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Laundette  Jones

Laundette Jones Ph.D.

Academic Title: Assistant Professor
Primary Appointment: Epidemiology & Public Health
Secondary Appointments: Pharmacology
Location: HH, Rm. 119
Phone: (410) 706-7331
Fax: (410) 706-0032
Lab: (410) 706-7335

Personal History:

Dr. Laundette Jones received her B.S. in Chemistry from Morgan State University in 1992 and then received her doctorate in the Department of Environmental Health Sciences, Division of Toxicological Sciences at the Johns Hopkins Bloomberg School of Public Health in May 2000.

After graduating from Hopkins, Dr. Jones spent a year as a postdoctoral fellow in the Laboratory of Experimental Carcinogenesis at the National Cancer Institute, National Institutes of Health where she analyzed the molecular mechanisms of mammary gland genotoxicity and carcinogencity of food derived heterocyclic amines. She completed a second postdoctoral fellowship at the Georgetown University, Lombardi Cancer Center where she investigated the role of the Breast Cancer Susceptibility 1 (BRCA1) gene in breast cancer development.

Dr. Jones was selected as a NIH BIRCWH (Building Interdisciplinary Research Careers in Women's Health) Scholar by the Women's Health Research Group at the University of Maryland and joined the faculty as a member of the Department of Pharmacology and Experimental Therapeutics in July 2005.

Research Interests:


  • Genetic and environmental modifiers of breast cancer risk
  • Biomarker Discovery
  • Mechanisms of chemical carcinogenesis
  • Environmental Toxicology


It is known that breast cancer originates in mammary epithelial cells (MEC) as a result of multiple genetic alterations, however these genetic alterations alone cannot explain the multistep nature of tumorigenesis and the diverse breast cancer subtypes observed in women. The projects in my lab are driven by the hypothesis that certain cell types in the microenvironment surrounding the mammary epithelium are key regulators in the conversion from a normal to a cancerous cell. We are utilizing preclinical mouse models of breast cancer and creating new in vitro culture models that effectively reproduce the breast tissue microenvironment to study how alterations in an individual's genes and/or exposure to environmental chemicals impact the ultimate fate of whether a MEC develops normally or turns cancerous. Experiments in our research program work together towards a common goal: To translate our mechanistic basic research to the clinic by identifying novel biomarkers for the early diagnosis of breast cancer that could yield new targets to block tumor progression.

Current research projects in my lab focus on these three questions:

  1. What are the molecular and cellular mechanisms that determine how certain genetic variations and/or exposure to environmental chemicals impact the ultimate fate of whether a mammary epithelial cell develops normally or turns cancerous?
  2. How can we develop sensitive comprehensive biomarker assays for the early diagnosis of breast cancer that accommodate genetically diverse human populations?
  3. Which physiological biomarkers can accurately predict breast cancer risk from exposures to environmental chemicals?

Lab Techniques and Equipment:

  • Experimental Model Systems: Transgenic mouse models of breast cancer; Mammary gland whole organ culture; novel cell culture models of the breast
  • DNA/RNA analysis: Polymerase Chain Reaction (PCR), QPCR, Microarray
  • Protein expression analysis: Immunohistochemistry/immunofluorescence, western blot, ELISA


Knight, L.P., Primiano, T., Groopman, J.D., Kensler, T.W., and Sutter, T.R. (1999) cDNA cloning, expression and activity of a second human aflatoxin B1 metabolizing member of the aldo keto reductase superfamily, AKR7A3. Carcinogenesis, 20,1215 1223.

Snyderwine, E.G., Yoon, H.S., Knight-Jones, L.P., Tran, M., Schut, H.A., Yu, M. (2003) Mutagenesis and DNA adduct formation in the mouse mammary gland exposed to 2-hydroxyamino-1-methyl-6-phenylimidazo-[4,5-b]pyridine in whole organ culture. Mutagenesis, 18, 7-12.

Snyderwine, E.G., Yu, M, Schut, H.A., Knight-Jones, L., and Kimura S. Links. (2002) Effect of CYP1A2 deficiency on heterocyclic amine DNA adduct levels in mice. Food Chem Toxicol. 40, 1529-1533.

