Jia-Long Fang Ph.D.

Research Biologist — Division of Biochemical Toxicology

Jia-Long Fang, Ph.D.
(870) 543-7121
NCTRResearch@fda.hhs.gov

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Background

Jia-Long Fang received a bachelor’s degree in public health in 1985 from Shanghai Medical University, one of the most prestigious medical universities in China, and a master’s degree in toxicology in 1990 from Chinese Academy of Preventive Medicine, one of the top institutes for health research in China. In 1997, Dr. Fang received a Ph.D. in Molecular Epidemiology from the renowned Karolinska Institute in Stockholm, Sweden. He joined NCTR as an ORISE Postdoctoral Fellow in 1997 and rejoined NCTR as a Staff Fellow in 2004. He was converted to a Research Biologist in 2010.

Research Interests

Dr. Fang has over twenty years of research experience in biochemical carcinogenesis and toxicology. He has designed, developed, and executed in vitro and in vivo research studies that address the biological mechanisms underlying the toxicities of drugs and chemicals. Throughout his career at NCTR, Dr. Fang’s research has been focused on the biological mechanisms of action underlying the toxicity of chemicals regulated by ─ or of interest to ─ FDA. Some of these chemicals are ethanol, urethane, tolvaptan, and antiretroviral drugs, including zidovudine, lamivudine, and nevirapine. More recently, Dr. Fang has been leading a research team to investigate the toxicities of topically applied triclosan.

Professional Societies/National and International Groups

Society of Toxicology
Full member
2009 – Present

Selected Publications

Absorption and Metabolism of Triclosan After Application to the Skin of B6C3F1 Mice.
Fang J., Vanlandingham M., Gamboa da Costa G., and Beland F.
Environ Toxicol. 2016, 31(5):609-23.

Human Sulfotransferases Enhance the Cytotoxicity of Tolvaptan.
Fang J., Wu Y., Gamboa da Costa G., Chen S., Chitranshi P. and Beland F.
Toxicol Sci. 2016, 150(1):27-39.

Effect of Triclosan,Triclocarban, 2,2',4,4'-Tetrabromodiphenyl Ether, and Bisphenol A on the Iodide Uptake, Thyroid Peroxidase Activity, and Expression of Genes Involved in Thyroid Hormone Synthesis.
Wu Y., Beland F., and Fang J.
Toxicol In Vitro. 2016, 32:310-19.

Mechanisms of Tolvaptan-Induced Toxicity in HepG2 Cells.
Wu Y., Beland F., Chen S., Liu F., Guo L., and Fang J.
Biochem Pharmacol. 2015 Jun 15, 95(4):324-36.

Dose-Response Assessment of the Dermal Toxicity of Triclosan in B6C3F1 Mice.
Fang J., Vanlandingham M., Juliar B., Olson G., Patton R., and Beland F.
Toxicol. Res. 2015, 4:867-77.

Differential Effects of Triclosan on the Activation of Mouse and Human Peroxisome Proliferator-Activated Receptor Alpha.
Wu Y., Wu Q., Beland F., Ge P., Manjanatha M., and Fang J.
Toxicol Lett. 2014, 231(1):17-28.

Extracellular Signal-Regulated Kinases 1/2 and Akt Contribute to Triclosan-Stimulated Proliferation of JB6 Cl 41-5a Cells.
Wu Y., Beland F., Chen S., and Fang J.
Arch Toxicol. 2015, 89(8):1297-311.

Differential Gene Expression in Human Hepatocyte Cell Lines Exposed to the Antiretroviral Agent Zidovudine.
Fang J., Han T., Wu Q., Beland F., Chang C., Guo L., and Fuscoe J.
Arch Toxicol. 2014, 88(3):609-23.

Differential Responses of Human Hepatocytes to the Non-Nucleoside HIV-1 Reverse Transcriptase Inhibitor Nevirapine.
Fang J. and Beland F.
J Toxicol Sci. 2013, 38(5):741-52.

XPC is Essential for Nucleotide Excision Repair of Zidovudine-Induced DNA Damage in Human Hepatoma Cells.
Wu Q., Beland F., Chang C., and Fang J.
Toxicol Appl Pharmacol. 2011, 251(2):155-62.

Occurrence, Efficacy, Metabolism, and Toxicity of Triclosan.
Fang J., Stingley R., Beland F., Harrouk W., Lumpkins D., and Howard P.
J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2010, 28(3):147-71.

Long-term Exposure to Zidovudine Delays Cell Cycle Progression, Induces Apoptosis, and Decreases Telomerase Activity in Human Hepatocytes.
Fang J. and Beland F.
Toxicol Sci. 2009, 111(1):120-30.

Interference of Cell Cycle Progression by Zidovudine and Lamivudine in NIH 3T3 Cells.
Fang J., McGarrity L., and Beland F.
Mutagenesis. 2009, 24(2):133-41.

Correlation Between the UDP-Glucuronosyltransferase (UGT1A1) TATAA Box Polymorphism and Carcinogen Detoxification Phenotype: Significantly Decreased Glucuronidating Activity Against Benzo(a)pyrene-7,8-Dihydrodiol(-) in Liver Microsomes From Subjects with the UGT1A1*28 Variant.
Fang J. and Lazarus P.
Cancer Epidemiol Biomarkers Prev. 2004, 13(1):102-9.

Characterization of Benzo(a)pyrene-Trans-7,8-Dihydrodiol Glucuronidation by Human Tissue Microsomes and Overexpressed UDP-Glucuronosyltransferase Enzymes.
Fang J., Beland F., Doerge D., Wiener D., Guillemette C., Marques M. and Lazarus P.
Cancer Res. 2002 Apr 1;62(7):1978-86. Erratum in: Cancer Res. 2002, 62(11):3328.

Detection of DNA Adducts of Acetaldehyde in Peripheral White Blood Cells of Alcohol Abusers.
Fang J. and Vaca C.
Carcinogenesis. 1997, 18(4):627-32.

Lab Member

Yufeng Wu, Ph.D.
Staff Fellow
(870) 543-7121
NCTRResearch@fda.hhs.gov

Contact Information: Jia-Long Fang; (870) 543-7121

Expertise: Expertise

Approach

Domain

Technology & Discipline

Toxicology