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Mark Cannon, M.D., Ph.D.
Assistant Professor
Department of Medicine
Johns Hopkins School of Medicine, M.D. 1993
University College, London, Ph.D. 2007
canno101@umn.edu
612-624-8048 office
612-626-2527 lab
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Research Interests:
Viral Tumorigenesis
The Cannon lab studies how Kaposi’s sarcoma-associated
herpesvirus (KSHV) causes Kaposi’s sarcoma (KS) and
other hyperproliferative diseases. KS is among the most common
AIDS-related tumors and is the most common cancer in large
parts of Africa. Our focus is the KSHV encoded chemokine receptor
(vGPCR). vGPCR has the ability to affect several aspects of
KS development including cell proliferation, angiogenesis,
and the inflammatory component associated with early KS lesions.
vGPCR does this through its broad and constitutive signaling.
Our goal is to identify how vGPCR deregulates normal host
cell signaling pathways and to target them as part of an anti-vGPCR
and ultimately an anti-KSHV therapeutic approach. In collaboration
with the Bohjanen lab we are also investigating the effects
of vGPCR signaling on mRNA stability. Our lab also has an
interest in developing viral gene therapy vectors to specifically
target KSHV- and EBV-mediated malignancies.
Selected Recent Publications:
- Bottero, V. ,Sharma-Walia, N., Kerur, N., Paul, A., Sadagopan,
S., Cannon, M., Chandran, B. 2009. Kaposi Sarcoma-associated
herpes virus (KSHV) G protein-coupled receptor (vGPCR) activates
the ORF50 lytic switch promoter: A potential positive feedback
loop for sustained ORF50 gene expression. Virology,
in press
- Daniel Di Bartolo, Mark Cannon, Yi-Fang Liu, Rolf Renne,
Amy Chadburn, Chris Boshoff, and Ethel Cesarman. 2008. KSHV
LANA inhibits TGF-beta signaling through epigenetic silencing
of the TGF-beta type II receptor. Blood
111(9): 4731-40.
- Richard J. Vart, Leonid L. Nikitenko, Dimitrios Lagos,
Matthew W. B. Trotter, Mark Cannon, Dimitra Bourboulia,
Fiona Gratrix, Yasuhiro Takeuchi, Chris Boshoff. 2007.
Kaposi’s Sarcoma-associated Herpesvirus encoded IL6
and GPCR Regulate Angiopoietin-2 Expression in Lymphatic
Endothelial Cells. Cancer
Research 67(9):4042-51.
- Cannon, M., Cesarman, E., Boshoff, C. 2006. The KSHV
G protein-coupled receptor inhibits lytic gene transcription
in primary effusion lymphoma cells via a p21-mediated inhibition
of Cdk2. Blood
107(1), 277-284.
- Cannon, M. & Cesarman, E. 2004. The KSHV G protein-coupled
receptor signals via multiple pathways to induce transcription
factor activation in primary effusion lymphoma cells. Oncogene
23(2), 514-523.
- Tyson V. Sharp, Fernando Munoz, Dimitra Bourboulia, Nadege
Presneau, Eva Darai, Hsei-Wei Wang, Mark Cannon, David N.
Butcher, Andrew G. Nicholson, George Klein, Stephan Imreh,
and Chris Boshoff. 2004. LIM domains-containing
protein 1 (LIMD1), a tumor suppressor encoded at chromosome
3p21.3, binds pRB and represses E2F-driven transcription
PNAS
101, 16531-16536.
- Cannon, M., Philpott, N. J. & Cesarman, E. 2003. The
Kaposi's Sarcoma-Associated Herpesvirus G Protein-Coupled
Receptor Has Broad Signaling Effects in Primary Effusion
Lymphoma Cells. J
Virol 77:57-67.
Last modified on: August 11, 2009 |