Updated March, 2013

Chief, Laboratory of Human Carcinogenesis
Chief of Molecular Genetics & Carcinogenesis Section

Biography:Dr. Curtis C. Harris received his BA degree from Kansas University and his MD from Kansas University School of Medicine. His clinical training in Internal Medicine was completed at the University of California at Los Angeles and the National Cancer Institute. He is the Chief of the Laboratory of Human Carcinogenesis and chief of its Molecular Genetics and Carcinogenesis Section. He also is Clinical Professor of Medicine and Oncology at Georgetown University School of Medicine.

The outstanding scientific contributions of Curtis C. Harris, M.D., to the fields of molecular carcinogenesis and molecular epidemiology of human cancer, has placed him at the international forefront. His research on environmental carcinogenesis, cancer risk factors and molecular genetics of human carcinogenesis, p53 and microRNA pathways, has significantly impacted the field of cancer risk assessment and our understanding of the molecular pathogenesis of human cancer.

Dr. Harris's Interview with Science Watch.

Dr. Harris's Interview at AACRNews

Click here to watch.

Dr. Harris's article about MicroRNAs.

Extended Biography:

Harris received his M.D. from Kansas University School of Medicine. He completed his clinical training in internal medicine at the University of California-Los Angeles, and at the NCI. He has held positions of increasing responsibility at the NCI, and is also a Clinical Professor of Medicine and Oncology at Georgetown University School of Medicine. Harris has received numerous honors throughout his distinguished career including the Alton Ochsner Award relating Smoking and Health (American College of Physicians), Deichmann Award (International Union of Toxicology), Charles Heidelberger Award (International Society of Gastroenterological Carcinogenesis) and the Distinguished Service Medal (the highest honor of the U.S. Public Health Service), NCI Outstanding Mentor Award, and the AACR-Princess Takamatsu Award. Harris has published more than 500 journal articles, 100 book chapters, and 10 books, and holds more than 25 patents owned by the U.S. Government. He also serves as Editor-in-Chief for the journal, Carcinogenesis, and has held or currently holds elected offices in scholarly societies and non-profit foundations including the American Association of Cancer Research, the International Society of Differentiations, the Keystone Symposia on Molecular and Cellular Biology and Aspen Cancer Conference. Harris has a wide range of scientific interests and accomplishments spanning molecular genetics of human cancer to molecular epidemiology of human cancer risk.


Our productive collaborations with intramural scientists and extramural investigators worldwide have led to significant discoveries and productivity (H-factor of more than 100; ISI Web of Science). In the last few years, we have published 36 papers in peer-reviewed journals, 6 invited reports/reviews (mostly peer reviewed), 4 book chapters, edited one book, and filed 7 patent applications for the U.S. Government. Harris served on the NCI-CCR Advisory Board and currently serves on the Steering Committee of the Center of Excellence in Integrative Cancer Biology and Genomics, CCR. He is the elected Chairman of the Board of Directors of two nonprofit foundations, the Keystone Symposia of Molecular and Cellular Biology and the Aspen Cancer Conference. Harris holds the position of Clinical Professor of Medicine (Oncology) at the Georgetown University School of Medicine and serves as Editor-in-Chief of the journal Carcinogenesis. Harris presented 5 keynote addresses and other invited presentations at national and international conferences. He received the NCI Outstanding Mentor Award in 2007 and the AACR-Princess Takamatsu Award in 2009.

Current Research Projects

Project 1: Molecular Epidemiology of Human Cancer and Clinical Biomarkers of Cancer Diagnosis, Prognosis, and Therapeutic Outcome. Gene-environment interaction is a seminal concept in the molecular epidemiology of human cancer. Our case-control (using hospital- and population-based controls) studies focus on lung cancer, a tobacco-related cancer, and colon, a cancer type more associated with chronic inflammation. These studies require the integration of data from genetic association studies, analysis of carcinogen exposure, rapidly developing technologies, bioinformatics, social-ethical concerns, and epidemiological study-design methods and the hypothesis, aims, and demographic characteristics of study subjects of multiple investigations. We also validate our results with independent cohorts, e.g., The NCI Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial, Mayo Clinic Never Smoker Lung Cancer cohort (P. Yang), Black Women Health Study (J. Palmer and L. Adams-Campbell), and Hong Kong Colon Cancer cohort (S.Y. Leung), and contribute data to the large multi-institutional International Lung Cancer Consortium, e.g., replication of susceptibility loci identified in Genome-Wide Association Studies. For example, we discovered from 2 independent cohorts that childhood exposure to secondhand smoke and a hyperactive innate immune system is associated with an increased the lung cancer risk in never smokers. Our studies have also provided genetic and biological evidence of racial health disparity of lung and colon cancer in African Americans: common genetic variations in TP53 are associated with increased lung cancer risk and poor prognosis; a less efficient G2/M cell cycle checkpoint is associated with increased lung cancer risk; and an increased risk and/or poor survival of colon cancer are associated with either specific microRNA expression or SNPs in the MBL2 gene. Cancer cases were also utilized to develop clinical biomarkers. For example, microRNAs and selected inflammatory cytokines were found to be diagnostic and prognostic biomarkers of human lung, esophageal, and colon cancer in their early TNM stages. Some of these biomarkers are also associated with therapeutic outcome. We continue to focus on tobacco-related cancer, inflammation-associated cancer, and cancer-related health disparities.

