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Carter Van Waes, M.D., Ph.D.

Photo of Dr. Carter Van Waes

Chief, Head and Neck Surgery Branch

Clinical Director, NIDCD, NIH

Building 10, CRC Room 4-2732
9000 Rockville Pike
Bethesda, MD 20892
Phone: (301) 402-4216
Fax: (301) 402-1140

Ph.D., University of Chicago, 1985
M.D., University of Chicago, 1987
Otolaryngology, Head and Neck Surgery residency, University of Michigan, 1993

Research Statement

The Head and Neck Surgery Branch (HNSB) includes the Tumor Biology Section (TBS) and Clinical Genomics Unit (CGU), which conduct laboratory clinical studies and trials concerning the pathogenesis, prevention, diagnosis, and treatment of head and neck neoplasms that affect human communication. Head and neck squamous cell carcinoma (HNSCC) is the most prevalent malignancy involving the upper aerodigestive tract which affects voice, speech, taste, smell, hearing, and balance as well as survival. More than 42,000 Americans develop neoplasms of the upper aerodigestive tract each year, and approximately 320,000 Americans currently suffer significant impairment of communication and other disability as a result of tumor destruction or ablative surgical and radiation therapy. Despite therapy, more than 8,000 of these patients die annually in the U.S. New modalities for prevention and therapy are needed in order to improve survival and preservation of function.

Dr. Carter Van Waes with lab personnel
Dr. Van Waes with Medical Research Scholars
Program students Danielle Eytan and Suresh
Mohan in the Clinical Genomics Unit.

Dr. Carter Van Waes's lab personnel
Anthony Saleh, research fellow, presenting his
work on microRNAs in head and neck cancer
at a conference.

Dr. Carter Van Waes's lab personnel
Howard Hughes Scholar Carol Yan presents her
poster on kinase CK2 and transcription factor
p73 in cancer stem cells at a conference.

Current Areas of Interest

Genomics of Head and Neck Cancer

A major current focus of the HNSB is to identify and determine the function of genomic alterations in head and neck cancers. We have collaborated with the Cancer Genome Atlas Network to complete a comprehensive genomic analysis of HNSCC, and multi-platform analysis across 12 cancer types, which are currently submitted. Additionally, we are completing structural and functional genomic studies of HNSCC lines using genome wide exome, RNA, and RNAi screening, and using genetically engineered mouse models of HNSCC to establish the function of genomic and molecular alterations. These studies have identified key genomic drivers of signal pathway and transcription factor networks previously discovered by our and other laboratories, which will enable investigation of new molecularly targeted agents for therapy and prevention.

Signal Transcription Factors in Head and Neck Cancer

A major hypothesis and focus of the HNSB has been to identify and determine the mechanisms of activation of key signal activated transcription factors responsible for altered gene and protein expression and molecular pathogenesis that may serve as molecular targets for prevention and therapy of HNSCC. Our laboratory discovered that transcription factor Nuclear Factor-kappaB, initially identified as a transient activator of genes in response to injury and infection, is aberrantly turned on in HNSCC (Ondrey, Mol Carcinogenesis, 1999). NF-kappaB was found to be a key regulator of cancer cell survival and the multiple cytokines and factors that promote inflammation, angiogenesis, and tumorigenesis (Duffey, Cancer Res, 1999; Dong, Cancer Res, 1999). Using microarray gene expression profiling, we further showed that as many as ~60 percent of the genes abnormally expressed in murine and human SCC are NF-kappaB regulated genes, and their expression and the malignant phenotype may be reverted by inhibition of NF-kappaB (Dong Cancer Res, 2001; Loercher, Cancer Res, 2004; Yan, Genome Biology, 2007; Lee, Clin Cancer Res, 2007).

We have further demonstrated that NF-kappaB is part of a network of injury signal transcription factors altered in HNSCC. NF-kappaB contributes to activation of other prosurvival pathways and genes, such as IL-6-mediated STAT3 activation, and inhibition of pro-death pathways, notably tumor suppressor p53 (Hong, FASEB J., 2000; Friedman, Clin Cancer Res, 2007; Lee, Int J Cancer, 2008; Yan, Genome Biol, 2008). Through a collaboration with Dr. Wendy Weinberg of the U.S. Food and Drug Administration, a novel interaction between NF-kappaB subunits cREL, and TP53 family members deltaNp63 and TAp73 in deregulating key growth arrest cell death genes important in cancer has been discovered (King, Cancer Res, 2008; Lu, Cancer Res, 2011). RELA, and TP53 family member deltaNp63 also co-activate a repertoire of NF-kB inducible cytokine, growth factor, cell adhesion, and prosurvival genes important in pathogenesis of HNSCC and other cancers (Yang, Cancer Res, 2011). A current focus is to determine the activation and functional role of the alternative IKK-NF-kB pathway in HNSCC.

Molecular Targeted Therapy

The HNSB showed that inhibitors of PI3K signaling block NF-kB activation, cell proliferation, and angiogenic cytokine expression (Bancroft, Int J Cancer, 2002). Subsequent studies by other investigators have implicated PI3K downstream signaling via mTOR and IKK in NF-kB activation. A study of rapamycin targeting mTOR prior to surgery was recently completed and undergoing follow-up and analysis. Prior clinical studies revealed limited activity of agents targeting EGFR and proteasome mediated activation of NF-kB (Van Waes, Int J Rad Oncol Biol Phys, 2010; Argiris, Clin Can Res, 2011; Gilbert, Head Neck, 2013). Preclinical studies of new agents targeting a combination of genetic drivers and pathways uncovered by our previous studies and by the TCGA are underway.

Lab Personnel

Head and Neck Surgery Branch

Zhong Chen, M.D., Ph.D., staff scientist, Clinical Genomics (Send email)
Xinping Yang, biologist (Send email)
Anthony Saleh, contract scientist (Send email)
Hui Cheng, post-doctoral visiting fellow (Send email)
Tony Chen, post-doctoral IRTA fellow (Send email)
Paul Clavijo, post-doctoral IRTA fellow (Send email)
ZhengBo Hu, pre-doctoral visiting fellow (Send email)
Ru Wang, pre-doctoral visiting fellow (Send email)
Sophie Carlson, technical IRTA (Send email)
Rita Das, technical IRTA (Send email)
Jianhong Chen, special volunteer (Send email)
Adeeb Derakhshan, medical research scholar program (Send email)

Office of the Clinical Director

Clint Allen, collaborator (clinical) (Send email)
Nicole Schmitt, collaborator (clinical) (Send email)
David Bianchi, staff clinician (Send email)
Brian Driscoll, staff clinician (Send email)
Kenneth Hauck, staff clinician (Send email)
Hung Kim, staff clinician (Send email)
Wojchiech Mydlarz, staff clinician (Send email)
Susannah Wargo, research nurse practitioner (Send email)
Regal Cameron, intramural office manager (Send email)  

Clinical Trials Recruitment

Patients with Recurrent Head and Neck Cancer

Screening Protocol for Head and Neck Surgery Branch Protocols (01-DC-0099)

For information about eligibility, contact:
Susannah Wargo, RN, Ph.D., CRNP
Phone: 301-496-4887

Employment Opportunities

For information about employment opportunities, contact:

Carter Van Waes
Chief, Head and Neck Surgery Branch
Clinical Director, NIDCD
Building 10, CRC Room 4-2732
9000 Rockville Pike
Bethesda, MD 20892
Phone: (301) 402-4216
Fax: (301) 402-1140

Selected Publications