Chengcheng Hu

Chengcheng Hu

Director, Biostatistics - Phoenix Campus
Professor, Public Health
Professor, Statistics-GIDP
Professor, BIO5 Institute
Primary Department
Department Affiliations
Contact
(520) 626-9308

Work Summary

Chengcheng Hu has worked on a broad range of areas including cancer, occupational health, HIV/AIDS, and aging. He has extensive collaborative research in conducting methodological research in the areas of survival analysis, longitudinal data, high-dimensional data, and measurement error. His current methodological interest, arising from studies of viral and human genetics and biomarkers, is to develop innovative methods to investigate the relationship between high-dimensional information and longitudinal outcomes or survival endpoints.

Research Interest

Chengcheng Hu, Ph.D., is an Associate Professor, Public Health and Director, Biostatistics, Phoenix campus at the Mel and Enid Zuckerman College of Public Health, University of Arizona. He is also Director of the Biometry Core on the Chemoprevention of Skin Cancer Project at the University of Arizona Cancer Center. Hu has worked on multiple federal grants in a broad range of areas including cancer, occupational health, HIV/AIDS, and aging. In addition to extensive experience in collaborative research, he has conducted methodological research in the areas of survival analysis, longitudinal data, high-dimensional data, and measurement error. His current methodological interest, arising from studies of viral and human genetics and biomarkers, is to develop innovative methods to investigate the relationship between high-dimensional information and longitudinal outcomes or survival endpoints. Hu joined the UA Mel and Enid Zuckerman College of Public Health in 2008. Prior to this he was an assistant professor of Biostatistics at the Harvard School of Public Health from 2002 to 2008. While at Harvard, he also served as senior statistician in the Pediatric AIDS Clinical Trials Group (PACTG) and the International Maternal Pediatric Adolescent AIDS Clinical Trials Group (IMPAACT). Hu received his Ph.D. and M.S. in Biostatistics from the University of Washington and a M.A. in Mathematics from the Johns Hopkins University.

Publications

Griffin, S. C., Bui, D. P., Gowrisankaran, G., Lutz, E. A., He, C., Hu, C., & Burgess, J. L. (2017). Risk Management Interventions to Reduce Injuries and Maximize Economic Benefits in U.S. Mining. Journal of occupational and environmental medicine.

Risk management (RM) is a cyclical process of identifying and ranking risks, implementing controls, and evaluating their effectiveness. This study aims to identify effective RM interventions in the U.S. mining industry.

Bobrow, B. J., Spaite, D. W., Vadeboncoeur, T. F., Hu, C., Mullins, T., Tormala, W., Dameff, C., Gallagher, J., Smith, G., & Panczyk, M. (2016). Implementation of a Regional Telephone Cardiopulmonary Resuscitation Program and Outcomes After Out-of-Hospital Cardiac Arrest. JAMA cardiology, 1(3), 294-302.

Bystander cardiopulmonary resuscitation (CPR) significantly improves survival from out-of-hospital cardiac arrest but is provided in less than half of events on average. Telephone CPR (TCPR) can significantly increase bystander CPR rates and improve clinical outcomes.

Diep, C. H., Zucker, K. M., Hostetter, G., Watanabe, A., Hu, C., Munoz, R. M., Von Hoff, D. D., & Han, H. (2012). Down-regulation of Yes Associated Protein 1 expression reduces cell proliferation and clonogenicity of pancreatic cancer cells. PloS one, 7(3), e32783.

The Hippo pathway regulates organ size by inhibiting cell proliferation and promoting cell apoptosis upon its activation. The Yes Associated Protein 1 (YAP1) is a nuclear effector of the Hippo pathway that promotes cell growth as a transcription co-activator. In human cancer, the YAP1 gene was reported as amplified and over-expressed in several tumor types.

Jacobson, S. A., Morshed, T., Dugger, B. N., Beach, T. G., Hentz, J. G., Adler, C. H., Shill, H. A., Sabbagh, M. N., Belden, C. M., Sue, L. I., Caviness, J. N., & Hu, C. (2014). Plaques and tangles as well as Lewy-type alpha synucleinopathy are associated with formed visual hallucinations. Parkinsonism & related disorders, 20(9), 1009-14.

Previous research has linked complex or formed visual hallucinations (VH) to Lewy-type alpha-synucleinopathy (LTS) in neocortical and limbic areas. As Alzheimer's disease pathology often co-occurs with LTS, we questioned whether this pathology - amyloid plaques and neurofibrillary tangles - might also be linked to VH.

LeRoy, E. C., Moore, J. H., Hu, C., Martínez, M. E., Lance, P., Duggan, D., & Thompson, P. A. (2011). Genes in the insulin and insulin-like growth factor pathway and odds of metachronous colorectal neoplasia. Human genetics, 129(5), 503-12.

Insulin and insulin-like growth factor (IGF) genes are implicated in colorectal carcinogenesis. Gene-by-gene interactions that influence the insulin/IGF pathways were hypothesized as modifiers of colorectal neoplasia risk. We built a classification tree to detect interactions in 18 IGF and insulin pathway-related genes and metachronous colorectal neoplasia among 1,439 subjects pooled from two chemoprevention trials. The probability of colorectal neoplasia was greatest (71.8%) among carriers of any A allele for rs7166348 (IGF1R) and AA genotype for rs1823023 (PIK3R1). In contrast, carriers of any A at rs7166348 (IGF1R), any G for the PIK3R1 variant, and AA for rs10426094 (INSR) had the lowest probability (14.3%). Logistic regression modeling showed that any A at rs7166348 (IGF1R) with the AA genotype at rs1823023 (PIK3R1) conferred the highest odds of colorectal neoplasia (OR 3.7; 95% CI 2.2-6.5), compared with carriage of GG at rs7166348 (IGF1R). Conversely, any A at rs7166348 (IGFR1), any G allele at rs1823023 (PIK3R1), and the AA genotype at rs10426094 (INSR) conferred the lowest odds (OR 0.22; 95% CI 0.07-0.66). Stratifying the analysis by parent study and intervention arm showed highly consistent trends in direction and magnitude of associations, with preliminary evidence of genotype effects on measured IGF-1 levels in a subgroup of subjects. These results were compared to those from multifactor dimensionality reduction, which identified different single nucleotide polymorphisms in the same genes (INSR and IGF1R) as effect modifiers for colorectal neoplasia. These results support a role for genetic interactions in the insulin/IGF pathway genes in colorectal neoplasia risk.