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Sinonasal and Skull Base Tumor Program
Nyall R. London Jr., M.D., Ph.D., Otolaryngology Surgeon-Scientist
Our laboratory is focused on understanding how and why malignant tumors develop in the nasal cavity, sinuses, and base of the skull. We seek to translate these results into better therapies. We are particularly interested in a type of malignancy called olfactory neuroblastoma (also known as esthesioneuroblastoma), which researchers think arises from the olfactory epithelium, the area of the nose important for the sense of smell.
The goals of the Sinonasal and Skull Base Tumor Program are to 1) understand the impact that standard surgical, radiation, and chemotherapy treatments have on the sense of smell, 2) identify critical genes that drive tumor development, and determine their mechanism of action, and 3) assess the potential of these genes as therapeutic targets.
Our laboratory utilizes a variety of in vitro and in vivo experimental approaches and immunotherapeutic and other treatment platforms to achieve these goals. We are actively developing a series of clinical trials to improve treatment effectiveness and survival in patients with sinonasal and skull base cancers.
- Wolfe AR, Blakaj D, London NR Jr, Blakaj A, Klamer B, Pan J, Wakely P, Prevedello L, Bonomi M, Bhatt A, Raval R, Palmer J, Prevedello D, Carrau, R. Clinical outcomes and multidisciplinary patterns of failure for olfactory neuroblastoma: The Ohio State experience. J Neurol Surg B. 2019 May 8.
- London NR Jr, Tharakan A, Mendiola M, Chen M, Dobzanski A, Sussan TE, Zaykaner M, Han AH, Lane AP, Sidhaye V, Biswal S, Ramanathan M Jr. Nrf2 activation via Keap1 deletion or sulforaphane treatment reduces Ova-induced sinonasal inflammation. Allergy. 2019 Mar 6.
- London NR Jr, Ishii M, Gallia G, Boahene K. Technique for reconstruction of large clival defects through an endoscopic-assisted tunneled retropharyngeal approach. International Forum of Allergy and Rhinology. 2018 Aug 2.
- London NR Jr, Tharakan A, Rule A, Lane A, Biswal S, Ramanathan M. Air pollutant mediated disruption of sinonasal epithelial cell barrier function is reversed by activation of the Nrf2 pathway. Journal of Allergy and Clinical Immunology. 2016 Dec;138(6):1736-1738.e4.
- Zhu W*, London NR Jr*, Gibson C*, Davis C, Tong Z, Sorensen L, Shi D, Guo J, Smith M, Grossmann A, Thomas K, Li D. Interleukin receptor activates a MYD88-ARNO-ARF6 cascade to disrupt vascular stability. Nature. 2012 Dec 13; 492(7428):252-5.
- London NR Jr*, Zhu W*, Bozza F, Smith M, Greif D, Sorensen L, Chen L, Kaminoh Y, Passi S, Day C, Barnard D, Zimmerman G, Krasnow M, Li D. Targeting Robo4-dependent Slit signaling to survive the cytokine storm in sepsis and influenza. Science Translational Medicine. 2010 Mar 17;2(23):23ra19.
- Jones C*, Nishiya N*, London NR Jr*, Zhu W, Sorensen L, Chan A, Lim C, Chen H, Zhang Q, Schultz P, Hayallah A, Thomas K, Famulok M, Zhang K, Ginsberg M, Li D. Slit2-Robo4 signalling promotes vascular stability by blocking Arf6 activity. Nature Cell Biology. 2009 Nov;11(11):1325-31.
- Jones C*, London NR Jr*, Chen H, Park K, Sauvaget D, Stockton R, Wythe J, Suh W, Larrieu-Lahargue F, Mukouyama Y, Lindblom P, Seth P, Frias A, Nishiya N, Ginsberg M., Gerhardt H, Zhang K, Li D. Robo4 stabilizes the vascular network by inhibiting pathological angiogenesis and endothelial hyperpermeability. Nature Medicine. 2008 Apr; 14(4):448-453.
*Indicates equal contribution to the work in this publication.