Frech, M.S.*, Jones, L.P.*, and Furth P.A. (2005) Validation of transgenic models of breast cancer: Ductal Carcinoma In Situ (DCIS) and Brca1 mutation related breast cancer. Breast Cancer Online, Vol. 8, Issue 8.(*Equal contribution).

Jones, L.P., Li, M., Halama, E., Ma, Y., Lubet, R., Grubbs, C.J., Deng, C-X, Rosen, E., Furth, P.A. (2005) Promotion of mammary cancer development by tamoxifen in a mouse model of Brca1-mutation related breast cancer. Oncogene 24: 3554-3562. 

Ma, Y, Katiyar, P, Jones, LP, Fan, S, Zhang, Y, Furth, PA and Rosen, EM. (2006) The Breast Cancer Susceptibility Gene BRCA1 Regulates Progesterone Receptor Signaling in Mammary Epithelial Cells. Molecular Endocrinology, 20:14-34.

Herschkowitx, JI, Simin, K, Weigman, VJ, Mikaelian, I, Usary, J, Hu, Z, Rasmussen, KE, Jones, LP, Assfnia, S, Chandrasekharan, S., Backlund, MG, Yin, Y., Khramtsov, AI, Bastein, R, Quac,enbush, J, Glazer, RI, Brown, PH, Green, JE, Kopelovich, L., Furth, PA, Palazzo, JP, Olopade, OI, Bernard, PS, Churchhill, GA, Dyke, TV, and Perou, CM. (2007) Identification of conserved gene expression features between murine mammary carcinoma models and human breast tumors. Genome Biology, 8:R76.

Tilli, M.T., Parrish, A.R., Cotarla, I., Jones, L.P. Johnson, M. and Furth, PA. (2008) Comparison of mammary gland imaging techniques and applications: reflectance confocal microscopy, GFP imaging, and ultrasound. BMC Cancer. 8:21.

Bodreddigari, S*, Jones, L*, Egner, P, Groopman, J, Sutter, C, Roebuck,B, Guengerich, F., Kensler, T, and Sutter, T. (2008) Protection Against Aflatoxin B1-induced Cytotoxicity by Expression of the Cloned Aflatoxin B1-aldehyde Reductases Rat AKR7A1 and Human AKR7A3. Chem Res Toxicol. 21:1134-42 (*Equal contribution).

Jones, L. P., Tilli, M.T., Assefnia, S., Torre, K., Halama, E, Parrish, A., Rosen, E. M., Furth, P. (2008) Activation of estrogen signaling pathways collaborates with loss of Brca1 to promote development of ERa negative and ERa positive mammary preneoplasia and cancer. Oncogene. 27:794-802.

Jones, LP, Sampson, A, Kang, HJ, Kim, HJ, Yi, YW, Kwon, SY, Babus, JK, Bae, I., (2010) Loss of BRCA1 leads to an increase sensitivity to Bisphenol A. Toxicology Letters, 199:261-268.

Jones, LP, Stefansson, S, Kim, M, Ahn, SN. (2011) Comparison of Radioimmuno and Carbon Nanotube Field-Effect Transistor Assays for Measuring Insulin-Like Growth Factor-1 in a Preclinical Model of Human Breast Cancer. J. Nanobiotechnology, 9:36.

Jones LP, Buelto D, Tago E, Owusu-Boaitey K. (2011) Abnormal mammary adipose tissue environment of Brca1 mutant mice show a persistent deposition of highly vascularized multilocular adipocytes. Journal of Cancer Science & Therapy.

Cao Q, Hersl J, La H, Smith M, Jenkins J, Goloubeva O, Vasken Dilsizian,Tkaczuk  K, Chen W, Jones L.  (2014) A Pilot Study of FDG PET/CT Detects a Link Between Brown Adipose Tissue and Breast Cancer.  BMC Cancer. 2014;14:126.   doi:10.1186/1471-2407-14-126