Title

Histological Characterization of Vitamin D-induced Apoptosis in a Hamster Buccal Pouch Model of Head and Neck Squamous Cell Carcinoma

Poster Number

42

Lead Author Major

Biological Sciences

Format

Poster Presentation

Faculty Mentor Name

Joanna Albala

Faculty Mentor Department

Biological Sciences

Abstract/Artist Statement

Head and neck squamous cell carcinoma (HNSCC) remains a major cause of mortality and morbidity in the U.S. and around the world. Vitamin D3 (VD3), in addition to its primary role in maintaining calcium homeostasis, has been shown to induce differentiation and suppress the growth of squamous cell carcinomas in vitro. As such, proteins and compounds that act in the vitamin D pathway are potential candidates for therapeutic intervention for treatment of HNSCC. Previous work in the Albala lab has demonstrated that VD3 was chemopreventive in cancer formation in the hamster buccal pouch model. The hamster buccal pouch tumor model is a well-characterized model system since the progression from normal epithelium to carcinoma closely resembles those changes in humans. Rad51 protein plays an important role in is cell proliferation and homologous recombinational DNA repair. Defects in the pathway may render cells sensitive to DNA cross-linking agents and ionizing radiation, while up-regulation of the pathway can render cellular DNA more resistant to damage, and strengthen cellular resistance to radiation therapy and selective chemotherapeutic agents. Studies have documented the elevation of Rad51 levels in several cancer cell lines, including immortalized cells. Previous studies in the Albala lab have demonstrated the down- regulation of Rad51 by VD3 in the hamster buccal cheek pouch model. This work aims to demonstrate a correlation between the reduction of Rad51 protein by VD3 in this hamster model and the effects of 7,12- dimethylbenz[a]anthracene (DMBA) as a carcinogen, inducing the repair mechanism when administered to the hamster buccal pouches.

Location

Grave Covell

Start Date

21-4-2012 10:00 AM

End Date

21-4-2012 12:00 PM

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Apr 21st, 10:00 AM Apr 21st, 12:00 PM

Histological Characterization of Vitamin D-induced Apoptosis in a Hamster Buccal Pouch Model of Head and Neck Squamous Cell Carcinoma

Grave Covell

Head and neck squamous cell carcinoma (HNSCC) remains a major cause of mortality and morbidity in the U.S. and around the world. Vitamin D3 (VD3), in addition to its primary role in maintaining calcium homeostasis, has been shown to induce differentiation and suppress the growth of squamous cell carcinomas in vitro. As such, proteins and compounds that act in the vitamin D pathway are potential candidates for therapeutic intervention for treatment of HNSCC. Previous work in the Albala lab has demonstrated that VD3 was chemopreventive in cancer formation in the hamster buccal pouch model. The hamster buccal pouch tumor model is a well-characterized model system since the progression from normal epithelium to carcinoma closely resembles those changes in humans. Rad51 protein plays an important role in is cell proliferation and homologous recombinational DNA repair. Defects in the pathway may render cells sensitive to DNA cross-linking agents and ionizing radiation, while up-regulation of the pathway can render cellular DNA more resistant to damage, and strengthen cellular resistance to radiation therapy and selective chemotherapeutic agents. Studies have documented the elevation of Rad51 levels in several cancer cell lines, including immortalized cells. Previous studies in the Albala lab have demonstrated the down- regulation of Rad51 by VD3 in the hamster buccal cheek pouch model. This work aims to demonstrate a correlation between the reduction of Rad51 protein by VD3 in this hamster model and the effects of 7,12- dimethylbenz[a]anthracene (DMBA) as a carcinogen, inducing the repair mechanism when administered to the hamster buccal pouches.