-mediated apoptosis. As a transporter of metabolites, VDAC1 contributes to the metabolic phenotype of cancer cells and is overexpressed in many cancer types. Moreover, silencing of VDAC1 expression has been shown to induce inhibition of tumor development. Hypothesis VDAC1 expression in OSCC and premalignant lesions in the oral cavity will be increased in comparison to controls. Objectives Exploration and evaluation of VDAC1 expression in biopsies of premalignant and OSCC lesions in the oral cavity, alongside to clinico-pathologic information of the cases. Results Significant differences were indicated between the control group (fibrous hyperplasia) and the premalignant and OSCC groups (p < .01), as control biopsies (Mean = 1.45, SD = 0.93) had higher VDAC than pre-malignant (Mean = 0.61, SD = 0.77) and OSCC (Mean = 0.63, SD = 0.82) biopsies (p < .01 for both, Bonferroni corrected). Conclusions OSCC and premalignant lesions of the oral cavity demonstrated decreased expression of VDAC1 compared to controls. Further research on larger study groups should be done in order to better evalute and explain VDAC1 expression in OSCC and premalignant lesions of the oral cavity and to explain the difference between OSCC and other types of cancer.