Project 2: p53 and Cancer. The p53 pathway is an intrinsic monitor and response pathway of telomeric attrition involved in cellular aging and senescence. Cellular senescence is a tumor suppressive mechanism that can be activated by p53 in cancer cells. We are currently studying the molecular mechanisms of cellular senescence in normal human cells and the role of the telometric multiprotein complex, shelterin, that includes TRF2 and POT1 in aging and carcinogenesis. We are focussed on the integrative p53 microRNA pathways in tumor suppression.

Project 3: Inflammation and Cancer. Chronic inflammation can increase cancer risk. We are investigating the interaction between nitric oxide (NO*) and p53 as a crucial pathway in inflammatory-mediated carcinogenesis. We have shown that NO* induces ATM- and ATR-dependent p53 posttranslational modifications leading to a p53 stress response in human cells in vitro, in an admixture of activated macrophages and human cells in vitro, and in colon tissue from patients with ulcerative colitis or Crohn's, both of which are cancer prone, chronic inflammatory diseases. Furthermore, NO* can suppress or enhance tumorigenesis in an animal model of the Li- Fraumeni Syndrome, depending on NO* concentration.

Selected Recent References
( with PubMed hyperlinks )

1. Okayama, H., Saito, M., Oue, N., Weiss, J. M., Stauffer, J., Takenoshita, S., Wiltrout, R. H., Hussain, S. P. and Harris, C. C.: NOS2 enhances KRAS-iduced lung carcinogenesis, inflammation and microRNA-21 expression. Int J. Cancer, 132: 9-18, 2013.

2. Nguyen, G. H., Dexheimer, T. S., Rosenthal, A. S., Chu, W. K., Singh, D. K., Mosedale, G., Bachrati, C. Z., Schultz, L., Sakurai, M., Savitsky, P., Abu, M., McHugh, P. J., Bohr, V. A., Harris, C. C., Jadhav, A., Gileadi, O., Maloney, D. J., Simeonov, A. and Hickson, I. D.: A Small Molecule Inhibitor of the BLM Helicase Modulates Chromosome Stability in Human Cells. Chem Biol., 20: 55-62, 2013.

3. Cui, X., Witalison, E. E., Chumanevich, A. P., Chumanevich, A. A., Poudyal, D., Subramanian, V., Schetter, A. J., Harris, C. C., Thompson, P. R. and Hofseth, L. J.: The induction of microRNA-16 in colon cancer cells by protein arginine deiminase inhibition causes a p53-dependent cell cycle arrest. PLoS One, 8: e53791, 2013.

4. Weng, M. T., Lee, J. H., Wei, S. C., Li, Q., Shahamatdar, S., Hsu, D., Schetter, A. J., Swatkoski, S., Mannan, P., Garfield, S., Gucek, M., Kim, M. K. H., Annunziata, C. M., Creighton, C. J., Emanuele, M. J., Harris, C. C., Sheu, J. C., Giaccone, G. and Luo, J.: The evolutionarily conserved protein ERH controls CENP-E mRNA splicing and is required for the survival of KRAS mutant cancer cells. Proc. Natl. Acad. Science, 109: E3659-67, 2012.

5. Sohn, J. J., Schetter, A. J., Yfantis, H. G., Ridnour, L. A., Khan, M. A., Robles, A. I., Hussain, S. P., Goto, A., Bowman, E. D., Hofseth, L. J., Bartkova, J., Bartek, J., Wogan, G. N., Wink, D. A. and Harris, C. C.: Macrophages, nitric oxide and microRNAs are associated with DNA damage response pathway and senescence in inflammatory bowel disease. PLoS One, 7: e44156, 2012.

6. Tang, Y., Horikawa, I., Ajiro, M., Robles, A. I., Fujita, K., Mondal, A. M., Stauffer, J. K., Zheng, Z. M. and Harris, C. C.: Downregulation of splicing factor SRSF3 induces p53_, an alternatively spliced isoform of p53 that promotes cellular senescence. Oncogene. 2012 July 9 [Epub ahead of print].

E-mail address: Curtis_Harris@nih.gov

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