The aim of this study was to assess whether vascular endothelial growth factor (VEGF) expression in oral tissues is associated with angiogenesis, disease progression or field cancerisation. Vascularity and VEGF immunoreactivity were quantified in 68 archival specimens including normal oral mucosa (NOM), dysplasia (DYS) and squamous cell carcinoma (SCC). Vascularity increased significantly with disease progression; it was also higher in NOM adjacent to SCC than in NOM from healthy tissue, suggesting an association with field cancerisation. VEGF expression in epithelial cells was evaluated using two antibodies and three indices. VEGF indices and vascularity were not directly correlated. The expression of VEGF was similar in all DYS and NOM specimens, whether or not adjacent to a concurrent lesion. A comparison of SCC with NOM or DYS led to opposite results, depending on the VEGF antibody and index used. We conclude that VEGF expression in the oral mucosa may play a physiological role, but does not appear to be associated with angiogenesis, field cancerisation or transition to dysplasia. Further studies concerned with tumour development require examining specific VEGF isoforms and standardisation of the methodology.

Aims-High expression of the angiogenic factor vascular endothelial growth factor (VEGF) in tumours has been found to be associated with poor prognosis in some studies, but not in others. The aims of this study were to determine the prognostic value of VEGF in operable non-small cell lung cancer (NSCLC) and its possible association with vascularity.

The purpose of pharmacogenetic testing is to determine the risk of adverse reactions and/or likelihood of a medication's effectiveness. Pharmacogenetic testing can assist primary care providers in tailoring treatment according to a patient's genetic traits and his or her ability to metabolize certain medication. This article will discuss the benefits and limitations of pharmacogenetic testing and how to interpret results.

Background: Adenoid Cystic Carcinoma (ACC) is an uncommon cancer of the head and neck which typically originates in the salivary glands. Treatment options for ACC resection and local radiation therapy although chemotherapy is sometimes used to control metastatic or locally recurrent disease. Patients with ACC may survive for years due to latent tumor growth and lack of lymph node metastasis; however, the high rate of recurrence and metastasis to the lungs lead to a poor prognosis beyond ten years. While no standard of care currently exists, improved understanding of ACC tumor biology and oncogenesis has provided some molecular targets for its treatment. Mutations and alterations of MYB, NFIB and molecules in the FGF, IGF, PI3K and NOTCH signaling pathways amongst others, may serve as targets for current and future therapies. Due to a lack of ACC derived cell lines, a panel of low passage ACC xenograft models designated ACCx5M1, ACCx6, ACCx9, ACCx14 and ACCx16 have been established and through the Adenoid Cystic Carcinoma Research Foundation (ACCRF) are routinely utilized to test agents which target pathways important in ACC. Methods: Low passage ACC models were established in immune-deficient mice from primary or metastatic patient tissue and once established were confirmed by histologic comparative analysis. Drug sensitivity studies are performed evaluating models towards chemotherapy and targeted agents. Study endpoints included tumor volume and time from treatment initiation with tumor growth inhibition and regression reported at study completion. Results: To date over seventy FDA-approved and investigational therapies have been evaluated and data has been generated that have contributed to the initiation of two Phase 2 clinical trials in ACC. In addition to chemotherapies, therapies targeting FGF, IGF, VEGF and NOTCH pathways have been tested and we are currently evaluating agents targeting MYB dysregulation. Conclusion: Low passage ACC models have been used to identify agents potentially useful in the treatment of ACC and models are available through the ACCRF to evaluate potential therapies for the treatment of adenoid cystic carcinoma. Citation Information: Mol Cancer Ther 2013;12(11 Suppl):A106. Citation Format: Justin Meade, Michael J. Wick, Teresa L. Vaught, Jennifer Carlile, Anthony W. Tolcher, Drew Rasco, Amita Patnaik, Jeffrey Kaufman, Chris Moskaluk, Kyriakos P. Papadopoulos. Utilization of low passage adenoid cystic carcinoma (ACC) models to identify novel therapies. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2013 Oct 19-23; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2013;12(11 Suppl):Abstract nr A106.